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Sample records for overt heart failure

  1. Heart Failure

    MedlinePLUS

    ... version of this page please turn Javascript on. Heart Failure What is Heart Failure? In heart failure, the heart cannot pump ... the lungs, where it picks up oxygen. The Heart's Pumping Action In normal hearts, blood vessels called ...

  2. Heart Failure

    MedlinePLUS

    ... page from the NHLBI on Twitter. What Is Heart Failure? Heart failure is a condition in which the heart can' ... force. Some people have both problems. The term "heart failure" doesn't mean that your heart has stopped ...

  3. Heart Failure

    MedlinePLUS

    Heart failure is a condition in which the heart can't pump enough blood to meet the body's needs. Heart failure does not mean that your heart has stopped ... Tiredness and shortness of breath Common causes of heart failure are coronary artery disease, high blood pressure and ...

  4. Heart Failure

    MedlinePLUS

    ... this? Submit What's this? Submit Button Related CDC Web Sites Heart Disease Stroke High Blood Pressure Salt ... to Prevent and Control Chronic Diseases Million Hearts® Web Sites with More Information About Heart Failure For ...

  5. Types of Heart Failure

    MedlinePLUS

    ... Blood Pressure Tools & Resources Stroke More Types of Heart Failure Updated:Mar 23,2016 Left-sided heart failure ... content was last reviewed on 04/06/2015. Heart Failure • Home • About Heart Failure Introduction Types of Heart ...

  6. Heart failure - medicines

    MedlinePLUS

    CHF - medicines; Congestive heart failure - medicines; Cardiomyopathy - medicines; HF - medicines ... You will need to take most of your heart failure medicines every day. Some medicines are taken ...

  7. Heart Failure

    MedlinePLUS

    ... tests: Blood tests Urine tests Chest X-ray Electrocardiogram (also called EKG or ECG) Echocardiogram Radionuclide ventriculography An electrocardiogram records the electrical activity of your heart. It ...

  8. Advanced Heart Failure

    MedlinePLUS

    ... High Blood Pressure Tools & Resources Stroke More Advanced Heart Failure Updated:Oct 8,2015 When heart failure (HF) ... content was last reviewed on 04/06/2015. Heart Failure • Home • About Heart Failure • Causes and Risks for ...

  9. Classes of Heart Failure

    MedlinePLUS

    ... Blood Pressure Tools & Resources Stroke More Classes of Heart Failure Updated:Sep 30,2015 Doctors usually classify patients' ... content was last reviewed on 04/06/2015. Heart Failure Questions to Ask Your Doctor Use these questions ...

  10. Heart failure - home monitoring

    MedlinePLUS

    ... body and the symptoms that tell you your heart failure is getting worse will help you stay healthier ... Januzi JL, Mann DL. Clinical assessment of heart failure. In: ... of Cardiovascular Medicine . 10th ed. Philadelphia, PA: Elsevier ...

  11. Antithrombotics in heart failure.

    PubMed

    Mili?i?, Davor; Samardi?, Jure; Petri?evi?, Mate

    2014-12-01

    Heart failure is a common clinical condition associated with high morbidity and mortality rate despite significant improvements in pharmacotherapy and implementation of medical procedures. Patients with heart failure are at an increased risk of developing arterial and venous thrombosis, which contribute to the high rate of adverse events and fatal outcomes. Many heart failure patients routinely receive antithrombotic therapy due to the presence of a specific indication for its use, like ischemic heart disease or atrial fibrillation. However, there is no solid evidence to support the routine use of antithrombotic agents in all heart failure patients. This article reviews the evidence for using antithrombotic therapy in heart failure patients. PMID:25559833

  12. Antithrombotics in heart failure

    PubMed Central

    Mili?i?, Davor; Samardi?, Jure; Petri?evi?, Mate

    2014-01-01

    Heart failure is a common clinical condition associated with high morbidity and mortality rate despite significant improvements in pharmacotherapy and implementation of medical procedures. Patients with heart failure are at an increased risk of developing arterial and venous thrombosis, which contribute to the high rate of adverse events and fatal outcomes. Many heart failure patients routinely receive antithrombotic therapy due to the presence of a specific indication for its use, like ischemic heart disease or atrial fibrillation. However, there is no solid evidence to support the routine use of antithrombotic agents in all heart failure patients. This article reviews the evidence for using antithrombotic therapy in heart failure patients. PMID:25559833

  13. Heart Failure: A Primer.

    PubMed

    Lee, Christopher S; Auld, Jonathan

    2015-12-01

    Heart failure is a complex and multisystem clinical syndrome that results from impaired ventricular contractility and/or relaxation. Hypertension, diabetes mellitus, and coronary artery disease are common antecedents to heart failure. The main pathogenic mechanisms involved in heart failure include sympathetic nervous and renin-angiotensin-aldosterone system activation, as well as inflammation. A detailed history and physical examination and additional diagnostic tests may be needed to diagnose heart failure. Most treatment strategies target neurohormonal systems. Nonpharmacologic interventions and effective engagement in self-care are also important in overall heart failure management. Therapeutic strategies are geared toward prolonging life and optimizing quality of life. PMID:26567488

  14. Heart failure - tests

    MedlinePLUS

    CHF - tests; Congestive heart failure - tests; Cardiomyopathy - tests; HF - tests ... An echocardiogram (Echo) is a test that uses sound waves to create a moving picture of the heart. The picture is much more detailed than a plain ...

  15. Heart Failure Society of America

    MedlinePLUS

    ... Press Releases Awards CEO Update Corporate Members Quick Heart Failure Facts Link Exchanges Use of Our Name Social ... App Education Modules What You Should Know About Heart Failure Living With Heart Failure Quick Tips and Topics ...

  16. Heart Failure Medications

    MedlinePLUS

    ... you may not need to take anymore, improper dosages of medicines, and mistakes that you may be making in taking them. Call your doctor ... • Home • About Heart Failure • Causes and Risks for ...

  17. Devices in Heart Failure

    PubMed Central

    Munir, Shahzeb M.; Bogaev, Roberta C.; Sobash, Ed; Shankar, K. J.; Gondi, Sreedevi; Stupin, Igor V.; Robertson, Jillian; Brewer, M. Alan; Casscells, S. Ward; Delgado, Reynolds M.; Ahmed, Amany

    2008-01-01

    Congestive heart failure has long been one of the most serious medical conditions in the United States; in fact, in the United States alone, heart failure accounts for 6.5 million days of hospitalization each year. One important goal of heart-failure therapy is to inhibit the progression of congestive heart failure through pharmacologic and device-based therapies. Therefore, there have been efforts to develop device-based therapies aimed at improving cardiac reserve and optimizing pump function to meet metabolic requirements. The course of congestive heart failure is often worsened by other conditions, including new-onset arrhythmias, ischemia and infarction, valvulopathy, decompensation, end-organ damage, and therapeutic refractoriness, that have an impact on outcomes. The onset of such conditions is sometimes heralded by subtle pathophysiologic changes, and the timely identification of these changes may promote the use of preventive measures. Consequently, device-based methods could in the future have an important role in the timely identification of the subtle pathophysiologic changes associated with congestive heart failure. PMID:18612451

  18. Pathophysiology of Heart Failure.

    PubMed

    Tanai, Edit; Frantz, Stefan

    2015-01-01

    Heart failure is considered an epidemic disease in the modern world affecting approximately 1% to 2% of adult population. It presents a multifactorial, systemic disease, in which--after cardiac injury--structural, neurohumoral, cellular, and molecular mechanisms are activated and act as a network to maintain physiological functioning. These coordinated, complex processes lead to excessive volume overload, increased sympathetic activity, circulation redistribution, and result in different, parallel developing clinical signs and symptoms. These signs and symptoms sum up to an unspecific clinical picture; thus invasive and noninvasive diagnostic tools are used to get an accurate diagnosis and to specify the underlying cause. The most important, outcome determining factor in heart failure is its constant progression. Constant optimizing of pharmatherapeutical regimes, novel targets, and fine regulation of these processes try to keep these compensatory mechanisms in a physiological range. Beside pharmacological therapy, interventional and surgical therapy options give new chances in the management of heart failure. For the optimization and establishment of these and novel therapeutical approaches, complete and comprehensive understanding of the underlying mechanisms is essentially needed. Besides diagnosis and treatment, efforts should be made for better prevention in heart failure by treatment of risk factors, or identifying and following risk groups. This summary of the pathophysiology of heart failure tries to give a compact overview of basic mechanisms and of the novel unfolding, progressive theory of heart failure to contribute to a more comprehensive knowledge of the disease. 2016 American Physiological Society. Compr Physiol 6:187-214, 2016. PMID:26756631

  19. Dissecting heart failure.

    PubMed

    Verma, Sameer; Gupta, Sameer; Guglin, Maya

    2014-06-01

    Dissection of ascending aorta is a medical emergency typically presenting with acute chest or back pain and hemodynamic instability. We are reporting a very unusual case of dissection of a large ascending aortic aneurysm presenting as a new onset heart failure. A 46-year-old man presented with gradually increasing dyspnea and orthopnea. His physical examination and laboratory findings were consistent with heart failure. The only unusual feature was a diastolic murmur, which prompted echocardiographic evaluation. Besides left ventricular dilatation, hypertrophy, and severe global hypokinesis, which were expected, we also found severely dilated aortic root with aortic regurgitation and a 8.69.7 cm ascending aortic aneurysm with dissection. The patient had a brother who died several years earlier from aortic dissection. Surgical treatment was successful. Type A aortic dissection may rarely present as heart failure. Aortic dissection at young age should prompt screening of first-degree relatives because genetic nature of the disease is very likely. PMID:24418447

  20. Overt hyperthyroidism and hypothyroidism during pregnancy.

    PubMed

    Stagnaro-Green, Alex

    2011-09-01

    The present manuscript provides a definition for, and evaluates the prevalence and maternal/fetal/child impact of, overt hyperthyroidism and overt hypothyroidism. The prevalence of overt hyperthyroidism is 0.5% and the prevalence of overt hyperthyroidism is 0.3%. Overt maternal hyperthyroidism is associated with heart failure, preeclampsia, preterm delivery, still birth, and neonatal mortality. Overt maternal hypothyroidism is associated with preeclampsia, gestational hypertension, cretinism, fetal deaths, and spontaneous abortion. A cost-effective analysis for screening and treating overt thyroid disease during pregnancy is warranted. PMID:21857178

  1. Your Heart Failure Healthcare Team

    MedlinePLUS

    ... Pressure Tools & Resources Stroke More Your Heart Failure Healthcare Team Updated:Mar 25,2016 Patients with heart failure may work with multiple healthcare professionals. It's important to develop good relationships with ...

  2. Warning Signs of Heart Failure

    MedlinePLUS

    ... Pressure Tools & Resources Stroke More Warning Signs of Heart Failure Updated:Mar 25,2016 By themselves, any one ... to the Terms and Conditions and Privacy Policy Heart Failure Questions to Ask Your Doctor Use these questions ...

  3. Lifestyle Changes for Heart Failure

    MedlinePLUS

    ... Pressure Tools & Resources Stroke More Lifestyle Changes for Heart Failure Updated:Sep 25,2015 Following recommendations about diet, ... content was last reviewed on 04/06/2015. Heart Failure • Home • About Heart Failure • Causes and Risks for ...

  4. Ejection Fraction Heart Failure Measurement

    MedlinePLUS

    ... Blood Pressure Tools & Resources Stroke More Ejection Fraction Heart Failure Measurement Updated:Mar 25,2016 The ejection fraction ( ... to the Terms and Conditions and Privacy Policy Heart Failure • Home • About Heart Failure • Causes and Risks for ...

  5. Primary Prevention of Heart Failure

    PubMed Central

    Butler, Javed

    2012-01-01

    Most heart failure research and quality improvement efforts are targeted at treatment and secondary prevention of patients with manifest heart failure. This is distinct from coronary disease where primary prevention has been a focus for over three decades. Given the current importance and the projected worsening of heart failure epidemiology, a more focused effort on prevention is urgently needed. PMID:22957272

  6. REFRACTORY HEART FAILURE

    PubMed Central

    Sodeman, William A.

    1954-01-01

    Any patient with so-called refractory heart failure should be looked upon as suboptimally handled. The patient should be studied for possible development of new disturbances, either inside or outside the vascular system, which, at the same time, have a bearing upon the heart failure. The entire therapeutic program should be reviewed to be sure that all aspects of therapy have been evaluated satisfactorily and established optimally. If diuretics, especially mercurial diuretics, have been given, the possible complications of such therapy, particularly in terms of electrolyte imbalance, should be considered. It is only through a general survey of the patient for an evaluation of these factors that they may be found and therapy instituted to minimize or eliminate them. PMID:13190428

  7. [Drug-induced heart failure].

    PubMed

    Negrusz-Kawecka, M

    2001-09-01

    Heart failure is a clinical syndrome caused mainly by cardiovascular diseases such as coronary heart disease, hypertension and valvular disease, but several categories of drugs may potentially induce heart failure in patients without previous heart disease or precipitate revealing of heart failure symptoms in patients with preexisting left ventricle impairment. Pathophysiologically drugs that increase preload, afterload or have negative inotropic properties may be able to cause this adverse reaction. In the article the potential role in the occurrence of heart failure of cytostatics, immunomodulating drugs, nonsteroidal anti-inflammatory drugs, calcium channel blockers, beta-adrenoceptor antagonists, antiarrhythmics, anesthetics and antidepressants is reviewed. PMID:11761828

  8. Electrophysiological Remodeling in Heart Failure

    PubMed Central

    Wang, Yanggan; Hill, Joseph A.

    2010-01-01

    Heart failure affects nearly 6 million Americans, with a half-million new cases emerging each year. Whereas up to 50% of heart failure patients die of arrhythmia, the diverse mechanisms underlying heart failure-associated arrhythmia are poorly understood. As a consequence, effectiveness of antiarrhythmic pharmacotherapy remains elusive. Here, we review recent advances in our understanding of heart failure-associated molecular events impacting the electrical function of the myocardium. We approach this from an anatomical standpoint, summarizing recent insights gleaned from pre-clinical models and discussing their relevance to human heart failure. PMID:20096285

  9. [Hypocalcemia causing heart failure].

    PubMed

    Musse, N S; Albanesi Filho, F M; Barbosa, E C; Ginefra, P

    1992-11-01

    A 39-year-old female patient with refractory heart failure has been studied. On February, 1982 she was submitted to right lobar thyroidectomy for remotion of the left thyroid lobe. Following the surgery, she had signs of hypocalcemia and the diagnosis of secondary hypoparathyroidism and heart failure had been made. Seven months after she had acute pulmonary edema, cardiomegaly III (cardiothoracic index = 0.58) with predominant left atrial and left ventricular hypertrophy, which were confirmed by echocardiogram (ECO). The ECO also demonstrated low contractility of the left ventricle. The QT interval was increased on the electrocardiogram (QTc = 0.50 s), the calcium was 5.0 mg/dl with calciuria of 28 mg/day; phosphatemia was 4.8 mg/dl and phosphaturia of 214 mg/day. The level of thyroid hormones (T3 and T4) were in the normal ranges despite the TSH was increased in the beginning of the disease. She was first treated with digitalis, diuretic and vasodilator drugs, thyroid hormone and oral calcium. She had progressive hemodynamic improvement when higher doses of calcium were given with D3 vitamin. The most significant result of this treatment was reduction of the heart size that come back to normal. At the present time patient is treated with thyroid hormone, calcium and D3 vitamin only. PMID:1340740

  10. Congestive heart failure.

    PubMed

    Yancy, C W; Firth, B G

    1988-08-01

    Congestive heart failure (CHF) is not a single entity but a symptom complex that may represent the consequence of mechanical abnormalities, myocardial abnormalities, and/or disturbances of cardiac rhythm. In turn, it affects virtually every organ system in the body. This review focuses on CHF due to systolic dysfunction of the left ventricle, which comprises the majority of cases of this condition. Recent data suggest that CHF may be the most frequent primary diagnosis in patients on medical services in nonmilitary hospitals in this country: it affects approximately 2% of the United States population, or some 4 million people. The mortality rate for CHF is also worse than for many forms of cancer; thus, new therapeutic alternatives are imperative. In order to devise new therapeutic strategies, a detailed understanding of the pathophysiology of this condition is required. The relative advantages and disadvantages of various pharmacologic and nonpharmacologic approaches are considered in detail. Certain medications, such as the angiotensin converting enzyme (ACE) inhibitors, have been shown to improve survival, and heart transplantation is clearly life-saving for those who are eligible for this therapy. However, the real challenge is to devise strategies to prevent the occurrence of heart failure, or interrupt its progress at a very early stage. PMID:3044719

  11. Heart Failure in South America

    PubMed Central

    Bocchi, Edimar Alcides

    2013-01-01

    Continued assessment of temporal trends in mortality and epidemiology of specific heart failure in South America is needed to provide a scientific basis for rational allocation of the limited health care resources, and strategies to reduce risk and predict the future burden of heart failure. The epidemiology of heart failure in South America was reviewed. Heart failure is the main cause of hospitalization based on available data from approximately 50% of the South American population. The main etiologies of heart failure are ischemic, idiopathic dilated cardiomyopathy, valvular, hypertensive and chagasic etiologies. In endemic areas, Chagas heart disease may be responsible by 41% of the HF cases. Also, heart failure presents high mortality especially in patients with Chagas etiology. Heart failure and etiologies associated with heart failure may be responsible for 6.3% of causes of deaths. Rheumatic fever is the leading cause of valvular heart disease. However, a tendency to reduction of HF mortality due to Chagas heart disease from 1985 to 2006, and reduction in mortality due to HF from 1999 to 2005 were observed in selected states in Brazil. The findings have important public health implications because the allocation of health care resources, and strategies to reduce risk of heart failure should also consider the control of neglected Chagas disease and rheumatic fever in South American countries. PMID:23597301

  12. Sleep and Heart Failure.

    PubMed

    Nelson, Kimberly A; Trupp, Robin J

    2015-12-01

    Sleep deprivation occurs for many reasons but, when chronic in nature, has many consequences for optimal health and performance. Despite its high prevalence, sleep-disordered breathing is underrecognized and undertreated. This is especially true in the setting of heart failure, where sleep-disordered breathing affects more than 50% of patients. Although the optimal strategy to best identify patients is currently unknown, concerted and consistent efforts to support early recognition, diagnosis, and subsequent treatment should be encouraged. Optimization of guideline-directed medical therapy and concurrent treatment of sleep-disordered breathing are necessary to improve outcomes in this complex high-risk population. PMID:26567495

  13. Heart failure - fluids and diuretics

    MedlinePLUS

    When you have heart failure, your heart does not pump out enough blood. This causes fluids to build up in your body. If you ... the amount of fluids you drink: When your heart failure is not very bad, you may not have ...

  14. Heart Failure - Multiple Languages: MedlinePlus

    MedlinePLUS

    ... Arabic (???????) Heart Failure (Arabic) ???? ????? - ??????? Bilingual PDF Health Information Translations Bosnian (Bosanski) Heart Failure Zatajenje srca - Bosanski (Bosnian) Bilingual PDF Health Information Translations Chinese - Simplified (????) Heart ...

  15. Heart failure and mouse models.

    PubMed

    Breckenridge, Ross

    2010-01-01

    Heart failure is a common, complex condition with a poor prognosis and increasing incidence. The syndrome of heart failure comprises changes in electrophysiology, contraction and energy metabolism. This complexity, and the interaction of the clinical syndrome with very frequently concurrent medical conditions such as diabetes, means that animal modelling of heart failure is difficult. The current animal models of heart failure in common use do not address several important clinical problems. There have been major recent advances in the understanding of cardiac biology in the healthy and failing myocardium, but these are, as yet, unmatched by advances in therapeutics. Arguably, the development of new animal models of heart failure, or at least adaptation of existing models, will be necessary to fully translate scientific advances in this area into new drugs. This review outlines the mouse models of heart failure in common usage today, and discusses how adaptations in these models may allow easier translation of animal experimentation into the clinical arena. PMID:20212081

  16. How Is Heart Failure Diagnosed?

    MedlinePLUS

    ... level of this hormone rises during heart failure. Echocardiography Echocardiography (echo) uses sound waves to create a ... your heart pumps blood when it beats. Doppler Ultrasound A Doppler ultrasound uses sound waves to measure ...

  17. Insomnia Self-Management in Heart Failure

    ClinicalTrials.gov

    2016-01-19

    Cardiac Failure; Heart Failure; Congestive Heart Failure; Heart Failure, Congestive; Sleep Initiation and Maintenance Disorders; Chronic Insomnia; Disorders of Initiating and Maintaining Sleep; Fatigue; Pain; Depressive Symptoms; Sleep Disorders; Anxiety

  18. Mitophagy and heart failure

    PubMed Central

    Shires, Sarah E.

    2015-01-01

    Cardiac mitochondria are responsible for generating energy in the form of ATP through oxidative phosphorylation and are crucial for cardiac function. Mitochondrial dysfunction is a major contributor to loss of myocytes and development of heart failure. Myocytes have quality control mechanisms in place to ensure a network of functional mitochondria. Damaged mitochondria are degraded by a process called mitochondrial autophagy, or mitophagy, where the organelle is engulfed by an autophagosome and subsequently delivered to a lysosome for degradation. Evidence suggests that mitophagy is important for cellular homeostasis, and reduced mitophagy leads to inadequate removal of dysfunctional mitochondria. In this review, we discuss the regulation of mitophagy and the emerging evidence of the cardioprotective role of mitophagy. We also address the prospect of therapeutically targeting mitophagy to treat patients with cardiovascular disease. PMID:25609139

  19. Copeptin in Heart Failure.

    PubMed

    Balling, Louise; Gustafsson, Finn

    2016-01-01

    Heart failure (HF) is one of the most common causes of hospitalization and mortality in the modern Western world and an increasing proportion of the population will be affected by HF in the future. Although HF management has improved quality of life and prognosis, mortality remains very high despite therapeutic options. Medical management consists of a neurohormonal blockade of an overly activated neurohormonal axis. No single marker has been able to predict or monitor HF with respect to disease progression, hospitalization, or mortality. New methods for diagnosis, monitoring therapy, and prognosis are warranted. Copeptin, a precursor of pre-provasopressin, is a new biomarker in HF with promising potential. Copeptin has been found to be elevated in both acute and chronic HF and is associated with prognosis. Copeptin, in combination with other biomarkers, could be a useful marker in the monitoring of disease severity and as a predictor of prognosis and survival in HF. PMID:26975969

  20. Acute Heart Failure Treatment

    PubMed Central

    Bellou, Abdel

    2013-01-01

    Dyspnea is the predominant symptom for patients with acute heart failure and initial treatment is largely directed towards the alleviation of this. Contrary to conventional belief, not all patients present with fluid overload and the approach to management is rapidly evolving from a solitary focus on diuresis to one that more accurately reflects the complex interplay of underlying cardiac dysfunction and acute precipitant. Effective treatment thus requires an understanding of divergent patient profiles and an appreciation of various therapeutic options for targeted patient stabilization. The key principle within this paradigm is directed management that aims to diminish the work of breathing through situation appropriate ventillatory support, volume reduction and hemodynamic improvement. With such an approach, clinicians can more efficiently address respiratory discomfort while reducing the likelihood of avoidable harm. PMID:24223323

  1. Heart failure - discharge

    MedlinePLUS

    ... Adults: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice ... Cardiovascular Nursing; American Heart Association Council on Clinical ... Heart Association Council on Nutrition, Physical Activity, ...

  2. Sweetened Drinks and Heart Failure

    MedlinePLUS Videos and Cool Tools

    ... of sweetened beverages per day are at increased risk of heart failure. Researchers tracked the health of around 42,000 men for more than ... of sweetened drinks had a 23 percent higher risk of developing heart failure compared to ... to you. Related MedlinePlus Health ...

  3. Congestive heart failure. New frontiers.

    PubMed Central

    Parmley, W. W.; Chatterjee, K.; Francis, G. S.; Firth, B. G.; Kloner, R. A.

    1991-01-01

    Congestive heart failure is a common syndrome with high mortality in its advanced stages. Current therapy includes the use of vasodilator drugs, which have been shown to prolong life. Despite current therapy, mortality remains high in patients with severe heart failure. Potent new inotropic vasodilators have improved ventricular performance but have not prolonged life in patients with end-stage heart failure. Serious arrhythmias are implicated in the sudden deaths of 30% to 40% of patients with severe heart failure, but the benefits of antiarrhythmic therapy have not been established. Upcoming trials will address this question. Ventricular remodeling and progressive dilatation after myocardial infarction commonly lead to congestive heart failure; early unloading of the ventricle with an angiotensin-converting enzyme inhibitor may attenuate these events. These findings support the concept that angiotensin-converting enzyme inhibitors may be useful in managing heart failure of all degrees of severity, including left ventricular dysfunction and end-stage heart failure. Part of the damage that may occur with acute myocardial infarction, particularly in this era of thrombolysis therapy, is reperfusion injury, which may be mediated by oxygen-derived free radicals. Better knowledge of the mechanisms and treatment of myocardial infarction, the leading cause of congestive heart failure, may help prevent or attenuate the development of this syndrome. PMID:1678903

  4. Biomarkers in acute heart failure.

    PubMed

    Mallick, Aditi; Januzzi, James L

    2015-06-01

    The care of patients with acutely decompensated heart failure is being reshaped by the availability and understanding of several novel and emerging heart failure biomarkers. The gold standard biomarkers in heart failure are B-type natriuretic peptide and N-terminal pro-B-type natriuretic peptide, which play an important role in the diagnosis, prognosis, and management of acute decompensated heart failure. Novel biomarkers that are increasingly involved in the processes of myocardial injury, neurohormonal activation, and ventricular remodeling are showing promise in improving diagnosis and prognosis among patients with acute decompensated heart failure. These include midregional proatrial natriuretic peptide, soluble ST2, galectin-3, highly-sensitive troponin, and midregional proadrenomedullin. There has also been an emergence of biomarkers for evaluation of acute decompensated heart failure that assist in the differential diagnosis of dyspnea, such as procalcitonin (for identification of acute pneumonia), as well as markers that predict complications of acute decompensated heart failure, such as renal injury markers. In this article, we will review the pathophysiology and usefulness of established and emerging biomarkers for the clinical diagnosis, prognosis, and management of acute decompensated heart failure. PMID:25911167

  5. What Causes Heart Failure?

    MedlinePLUS

    ... sugar) level is too high. The body normally breaks down food into glucose and then carries it to ... rigid. Congenital heart defects . Problems with the hearts structure ... or more of your heart valves doesnt work properly, which can be present at birth or ...

  6. Heart Failure in North America

    PubMed Central

    Blair, John E. A; Huffman, Mark; Shah, Sanjiv J

    2013-01-01

    Heart failure is a major health problem that affects patients and healthcare systems worldwide. Within the continent of North America, differences in economic development, genetic susceptibility, cultural practices, and trends in risk factors and treatment all contribute to both inter-continental and within-continent differences in heart failure. The United States and Canada represent industrialized countries with similar culture, geography, and advanced economies and infrastructure. During the epidemiologic transition from rural to industrial in countries such as the United States and Canada, nutritional deficiencies and infectious diseases made way for degenerative diseases such as cardiovascular diseases, cancer, overweight/obesity, and diabetes. This in turn has resulted in an increase in heart failure incidence in these countries, especially as overall life expectancy increases. Mexico, on the other hand, has a less developed economy and infrastructure, and has a wide distribution in the level of urbanization as it becomes more industrialized. Mexico is under a period of epidemiologic transition and the etiology and incidence of heart failure is rapidly changing. Ethnic differences within the populations of the United States and Canada highlight the changing demographics of each country as well as potential disparities in heart failure care. Heart failure with preserved ejection fraction makes up approximately half of all hospital admissions throughout North America; however, important differences in demographics and etiology exist between countries. Similarly, acute heart failure etiology, severity, and management differ between countries in North America. The overall economic burden of heart failure continues to be large and growing worldwide, with each country managing this burden differently. Understanding the inter-and within-continental differences may help improve understanding of the heart failure epidemic, and may aid healthcare systems in delivering better heart failure prevention and treatment. PMID:23597296

  7. Heart failure in North America.

    PubMed

    Blair, John E A; Huffman, Mark; Shah, Sanjiv J

    2013-05-01

    Heart failure is a major health problem that affects patients and healthcare systems worldwide. Within the continent of North America, differences in economic development, genetic susceptibility, cultural practices, and trends in risk factors and treatment all contribute to both inter-continental and within-continent differences in heart failure. The United States and Canada represent industrialized countries with similar culture, geography, and advanced economies and infrastructure. During the epidemiologic transition from rural to industrial in countries such as the United States and Canada, nutritional deficiencies and infectious diseases made way for degenerative diseases such as cardiovascular diseases, cancer, overweight/obesity, and diabetes. This in turn has resulted in an increase in heart failure incidence in these countries, especially as overall life expectancy increases. Mexico, on the other hand, has a less developed economy and infrastructure, and has a wide distribution in the level of urbanization as it becomes more industrialized. Mexico is under a period of epidemiologic transition and the etiology and incidence of heart failure is rapidly changing. Ethnic differences within the populations of the United States and Canada highlight the changing demographics of each country as well as potential disparities in heart failure care. Heart failure with preserved ejection fraction makes up approximately half of all hospital admissions throughout North America; however, important differences in demographics and etiology exist between countries. Similarly, acute heart failure etiology, severity, and management differ between countries in North America. The overall economic burden of heart failure continues to be large and growing worldwide, with each country managing this burden differently. Understanding the inter-and within-continental differences may help improve understanding of the heart failure epidemic, and may aid healthcare systems in delivering better heart failure prevention and treatment. PMID:23597296

  8. Heart Failure Questions to Ask Your Doctor

    MedlinePLUS

    ... Pressure High Blood Pressure Tools & Resources Stroke More Heart Failure Questions to Ask Your Doctor Updated:Mar 25, ... to the Terms and Conditions and Privacy Policy Heart Failure • Home • About Heart Failure • Causes and Risks for ...

  9. Heart Failure: Unique to Older Adults

    MedlinePLUS

    ... our e-newsletter! Aging & Health A to Z Heart Failure Unique to Older Adults This section provides ... or maintain quality of life. Urinary Incontinence and Heart Failure If you have heart failure, you may ...

  10. Who Is at Risk for Heart Failure?

    MedlinePLUS

    ... Failure? Explore Heart Failure What Is... Other Names Causes Who Is at Risk Signs & Symptoms Diagnosis Treatments Prevention Living With Clinical Trials Links Related Topics Arrhythmia Congenital Heart Defects Coronary Heart Disease Heart Valve Disease High Blood Pressure Send a ...

  11. [Competence Network Heart Failure (CNHF) : Together against heart failure].

    PubMed

    Ertl, Georg; Störk, Stefan; Börste, Rita

    2016-04-01

    Heart failure is one of the most urgent medical and socio-economic challenges of the 21(st) century. Up to three million people are affected in Germany; this means one in ten people over the age of 65  live with heart failure. The current demographic changes will accentuate the importance of this grave health problem. The care of patients with heart failure, as well as the associated research mandates a comprehensive, multidisciplinary approach. The Competence Network Heart Failure (CNHF) pursues this objective. CNHF is a research alliance with 11 sites in Germany and was funded by the Federal Ministry of Research (BMBF) from 2003 through 2014. Since January 2015, the network has been an associate cooperating partner of the German Centre for Cardiovascular Research (DZHK). During the 12-year funding period by the BMBF, scientists in the field of heart failure from 30 university hospitals, 5 research institutes, 7 heart centers, 17 cardiovascular clinics, over 200 general practitioners, 4 rehabilitation clinics, as well as numerous organizations and associations were involved in cooperative CNHF research. In the context of 22 projects, the CNHF covered basic, clinical, and health care research, and generated numerous groundbreaking insights into disease mechanisms, as well as diagnosis and treatment of heart failure, which are documented in more than 350 publications. With its central study database and bank of biomaterials, the network has set up a Europe-wide unique research resource, which can be used in the future for national and international cooperations with the DZHK and other partners. Furthermore, the CNHF strongly promotes nation- and Europe-wide public relations and heart failure awareness activities. PMID:26979718

  12. Ivabradine for chronic heart failure?

    PubMed

    2012-10-01

    In the UK, over 900,000 patients have chronic heart failure and more than 60,000 develop the condition each year.(1,2) Patients with heart failure suffer significantly reduced quality of life and have a poor prognosis. It is estimated that heart failure accounts for around 2% of the total NHS budget, 70% of which is related to the costs of hospitalisation.(3) The main pharmacological interventions that are currently used to manage heart failure include angiotensin converting enzyme (ACE) inhibitors, angiotensin receptor antagonists (AIIRAs), beta-blockers and aldosterone antagonsists. Ivabradine (Procoralan - Servier) is a "pure heart rate lowering agent, acting by selective and specific inhibition of the cardiac pacemaker I(f) current that controls the spontaneous diastolic depolarisation in the sinus node and regulates heart rate".(4) It has been licensed in the UK since 2006 for the symptomatic treatment of chronic stable angina in patients with normal sinus rhythm.(5) Earlier this year ivabradine was granted marketing authorisation for the treatment of chronic heart failure. Here we review the role of ivabradine for this new indication. PMID:23065752

  13. The molecular and cellular pathophysiology of heart failure.

    PubMed

    Piano, M R; Bondmass, M; Schwertz, D W

    1998-01-01

    In the United States, it is estimated that heart failure develops in 465,000 people each year. Heart failure occurs in both men and women and is associated with a high morbidity and mortality rate in both sexes and in all races. Our knowledge of the pathophysiology of heart failure has advanced beyond the cardiorenal-neurohumoral model and now includes changes in myocyte structure and function. Cellular changes in heart failure include myocyte hypertrophy, abnormalities in calcium homeostasis, excitation-contraction coupling, cross-bridge cycling, and changes in the cytoskeletal architecture. Data also indicate that some of these changes are found during the compensated stage of heart failure; whereas other changes are found during overt decompensation and are associated with changes in systolic and diastolic function. The transition from compensated to decompensated heart failure is more than likely related to the overexpression of neurohormones and peptides such as norepinephrine, angiotensin II, and proinflammatory cytokines. The purpose of this article is to review the epidemiology and cellular pathophysiology of heart failure. PMID:9493878

  14. Heart failure - overview

    MedlinePLUS

    ... about what you should do if your weight goes up or you develop more symptoms. Limit how ... prevented by living a healthy lifestyle and taking steps aimed at reducing your risk for heart disease . .

  15. Acute Decompensated Heart Failure Update

    PubMed Central

    Teerlink, John R; Alburikan, Khalid; Metra, Marco; Rodgers, Jo E

    2015-01-01

    Acute decompensated heart failure (ADHF) continues to increase in prevalence and is associated with substantial mortality and morbidity including frequent hospitalizations. The American Heart Association is predicting that more than eight million Americans will have heart failure by 2030 and that the total direct costs associated with the disease will rise from $21 billion in 2012 to $70 billion in 2030. The increase in the prevalence and cost of HF is primarily the result of shifting demographics and a growing population. Although many large, randomized, controlled clinical trials have been conducted in patients with chronic heart failure, it was not until recently that a growing number of studies began to address the management of ADHF. It is the intent of this review to update the clinician regarding the evaluation and optimal management of ADHF. PMID:24251454

  16. Diastolic Function in Heart Failure

    PubMed Central

    Kovács, Sándor J

    2015-01-01

    Heart failure has reached epidemic proportions, and diastolic heart failure or heart failure with preserved ejection fraction (HFpEF) constitutes about 50% of all heart failure admissions. Long-term prognosis of both reduced ejection fraction heart failure and HFpEF are similarly dismal. No pharmacologic agent has been developed that actually treats or repairs the physiologic deficit(s) responsible for HFpEF. Because the physiology of diastole is both subtle and counterintuitive, its role in heart failure has received insufficient attention. In this review, the focus is on the physiology of diastole in heart failure, the dominant physiologic laws that govern the process in all hearts, how all hearts work as a suction pump, and, therefore, the elucidation and characterization of what actually is meant by “diastolic function”. The intent is for the reader to understand what diastolic function actually is, what it is not, and how to measure it. Proper measurement of diastolic function requires one to go beyond the usual E/A, E/E′, etc. phenomenological metrics and employ more rigorous causality (mathematical modeling) based parameters of diastolic function. The method simultaneously provides new physiologic insight into the meaning of in vivo “equilibrium volume” of the left ventricle (LV), longitudinal versus transverse volume accommodation of the chamber, diastatic “ringing” of the mitral annulus, and the mechanism of L-wave generation, as well as availability of a load-independent index of diastolic function (LIIDF). One important consequence of understanding what diastolic function is, is the recognition that all that current therapies can do is basically alter the load, rather than actually “repair” the functional components (chamber stiffness, chamber relaxation). If beneficial (biological/structural/metabolic) remodeling due to therapy does manifest ultimately as improved diastolic function, it is due to resumption of normal physiology (as in alleviation of ischemia) or activation of compensatory pathways already devised by evolution. In summary, meaningful quantitative characterization of diastolic function in any clinical setting, including heart failure, requires metrics based on physiologic mechanisms that quantify the suction pump attribute of the heart. This requires advancing beyond phenomenological global indexes such as E/A, E/E′, Vp, etc. and employing causality (mathematical modeling) based parameters of diastolic function easily obtained via the parametrized diastolic function (PDF) formalism. PMID:25922587

  17. Understand Your Risk for Heart Failure

    MedlinePLUS

    ... Tools & Resources Stroke More Causes and Risks for Heart Failure Updated:Feb 1,2016 Who Develops Heart Failure ( ... HF. This content was last reviewed April 2015. Heart Failure • Home • About Heart Failure • Causes and Risks for ...

  18. Heart failure - what to ask your doctor

    MedlinePLUS

    ... a pump that moves blood through your body. Heart failure occurs when blood does not move well and ... often, fluid collects in your lungs and legs. Heart failure most often occurs because your heart muscle is ...

  19. Metabolic and signaling alterations in dystrophin-deficient hearts precede overt cardiomyopathy.

    PubMed

    Khairallah, Maya; Khairallah, Ramzi; Young, Martin E; Dyck, Jason R B; Petrof, Basil J; Des Rosiers, Christine

    2007-08-01

    The cytoskeletal protein dystrophin has been implicated in hereditary and acquired forms of cardiomyopathy. However, much remains to be learned about the role of dystrophin in the heart. We hypothesized that the dystrophin-deficient heart displays early alterations in energy metabolism that precede overt cardiomyopathy. We evaluated the metabolic and functional phenotype of dystrophin-deficient mdx mouse hearts at 10-12 weeks, when no major histological or echocardiographic abnormalities are reported. Ex vivo working mdx heart perfusions with stable isotopes revealed a marked shift in substrate fuel selection from fatty acids to carbohydrates associated with enhanced oxygen consumption. They also unmasked in the mdx heart: (i) compromised cardiac contractile function and efficiency, (ii) reduced cellular integrity, and (iii) exacerbated alterations in mitochondrial citric acid cycle-related parameters and in nutrient signaling pathways related to Akt. The observed shift in substrate selection cannot be explained by metabolic gene remodeling. However, mdx mice hearts showed an increased expression of the atrial natriuretic factor (anf) gene, an activator of the nitric oxide (NO)/cGMP signaling pathway and marker of cardiac remodeling, and, only as the cardiomyopathy progresses (at 25 weeks of age), an increased expression of the alpha1 subunit of soluble guanylate cyclase, which is known to negatively correlate with the activity NO/cGMP pathway. Collectively, our results highlight early metabolic and signaling alterations in the dystrophin-deficient heart, which may predispose these hearts to contractile dysfunction and sarcolemmal fragility. They also suggest the presence of a "sub-clinical" defect in the NO/cGMP pathway, which in vivo, at an early age, may be compensated by enhanced anf gene expression. PMID:17583724

  20. Mechanisms of Heart Failure in Obesity

    PubMed Central

    Ebong, Imo A.; Goff, David C.; Rodriguez, Carlos J.; Chen, Haiying; Bertoni, Alain G.

    2014-01-01

    Heart failure is a leading cause of morbidity and mortality and its prevalence continues to rise. Because obesity has been linked with heart failure, the increasing prevalence of obesity may presage further rise in heart failure in the future. Obesity-related factors are estimated to cause 11% of heart failure cases in men and 14% in women. Obesity may result in heart failure by inducing hemodynamic and myocardial changes that lead to cardiac dysfunction, or due to an increased predisposition to other heart failure risk factors. Direct cardiac lipotoxicity has been described where lipid accumulation in the heart results in cardiac dysfunction inexplicable of other heart failure risk factors. In this overview, we discussed various pathophysiological mechanisms that could lead to heart failure in obesity, including the molecular mechanisms underlying cardiac lipotoxicity. We defined the obesity paradox and enumerated various premises for the paradoxical associations observed in the relationship between obesity and heart failure. PMID:25434909

  1. Heart failure and Alzheimer's disease.

    PubMed

    Cermakova, P; Eriksdotter, M; Lund, L H; Winblad, B; Religa, P; Religa, D

    2015-04-01

    It has recently been proposed that heart failure is a risk factor for Alzheimer's disease. Decreased cerebral blood flow and neurohormonal activation due to heart failure may contribute to the dysfunction of the neurovascular unit and cause an energy crisis in neurons. This leads to the impaired clearance of amyloid beta and hyperphosphorylation of tau protein, resulting in the formation of amyloid beta plaques and neurofibrillary tangles. In this article, we will summarize the current understanding of the relationship between heart failure and Alzheimer's disease based on epidemiological studies, brain imaging research, pathological findings and the use of animal models. The importance of atherosclerosis, myocardial infarction, atrial fibrillation, blood pressure and valve disease as well as the effect of relevant medications will be discussed. PMID:25041352

  2. How Can Heart Failure Be Prevented?

    MedlinePLUS

    ... Prevented? Explore Heart Failure What Is... Other Names Causes Who Is at Risk Signs & Symptoms Diagnosis Treatments Prevention Living With Clinical Trials Links Related Topics Arrhythmia Congenital Heart Defects Coronary Heart Disease Heart Valve Disease High Blood Pressure Send a ...

  3. Heart Failure in Children and Adolescents

    MedlinePLUS

    ... Pressure High Blood Pressure Tools & Resources Stroke More Heart Failure in Children and Adolescents Updated:Mar 25,2016 ... content was last reviewed on 04/06/2015. Heart Failure • Home • About Heart Failure Introduction Types of Heart ...

  4. [Thyrometabolic disorders and heart failure].

    PubMed

    Fater-Debska, Agata; Gworys, Przemysław; Brzeziński, Jan; Gawor, Zenon

    2007-01-01

    Thyroid hormones are essential to maintain normal function of many systems including the cardiovascular system. Their excess or deficiency may upset human body homeostasis. Hyperthyroidism leads to cardiovascular system's hyperdynamic status which is characterized by tachycardia, increased difference between systolic and diastolic arterial pressure, significant increase of the stroke volume and improvement of the left ventricular diastolic function. Long-lasting thyrotoxicosis in patient with heart disease may result in atrial fibrillation, deterioration of angina pectoris or congestive heart failure. Hypothyroidism leads to hemodynamic disturbances which are quite different than those observed in hyperthyroidism, but cardiac symptoms are scant in clinical practice. Hypothyroidism's clinical significance is limited to atherosclerosis progression and intensification of ischaemic heart disease symptoms. Both leads to symptomatic cardiovascular system failure or its deterioration. We should emphasize that cardiovascular system dysfunction associated with thyrometabolic disturbances subsides when euthyreosis is restored. It sounds promising that there are reports suggesting a potential advantage of thyroxin treatment in patients with acute or chronic cardiovascular system diseases. These hypotheses result from the observations that heart dysfunction in hypothyroidism is similar to that observed in heart failure. PMID:17940989

  5. Cardiotonic Modulation in Heart Failure

    PubMed Central

    Tang, W. H. Wilson; Huang, Yanming

    2014-01-01

    Medicinal herbs have been used over the past centuries for restoring the body's homeostatic balance. Contemporary use of herbal supplements remains widespread in many cultures as treatment for specific ailments. Many possess cardiovascular actions, and some interact with cardiac medications. However, there is variable scientific evidence with respect to their safety and efficacy, and few have been subjected to the same rigorous evaluation processes and regulations as contemporary pharmaceuticals (1). In the field of heart failure, we have also witnessed the failure of promising naturopathic therapies like hawthorn extract in translating their potential benefits in rigorous clinical trials (2,3). PMID:23747774

  6. Management of severe heart failure.

    PubMed

    Hiramitsu, Shinya; Miyagishima, Kenji; Kimura, Hisashi; Mori, Kazumasa; Shiino, Kenji; Yamada, Akira; Kato, Shigeru; Kato, Yasuchika; Morimoto, Shin-ichiro; Hishida, Hitoshi; Ozaki, Yukio

    2009-06-01

    Patients admitted to the hospital with heart failure (HF) include those with new-onset of acute HF and those with acute exacerbation of chronic HF (CHF). In therapy for new-onset acute HF associated with acute myocardial infarction, therapy to inhibit left ventricular (LV) remodeling in the convalescent phase is required in addition to that needed to overcome the acute phase. Hitherto, CHF therapy was aimed at improving LV contractability, whereas more recently the aim has shifted to resting the heart. Most patients with HF should be routinely managed with a combination of 3 types of drugs: a diuretic; an angiotensin converting enzyme inhibitor and/or an angiotensin II receptor blocker; and a beta-blocker. The administration of beta-blockers is of particular importance. For HF unresponsive to medical therapy, non-pharmacological therapies are considered. When a HF patient fails to respond to all available therapies, heart transplantation becomes necessary. Of the 1,000 HF patients admitted to our hospital, two cases received heart transplants. 11 cases were indicated for heart transplantation but died before registration. It should be remembered that although in Japan the possibility of receiving a heart transplant is very low, it is by no means entirely impossible. PMID:19474507

  7. Move More to Prevent Heart Failure

    MedlinePLUS

    ... rights reserved. More Health News on: Exercise and Physical Fitness Heart Diseases--Prevention Heart Failure Recent Health News Related MedlinePlus Health Topics Exercise and Physical Fitness Heart Diseases--Prevention Heart Failure About MedlinePlus Site Map FAQs ...

  8. [Hyponatremia in chronic heart failure].

    PubMed

    Shchekochikhin, D Iu; Kopylov, F Iu; Kozlovskaia, N L; Syrkin, A L

    2014-01-01

    Hyponatremia - lowering of sodium in blood serum below 135 mmol/l - is a frequent disorder of electrolyte metabolism in patients with chronic heart failure (CHF). Hyponatremia is a risk factor of elevated mortality, repetitive hospitalizations, and worsening of kidney function in patients with decompensation of CHF. In this review we present pathophysiology of hyponatremia and propose therapeutic approach to correction of this disorder. PMID:25178081

  9. Stress echocardiography in heart failure.

    PubMed

    Agricola, Eustachio; Oppizzi, Michele; Pisani, Matteo; Margonato, Alberto

    2004-01-01

    Echocardiography has the ability to noninvasively explore hemodynamic variables during pharmacologic or exercise stress test in patients with heart failure. In this review, we detail some important potential applications of stress echocardiography in patients with heart failure. In patients with coronary artery disease and chronic LV dysfunction, dobutamine stress echocardiography is able to distinguish between viable and fibrotic tissue to make adequate clinical decisions. Exercise testing, in combination with echocardiographic monitoring, is a method of obtaining accurate information in the assessment of functional capacity and prognosis. Functional mitral regurgitation is a common finding in patients with dilated and ischaemic cardiomyopathy and stress echocardiography in the form of exercise or pharmacologic protocols can be useful to evaluate the behaviour of mitral regurgitation. It is clinical useful to search the presence of contractile reserve in non ischemic dilated cardiomyopathy such as to screen or monitor the presence of latent myocardial dysfunction in patients who had exposure to cardiotoxic agents. Moreover, in patients with suspected diastolic heart failure and normal systolic function, exercise echocardiography could be able to demonstrate the existence of such dysfunction and determine that it is sufficient to limit exercise tolerance. Finally, in the aortic stenosis dobutamine echocardiography can distinguish severe from non-severe stenosis in patients with low transvalvular gradients and depressed left ventricular function. PMID:15285780

  10. [Diagnosis and therapy of chronic heart failure].

    PubMed

    Angermann, C E; Strk, S; Ertl, G

    2004-09-01

    Incidence and prevalence of chronic heart failure are continuously increasing. Today, heart failure of different etiologies represents the most frequent cause of death in industrialized countries. Improvements in heart failure diagnosis and treatment have decreased lethality. In this context, a valid diagnosis, causative therapy of treatable heart failure etiologies, and efficient pharmacological as well as non-pharmacological management strategies are of equal importance. The principal goals of therapy are prevention, maintenance or even improvement of quality of life and the decrease of heart-failure-related morbidity and mortality. PMID:15887699

  11. Heart Failure Update: Outpatient Management.

    PubMed

    Wojnowich, Katherine; Korabathina, Ravi

    2016-03-01

    Outpatient management of heart failure (HF) is aimed at treating symptoms and preventing hospitalizations and readmissions. Management is initiated in a stepwise approach. Blockade of the renin-angiotensin system is a cornerstone of therapy and should be started, along with beta blockers, as soon as the diagnosis of HF is made. Other drugs, including diuretics, aldosterone antagonists, hydralazine, and nitrates, may be added based on symptoms and American College of Cardiology/American Heart Association stage. Despite a great interest in and theoretical benefit of naturoceutical products in the mitigation of oxidative stress and HF progression, none has been proven to be beneficial, and concerns exist regarding their interactions with standard HF drugs. Other nonpharmacologic interventions, including sodium restriction, regular exercise, and/or cardiac rehabilitation, should be initiated at diagnosis. HF often is progressive, and clinicians should be aware of late stage management options, including implantable devices, cardiac transplantation, and hospice care. PMID:26974001

  12. [Baroreflexes and congestive heart failure].

    PubMed

    Aumont, M C; Himbert, D; Czitrom, D

    1995-04-01

    Abnormal responses are found in the early stages of heart failure with increased sympathetic and decreased parasympathetic activity, causing peripheral arteriolar vasconstriction and tachycardia respectively. The cardiopulmonary baroreflex may be studied by decreasing venous return ("low body negative pressure") and by measuring vascular resistance forearm. The arterial baroreflex may be studied by changing aortic pressures (by intravenous phenylephrine or nitroglycerin). Orthostatism and the tilt test deactivate the cardiopulmonary and arterial baroreflexes simultaneously. These baroreflexes are impaired in patients with heart failure. Their activation does not cause the usual sympatho-inhibition so contributing to increased sympathetic tone. This dysfunction may result from a change at any point on the reflex pathway: the baroreceptors themselves, the afferent, central and efferent pathways. It is selective as during the cold pressor test, the vasoconstrictor response remains intact. One of the possible mechanisms of baroreflex dysfunction in heart failure is loss of sensitivities of the baroreceptors. This may be multifactorial: structural abnormalities, changes in compliance or functional abnormality. Even if the loss of sensitivity is partially related to a change in compliance, other factors play a role. It is more functional than structural abnormalities because, after cardiac transplantation, the baroreceptors regain their sensitivity within 2 to 3 weeks. Excessive Na-K dependent ATPase activation of the smooth muscle cells of the carotid sinus could lead to hyperpolarization of the cell membrane, so reducing the excitability of the receptor. Aldosterone is one of the factors which could activate the Na-K ATPase, as this hormone directly increases pump activity and favorizes the synthesis of new pumps in the vascular smooth muscle cells.(ABSTRACT TRUNCATED AT 250 WORDS) PMID:7487298

  13. Heart Failure and Loss of Metabolic Control

    PubMed Central

    Wang, Zhao V.; Li, Dan L.; Hill, Joseph A.

    2014-01-01

    Heart failure is a leading cause of morbidity and mortality worldwide, currently affecting 5 million Americans. A syndrome defined on clinical terms, heart failure is the end-result of events occurring in multiple heart diseases, including hypertension, myocardial infarction, genetic mutations and diabetes, and metabolic dysregulation is a hallmark feature. Mounting evidence from clinical and preclinical studies suggests strongly that fatty acid uptake and oxidation are adversely affected, especially in end-stage heart failure. Moreover, metabolic flexibility, the heart’s ability to move freely among diverse energy substrates, is impaired in heart failure. Indeed, impairment of the heart’s ability to adapt to its metabolic milieu, and associated metabolic derangement, are important contributing factors in heart failure pathogenesis. Elucidation of molecular mechanisms governing metabolic control in heart failure will provide critical insights into disease initiation and progression, raising the prospect of advances with clinical relevance. PMID:24336014

  14. Heart Failure in Rural Communities.

    PubMed

    Verdejo, Hugo E; Ferreccio, Catterina; Castro, Pablo F

    2015-10-01

    Patients with chronic heart failure (CHF) living in rural areas face an increased risk of adverse cardiovascular events. Even in countries with universal access to health care, rural areas are characteristically underserved, with reduced health care providers supply, greater distance to health care centers, decreased physician density with higher reliance on generalists, and high health care staff turnover. On the other hand, patient-related characteristics vary widely among published data. This review describes the epidemiology of CHF in rural or remote settings, organizational and patient-related factors involved in cardiovascular outcomes, and the role of interventions to improve rural health care. PMID:26462091

  15. Socioeconomic Inequalities in Heart Failure.

    PubMed

    Daz-Toro, Felipe; Verdejo, Hugo E; Castro, Pablo F

    2015-10-01

    Prevalence and incidence of chronic heart failure (CHF) has increased during the past decades. Beyond its impact on mortality rates, CHF severely impairs quality of life, particularly with the elderly and vulnerable population. Several studies have shown that CHF takes its toll mostly on the uneducated, low-income population, who exhibit impaired access to health care systems, less knowledge regarding its pathology and poorer self-care behaviors. This review summarizes the available evidence linking socioeconomic inequalities and CHF, focusing on the modifiable factors that may explain the impaired health outcomes in socioeconomically deprived populations. PMID:26462090

  16. Micronutrients in chronic heart failure.

    PubMed

    Krim, Selim R; Campbell, Patrick; Lavie, Carl J; Ventura, Hector

    2013-03-01

    Heart failure (HF)-associated mortality remains high, despite guideline-recommended medical therapies. Poor nutritional status and unintentional cachexia have been shown to have a strong association with worse survival in HF patients. Importantly, micronutrient deficiencies are potential contributing factors to the progression of HF. This review aims to summarize contemporary evidence on the role of micronutrients in the pathophysiology and outcome of HF patients. Emphasis will be given to the most well-studied micronutrients, specifically, vitamin D, vitamin B complex, coenzyme Q10 and L-carnitine. PMID:23070580

  17. Right heart failure: toward a common language

    PubMed Central

    2013-01-01

    Abstract In this guideline, the International Right Heart Foundation Working Group moves a step forward to develop a common language to describe the development and defects that exemplify the common syndrome of right heart failure. We first propose fundamental definitions of the distinctive components of the right heart circulation and provide consensus on a universal definition of right heart failure. These definitions will form the foundation for describing a uniform nomenclature for right heart circulatory failure with a view to foster collaborative research initiatives and conjoint education in an effort to provide insight into mechanisms of disease unique to the right heart. PMID:25006413

  18. Right heart failure: toward a common language.

    PubMed

    Mehra, Mandeep R; Park, Myung H; Landzberg, Michael J; Lala, Anuradha; Waxman, Aaron B

    2013-12-01

    In this guideline, the International Right Heart Foundation Working Group moves a step forward to develop a common language to describe the development and defects that exemplify the common syndrome of right heart failure. We first propose fundamental definitions of the distinctive components of the right heart circulation and provide consensus on a universal definition of right heart failure. These definitions will form the foundation for describing a uniform nomenclature for right heart circulatory failure with a view to foster collaborative research initiatives and conjoint education in an effort to provide insight into mechanisms of disease unique to the right heart. PMID:25006413

  19. Right heart failure: toward a common language.

    PubMed

    Mehra, Mandeep R; Park, Myung H; Landzberg, Michael J; Lala, Anuradha; Waxman, Aaron B

    2014-02-01

    In this perspective, the International Right Heart Foundation Working Group moves a step forward to develop a common language to describe the development and defects that exemplify the common syndrome of right heart failure. We first propose fundamental definitions of the distinctive components of the right heart circulation and provide consensus on a universal definition of right heart failure. These definitions will form the foundation for describing a uniform nomenclature for right heart circulatory failure with a view to foster collaborative research initiatives and conjoint education in an effort to provide insight into echanisms of disease unique to the right heart. PMID:24268184

  20. Serelaxin and acute heart failure.

    PubMed

    Tietjens, Jeremy; Teerlink, John R

    2016-01-15

    Attempts at developing novel therapeutic agents for acute heart failure (AHF) over the past two decades have been marked by disappointment. Relaxin is a human peptide hormone believed to mediate many adaptive haemodynamic changes that occur during pregnancy. Because these effects may be useful for treating AHF, a recombinant version of human relaxin-2, serelaxin, has been developed as a novel therapeutic agent. Studies have confirmed serelaxin's haemodynamic effects of decreasing pulmonary and systemic resistance and increasing renal blood flow. A 1161-patient, placebo-controlled Phase III trial, RELAX-AHF, demonstrated significant improvement in symptoms, reduced worsening of heart failure, decreased hospital length of stay and increased 180-day survival after index hospitalisation. Additional Phase III trials (RELAX-AHF-2; RELAX-AHF-ASIA) are underway to further evaluate the efficacy of serelaxin in patients with AHF. This article will review the physiological function, mechanism of action, clinical trial results and future directions of serelaxin in the treatment of AHF. PMID:26603680

  1. [Heart failure. Current pharmacologic treatment].

    PubMed

    Coma-Canella, I; Castao, S; Nasarre, E

    2005-01-01

    Treatment of heart failure (HF) has changed in recent years, despite the paucity of new approved drugs. Current treatment is directed not only towards improving symptoms, but also to preventing the development from asymptomatic systolic dysfunction to symptomatic heart failure, to preventing cardiac remodelling, renal dysfunction and to reducing mortality. The main families of drugs currently used are: cardiac glycosides, diuretics, angiotensin-converting enzyme inhibitors (ACEI), beta-blocking drugs (BB), angiotensin-II receptor blockers (ARB) and aldosterone receptor antagonists. The combination isosorbide dinitrate + hydralazine is hardly used due to its side effects and none of the new positive inotropic drugs has been approved in chronic HF, because all of them increase mortality. Levosimendan is a new positive inotropic agent approved for acute HF by an intravenous route, with a favourable effect on prognosis vs placebo and vs dobutamine (which worsens the prognosis). The approved oral drugs can be given at the same time if the patient tolerates them, because their beneficial effect is additive. Mortality in two years in mild to moderate HF is 34% with glycosides + diuretics. It falls to 22% when an ACEI is added, to 14% when a BB is added and to 10% when an aldosterone antagonist is added. ARB can be given instead of an ACEI or be added to the other drugs. PMID:16400975

  2. The heart metabolism: pathophysiological aspects in ischaemia and heart failure.

    PubMed

    Abozguia, K; Shivu, G Nallur; Ahmed, I; Phan, T T; Frenneaux, M P

    2009-01-01

    The morbidity and mortality of coronary heart disease and of heart failure remain unacceptably high despite major advances in their management. The main focus of treatment has been revascularisation for ischaemic heart disease and neuro-humoral modification for heart failure. There is an urgent need for new modalities of treatment to improve mortality and morbidity. Recently, there has been a great deal of interest in the role of disturbances in cardiac energetics and myocardial metabolism in the pathophysiology of both ischaemic heart disease and heart failure and of therapeutic potential of metabolic modulation. The myocardium is a metabolic omnivore, but mainly uses fatty acids and glucose for generation of Adenosine-5'-triphosphate (ATP). This review focuses on the key changes that occur to the metabolism of the heart in ischaemia and in heart failure and its effects on cardiac energetics. PMID:19275646

  3. Pacific Islanders Perspectives on Heart Failure Management

    PubMed Central

    Kaholokula, Joseph Keaweaimoku; Saito, Erin; Mau, Marjorie K.; Latimer, Renee; Seto, Todd B.

    2008-01-01

    Objective To identify the health beliefs, attitudes, practices and social and family relations important in heart failure treatment among Pacific Islanders. Methods Four focus groups were convened with 36 Native Hawaiians and Samoans with heart failure and their family caregivers. Thematic data analysis was used to categorize data into four domains: health beliefs and attitudes, preferred health practices, social support systems, and barriers to heart failure care. Results Common coping styles and emotional experiences of heart failure in this population included avoidance or denial of illness, hopelessness and despair, and reliance on spiritual/religious beliefs as a means of support. Among study participants, more Samoans preferred to be treated by physicians whereas more Native Hawaiians preferred traditional Hawaiian methods of healing. Two types of social support (informational and tangible-instrumental) were identified as important in heart failure care. Barriers to heart failure care included poor knowledge of heart failure, lack of trust in physicians care, poor physician-patient relations, finances, dietary changes, and competing demands on time. Conclusion The recruitment, retention, and adherence of Pacific Islanders to heart failure interventions are affected by an array of psychosocial and socio-cultural factors. Practice Implications Interventions might be improved by offering participants accurate and detailed information about heart failure and its treatment, engaging the extended family in providing necessary supports, and providing tools to facilitate physician-patient relationships, among others, within the context of a larger socio-cultural system. PMID:18068939

  4. Mitochondrial dysfunction in heart failure

    PubMed Central

    Rosca, Mariana G.; Hoppel, Charles L.

    2013-01-01

    Heart failure (HF) is a complex chronic clinical syndrome. Energy deficit is considered to be a key contributor to the development of both cardiac and skeletal myopathy. In HF several components of cardiac and skeletal muscle bioenergetics are altered, such as oxygen availability, substrate oxidation, mitochondrial ATP production, and ATP transfer to the contractile apparatus via the creatine kinase shuttle. This review focuses on alterations in mitochondrial biogenesis and respirasome organization, substrate oxidation coupled with ATP synthesis in the context of their contribution to the chronic energy deficit, and mechanical dysfunction of the cardiac and skeletal muscle in HF. We conclude that HF is associated with decreased mitochondrial biogenesis and function in both heart and skeletal muscle, supporting the concept of a systemic mitochondrial cytopathy. The sites of mitochondrial defects are located within the electron transport and phosphorylation apparatus, and differ with the etiology and progression of HF in the two mitochondrial populations (subsarcolemmal and interfibrillar) of cardiac and skeletal muscle. The roles of adrenergic stimulation, the renin-angiotensin system, and cytokines are evaluated as factors responsible for the systemic energy deficit. We propose a cylic AMP-mediated mechanism by which increased adrenergic stimulation contributes to the mitochondrial dysfunction. PMID:22948484

  5. Focus on renal congestion in heart failure

    PubMed Central

    Afsar, Baris; Ortiz, Alberto; Covic, Adrian; Solak, Yalcin; Goldsmith, David; Kanbay, Mehmet

    2016-01-01

    Hospitalizations due to heart failure are increasing steadily despite advances in medicine. Patients hospitalized for worsening heart failure have high mortality in hospital and within the months following discharge. Kidney dysfunction is associated with adverse outcomes in heart failure patients. Recent evidence suggests that both deterioration in kidney function and renal congestion are important prognostic factors in heart failure. Kidney congestion in heart failure results from low cardiac output (forward failure), tubuloglomerular feedback, increased intra-abdominal pressure or increased venous pressure. Regardless of the cause, renal congestion is associated with increased morbidity and mortality in heart failure. The impact on outcomes of renal decongestion strategies that do not compromise renal function should be explored in heart failure. These studies require novel diagnostic markers that identify early renal damage and renal congestion and allow monitoring of treatment responses in order to avoid severe worsening of renal function. In addition, there is an unmet need regarding evidence-based therapeutic management of renal congestion and worsening renal function. In the present review, we summarize the mechanisms, diagnosis, outcomes, prognostic markers and treatment options of renal congestion in heart failure. PMID:26798459

  6. Focus on renal congestion in heart failure.

    PubMed

    Afsar, Baris; Ortiz, Alberto; Covic, Adrian; Solak, Yalcin; Goldsmith, David; Kanbay, Mehmet

    2016-02-01

    Hospitalizations due to heart failure are increasing steadily despite advances in medicine. Patients hospitalized for worsening heart failure have high mortality in hospital and within the months following discharge. Kidney dysfunction is associated with adverse outcomes in heart failure patients. Recent evidence suggests that both deterioration in kidney function and renal congestion are important prognostic factors in heart failure. Kidney congestion in heart failure results from low cardiac output (forward failure), tubuloglomerular feedback, increased intra-abdominal pressure or increased venous pressure. Regardless of the cause, renal congestion is associated with increased morbidity and mortality in heart failure. The impact on outcomes of renal decongestion strategies that do not compromise renal function should be explored in heart failure. These studies require novel diagnostic markers that identify early renal damage and renal congestion and allow monitoring of treatment responses in order to avoid severe worsening of renal function. In addition, there is an unmet need regarding evidence-based therapeutic management of renal congestion and worsening renal function. In the present review, we summarize the mechanisms, diagnosis, outcomes, prognostic markers and treatment options of renal congestion in heart failure. PMID:26798459

  7. [Diabetes and heart failure, a fatal association].

    PubMed

    Cohen-Solal, A; Logeart, D

    2007-01-01

    The prevalence of heart failure and diabetes are both increasing: 25 to 30% of patients with heart failure suffer from diabetes, and the latter aggravates heart failure. The presence of macro- or micro-angiopathy, cardiac neuropathy or renal failure worsens the clinical pattern and disturbs treatment strategies. Doppler-echocardiography and the dosage of BNP can probably help to detect and consequently to treat prematurely heart failure in the diabetic patient. The usual treatments in heart failure have similar or lower efficacy in the diabetic patient, and treatment intolerance is frequent. Treatments used for diabetes can be handled with difficulty in case of heart failure (metformin, glitazones). In the future, it is therefore extremely important: 1--to prevent the occurrence of diabetes in patients with glucose intolerance; 2--in diabetic patients, to prematurely detect cardiac dysfunction and optimally control diabetes, in order to avoid its occurrence; 3--and finally, in diabetic patients with heart failure, to optimize the medical treatment, in order that these patients have similar benefits compared to non-diabetic patients with heart failure. The ACE-inhibitors and angiotensin-2 antagonists seem to have an important role. Treatments breaking the glycation bridges, as well as statins, appear as interesting therapeutic options. Finally, the exact role of myocardial revascularization, either by angioplasty or surgery, might probably be important. PMID:17893636

  8. [Acute heart failure: precipitating factors and prevention].

    PubMed

    Aramburu Bodas, Oscar; Conde Martel, Alicia; Salamanca Bautista, Prado

    2014-03-01

    Acute heart failure episodes, whether onset or decompensation of a chronic form, are most often precipitated by a concurrent process or disease, described as precipitating factors of heart failure. In this article, we review these precipitating factors, their proportions and clinical relevance in general and in subgroups of patients, their relationship with prognosis, and their possible prevention. PMID:24930077

  9. The role of micronutrients in heart failure.

    PubMed

    McKeag, Nicholas A; McKinley, Michelle C; Woodside, Jayne V; Harbinson, Mark T; McKeown, Pascal P

    2012-06-01

    Heart failure is a common condition in the Western world, particularly among elderly persons and with an ever-aging population, the incidence is expected to increase. Diet in the setting of heart failure is important--patients with this condition are advised to consume a low-salt diet and monitor their weight closely. Nutritional status of patients with heart failure also is important--those with poor nutritional status tend to have a poor long-term prognosis. A growing body of evidence suggests an association between heart failure and micronutrient status. Reversible heart failure has been described as a consequence of severe thiamine and selenium deficiency. However, contemporary studies suggest that a more subtle relationship may exist between micronutrients and heart failure. This article reviews the existing literature linking heart failure and micronutrients, examining studies that investigated micronutrient intake, micronutrient status, and the effect of micronutrient supplementation in patients with heart failure, and focusing particularly on vitamin A, vitamin C, vitamin E, thiamine, other B vitamins, vitamin D, selenium, zinc, and copper. PMID:22709814

  10. Generation of Antigen Microarrays to Screen for Autoantibodies in Heart Failure and Heart Transplantation

    PubMed Central

    Chruscinski, Andrzej; Huang, Flora Y. Y.; Nguyen, Albert; Lioe, Jocelyn; Tumiati, Laura C.; Kozuszko, Stella; Tinckam, Kathryn J.; Rao, Vivek; Dunn, Shannon E.; Persinger, Michael A.; Levy, Gary A.; Ross, Heather J.

    2016-01-01

    Autoantibodies directed against endogenous proteins including contractile proteins and endothelial antigens are frequently detected in patients with heart failure and after heart transplantation. There is evidence that these autoantibodies contribute to cardiac dysfunction and correlate with clinical outcomes. Currently, autoantibodies are detected in patient sera using individual ELISA assays (one for each antigen). Thus, screening for many individual autoantibodies is laborious and consumes a large amount of patient sample. To better capture the broad-scale antibody reactivities that occur in heart failure and post-transplant, we developed a custom antigen microarray technique that can simultaneously measure IgM and IgG reactivities against 64 unique antigens using just five microliters of patient serum. We first demonstrated that our antigen microarray technique displayed enhanced sensitivity to detect autoantibodies compared to the traditional ELISA method. We then piloted this technique using two sets of samples that were obtained at our institution. In the first retrospective study, we profiled pre-transplant sera from 24 heart failure patients who subsequently received heart transplants. We identified 8 antibody reactivities that were higher in patients who developed cellular rejection (2 or more episodes of grade 2R rejection in first year after transplant as defined by revised criteria from the International Society for Heart and Lung Transplantation) compared with those who did have not have rejection episodes. In a second retrospective study with 31 patients, we identified 7 IgM reactivities that were higher in heart transplant recipients who developed antibody-mediated rejection (AMR) compared with control recipients, and in time course studies, these reactivities appeared prior to overt graft dysfunction. In conclusion, we demonstrated that the autoantibody microarray technique outperforms traditional ELISAs as it uses less patient sample, has increased sensitivity, and can detect autoantibodies in a multiplex fashion. Furthermore, our results suggest that this autoantibody array technology may help to identify patients at risk of rejection following heart transplantation and identify heart transplant recipients with AMR. PMID:26967734

  11. The Genomic Architecture of Sporadic Heart Failure

    PubMed Central

    Dorn, Gerald W

    2011-01-01

    Common or sporadic systolic heart failure (heart failure) is the clinical syndrome of insufficient forward cardiac output resulting from myocardial disease. Most heart failure is the consequence of ischemic or idiopathic cardiomyopathy. There is a clear familial predisposition to heart failure, with a genetic component estimated to confer between 20 and 30% of overall risk. The multifactorial etiology of this syndrome has complicated identification of its genetic underpinnings. Until recently, almost all genetic studies of heart failure were designed and deployed according to the common disease-common variant hypothesis, in which individual risk alleles impart a small positive or negative effect and overall genetic risk is the cumulative impact of all functional genetic variations. Early studies employed a candidate gene approach, focused mainly on factors within adrenergic and renin-angiotensin pathways that affect heart failure progression and are targeted by standard pharmacotherapeutics. Many of these reported allelic associations with heart failure have not been replicated. However, the preponderance of data support risk-modifier effects for the Arg389Gly polymorphism of β1-adrenergic receptors and the intron 16 in/del polymorphism of angiotensin converting enzyme. Recent unbiased studies using genome-wide single nucleotide polymorphism (SNP) microarrays have shown fewer positive results than when these platforms were applied to hypertension, myocardial infarction, or diabetes, possibly reflecting the complex etiology of heart failure. A new cardiovascular gene-centric sub-genome SNP array identified a common heat failure risk allele at 1p36 in multiple independent cohorts, but the biological mechanism for this association is still uncertain. It is likely that common gene polymorphisms account for only a fraction of individual genetic heart failure risk, and future studies using deep resequencing are likely to identify rare gene variants with larger biological effects. PMID:21566223

  12. Gene Therapy in Heart Failure

    PubMed Central

    Vinge, Leif Erik; Raake, Philip W.; Koch, Walter J.

    2008-01-01

    With increasing knowledge of basic molecular mechanisms governing the development of heart failure (HF), the possibility of specifically targeting key pathological players is evolving. Technology allowing for efficient in vivo transduction of myocardial tissue with long-term expression of a transgene enables translation of basic mechanistic knowledge into potential gene therapy approaches. Gene therapy in HF is in its infancy clinically with the predominant amount of experience being from animal models. Nevertheless, this challenging and promising field is gaining momentum as recent preclinical studies in larger animals have been carried out and, importantly, there are 2 newly initiated phase I clinical trials for HF gene therapy. To put it simply, 2 parameters are needed for achieving success with HF gene therapy: (1) clearly identified detrimental/beneficial molecular targets; and (2) the means to manipulate these targets at a molecular level in a sufficient number of cardiac cells. However, several obstacles do exist on our way to efficient and safe gene transfer to human myocardium. Some of these obstacles are discussed in this review; however, it primarily focuses on the molecular target systems that have been subjected to intense investigation over the last decade in an attempt to make gene therapy for human HF a reality. PMID:18566312

  13. Health Literacy and Heart Failure

    PubMed Central

    Cajita, Maan Isabella; Cajita, Tara Rafaela; Han, Hae-Ra

    2015-01-01

    Background Low health literacy affects millions of Americans, putting those who are affected at a disadvantage and at risk for poorer health outcomes. Low health literacy can act as a barrier to effective disease self-management; this is especially true for chronic diseases such as heart failure (HF) that require complicated self-care regimens. Purpose This systematic review examined quantitative research literature published between 1999 and 2014 to explore the role of health literacy among HF patients. The specific aims of the systematic review are to (1) describe the prevalence of low health literacy among HF patients, (2) explore the predictors of low health literacy among HF patients, and (3) discuss the relationship between health literacy and HF self-care and common HF outcomes. Methods A systematic search of the following databases was conducted, PubMed, CINAHL Plus, Embase, PsycINFO, and Scopus, using relevant keywords and clear inclusion and exclusion criteria. Conclusions An average of 39% of HF patients have low health literacy. Age, race/ethnicity, years of education, and cognitive function are predictors of health literacy. In addition, adequate health literacy is consistently correlated with higher HF knowledge and higher salt knowledge. Clinical Implications Considering the prevalence of low health literacy among in the HF population, nurses and healthcare professionals need to recognize the consequences of low health literacy and adopt strategies that could minimize its detrimental effect on the patient's health outcomes. PMID:25569150

  14. VT ablation in heart failure.

    PubMed

    Bnsch, D; Schneider, R; Akin, I; Nienaber, C A

    2012-03-01

    Ventricular tachycardias (VT), shocks, and clusters of shock are ominous signs in patients with implantable cardioverter-defibrillators and herald an increased risk of hospitalization and mortality. VT clusters have been associated with aggravation of heart failure (19%), acute coronary events (14%), and electrolyte imbalance (10%). Yet, any association of potential causative factors and aggravation of VT is vague. Maybe, in patients with any substrate for re-entry, progressive aggravation of ventricular dysrhythmias is to be expected. The high recurrence rate of electrical storm despite antiarrhythmic drug therapy supports this view. The optimal timing of VT ablation is unknown, but current convention is to perform VT ablation after shock clusters or incessant VT has occurred. Preemptive VT ablation before VT has occurred is rarely performed (only in 15% of active centers) and the majority of centers never perform VT ablation even after the first shock. Such practice is within guidelines that recommend VT ablation only in ICD patients with recurrent or incessant VT. However, there is strong data in support of preemptive VT ablation. PMID:22410757

  15. Community management of heart failure.

    PubMed Central

    McKelvie, R. S.

    1998-01-01

    OBJECTIVE: To review therapies for treating patients with heart failure (HF). QUALITY OF EVIDENCE: Recommendations in this paper are mainly based on the results of randomized controlled trials. To a lesser extent, data from smaller, more physiologic studies are included. Where appropriate, recommendations are based on the results of a consensus conference. MAIN MESSAGE: Although pharmacologic therapy is the main strategy for treating HF patients, general measures, such as counseling and advice about regular physical activity, are an important component of management. Use of angiotensin-converting enzyme inhibitors (ACE-I) is central to treating HF patients, because these agents decrease mortality and morbidity significantly. Digoxin does not reduce mortality but does reduce morbidity. Angiotensin II antagonists, although found to provide clinical benefit equal to ACE-I, have not been found as yet to have similar effects on mortality and morbidity. Diuretics and nitrates are useful for treating these patients' symptoms. Calcium channel blockers should generally be avoided. CONCLUSIONS: Angiotensin-converting enzyme inhibitors are the therapy of choice for HF patients and should be used in all cases unless there are contraindications or clear evidence of intolerance. All other therapies are used mainly for symptom relief. PMID:9870122

  16. Decongestion in Acute Heart Failure

    PubMed Central

    Mentz, Robert J.; Kjeldsen, Keld; Rossi, Gian Paolo; Voors, Adriaan A.; Cleland, John G.F.; Anker, Stefan D.; Gheorghiade, Mihai; Fiuzat, Mona; Rossignol, Patrick; Zannad, Faiez; Pitt, Bertram; OConnor, Christopher; Felker, G. Michael

    2015-01-01

    Congestion is a major reason for hospitalization in acute heart failure (HF). Therapeutic strategies to manage congestion include diuretics, vasodilators, ultrafiltration, vasopressin antagonists, mineralocorticoid receptor antagonists, and potentially also novel therapies such as gut sequesterants and serelaxin. Uncertainty exists with respect to the appropriate decongestion strategy for an individual patient. In this manuscript, we summarize the benefit and risk profiles for these decongestion strategies and provide guidance on selecting an appropriate approach for different patients. An evidence-based initial approach to congestion management involves high-dose intravenous diuretics with addition of vasodilators for dyspnea relief if blood pressure allows. To enhance diuresis or overcome diuretic resistance, options include dual nephron blockade with thiazide diuretics or natriuretic doses of mineralocorticoid receptor antagonists. Vasopressin antagonists may improve aquaresis and relieve dyspnea. If diuretic strategies are unsuccessful, then ultrafiltration may be considered. Ultrafiltration should be used with caution in the setting of worsening renal function. This review is based on discussions among scientists, clinical trialists and regulatory representatives at the 9th Global Cardio Vascular Clinical Trialists Forum in Paris, France, from November 30 to December 1, 2012. PMID:24599738

  17. Emerging Novel Therapies for Heart Failure

    PubMed Central

    Szema, Anthony M; Dang, Sophia; Li, Jonathan C

    2015-01-01

    Heart function fails when the organ is unable to pump blood at a rate proportional to the bodys need for oxygen or when this function leads to elevated cardiac chamber filling pressures (cardiogenic pulmonary edema). Despite our sophisticated knowledge of heart failure, even so-called ejection fraction-preserved heart failure has high rates of mortality and morbidity. So, novel therapies are sorely needed. This review discusses current standard therapies for heart failure and launches an exploration into emerging novel treatments on the heels of recently-approved sacubitril and ivbradine. For example, Vasoactive Intestinal Peptide (VIP) is protective of the heart, so in the absence of VIP, VIP knockout mice have dysregulation in key heart failure genes: 1) Force Generation and Propagation; 2) Energy Production and Regulation; 3) Ca+2 Cycling; 4) Transcriptional Regulators. VIP administration leads to coronary dilation in human subjects. In heart failure patients, VIP levels are elevated as a plausible endogenous protective effect. With the development of elastin polymers to stabilize VIP and prevent its degradation, VIP may therefore have a chance to satisfy the unmet need as a potential treatment for acute heart failure. PMID:26512208

  18. Heart failure - surgeries and devices

    MedlinePLUS

    ... use. Intra-aortic balloon pumps (IABP) help maintain heart function in people who are waiting for transplants. They ... who have a sudden and severe decline in heart function. The IABP is a thin, implanted balloon. Most ...

  19. Diet and Exercise Benefit People with Heart Failure

    MedlinePLUS

    ... 156532.html Diet and Exercise Benefit People With Heart Failure Combination approach greatly boosted oxygen consumption, study shows ... capacity in people with a particular form of heart failure, a new study reports. Heart failure with preserved ...

  20. Ca2+ Cycling in Heart Failure

    PubMed Central

    Luo, Min; Anderson, Mark E.

    2013-01-01

    Ca2+ plays a crucial role in connecting membrane excitability with contraction in myocardium. The hallmark features of heart failure are mechanical dysfunction and arrhythmias; defective intracellular Ca2+ homeostasis is a central cause of contractile dysfunction and arrhythmias in failing myocardium. Defective Ca2+ homeostasis in heart failure can result from pathological alteration in the expression and activity of an increasingly understood collection of Ca2+ homeostatic binding proteins, ion channels and enzymes. This review focuses on the molecular mechanisms of defective Ca2+ cycling in heart failure and consider how fundamental understanding of these pathways may translate into novel and innovative therapies. PMID:23989713

  1. Adrenal adrenoceptors in heart failure

    PubMed Central

    de Lucia, Claudio; Femminella, Grazia D.; Gambino, Giuseppina; Pagano, Gennaro; Allocca, Elena; Rengo, Carlo; Silvestri, Candida; Leosco, Dario; Ferrara, Nicola; Rengo, Giuseppe

    2014-01-01

    Heart failure (HF) is a chronic clinical syndrome characterized by the reduction in left ventricular (LV) function and it represents one of the most important causes of morbidity and mortality worldwide. Despite considerable advances in pharmacological treatment, HF represents a severe clinical and social burden. Sympathetic outflow, characterized by increased circulating catecholamines (CA) biosynthesis and secretion, is peculiar in HF and sympatholytic treatments (as ?-blockers) are presently being used for the treatment of this disease. Adrenal gland secretes Epinephrine (80%) and Norepinephrine (20%) in response to acetylcholine stimulation of nicotinic cholinergic receptors on the chromaffin cell membranes. This process is regulated by adrenergic receptors (ARs): ?2ARs inhibit CA release through coupling to inhibitory Gi-proteins, and ? ARs (mainly ?2ARs) stimulate CA release through coupling to stimulatory Gs-proteins. All ARs are G-protein-coupled receptors (GPCRs) and GPCR kinases (GRKs) regulate their signaling and function. Adrenal GRK2-mediated ?2AR desensitization and downregulation are increased in HF and seem to be a fundamental regulator of CA secretion from the adrenal gland. Consequently, restoration of adrenal ?2AR signaling through the inhibition of GRK2 is a fascinating sympatholytic therapeutic strategy for chronic HF. This strategy could have several significant advantages over existing HF pharmacotherapies minimizing side-effects on extra-cardiac tissues and reducing the chronic activation of the reninangiotensinaldosterone and endothelin systems. The role of adrenal ARs in regulation of sympathetic hyperactivity opens interesting perspectives in understanding HF pathophysiology and in the identification of new therapeutic targets. PMID:25071591

  2. Optimizing the treatment of heart failure.

    PubMed

    Giles, T D

    1994-07-01

    The introduction of new drugs, and a re-evaluation of older drugs, have radically changed the pharmacological management of heart failure. Angiotensin converting enzyme (ACE) inhibitors, digitalis, diuretics and the combination of nitrates and hydralazine are now used. The first Cooperative North Scandinavian Enalapril Survival Study (CONSENSUS I) and the second Vasodilator therapy in Heart Failure Trial (V-HeFT II) have demonstrated that patients with severe or advanced heart failure should be treated with ACE inhibitors, digitalis and diuretics (other vasodilators can be used if ACE inhibitors are contraindicated) to improve symptoms and duration of life. The Studies Of Left Ventricular Dysfunction (SOLVD) and the Munich Heart Failure trial have shown that patients with mild heart failure should be treated with ACE inhibitors. However, data from several large clinical registries suggest that only 40% of patients with heart failure are being given ACE inhibitors perhaps through fear of serious renal damage or hypotension; these fears are unfounded. Patients with anterior myocardial infarcts and reduced left ventricular function also benefit from ACE inhibitors. The fourth International Study of Infarct Survival (ISIS 4) and results from the Gruppo Italiano per Io Studio della Sopravvivenza nell'Infarto miocardico 3 (GISSI 3) have indicated that patients with acute myocardial infarction benefit from early ACE inhibitor therapy and that survival is increased. Heart failure treatment can be optimized by establishing a disease etiology and stressing the need to restrict dietary sodium. ACE inhibitors should be used for depressed left systolic ventricular function, including patients in New York Heart Association class I heart failure.(ABSTRACT TRUNCATED AT 250 WORDS) PMID:7827370

  3. Telerehabilitation for patients with heart failure

    PubMed Central

    Tousignant, Michel

    2015-01-01

    Heart failure is a chronic and progressive condition that is associated with high morbidity and mortality rates. Even though cardiac rehabilitation (CR) has been shown to be beneficial to heart failure patients, only a very small proportion of them will actually be referred and eventually participate. The low participation rate is due in part to accessibility and travel difficulties. Telerehabilitation is a new approach in the rehabilitation field that allows patients to receive a complete rehabilitation program at home in a safe manner and under adequate supervision. We believe that by increasing accessibility to CR, telerehabilitation programs will significantly improve heart failure patients functional capacity and quality of life. However, it is crucial to provide policy makers with evidence-based data on cardiac telerehabilitation if we want to see its successful implementation in heart failure patients. PMID:25774353

  4. Anticoagulation in Heart Failure: a Review

    PubMed Central

    Zeitler, Emily P.; Eapen, Zubin J

    2015-01-01

    Heart failure (HF) with reduced left ventricular function inflicts a large and growing burden of morbidity and mortality in the US and across the globe. One source of this burden is stroke. While it appears that HF itself may impose some risk of stroke, it is in the presence of other risk factors, like atrial fibrillation, that the greatest risks are observed. Therapeutic anticoagulation is the mainstay of risk reduction strategies in this population. While warfarin was the only available therapy for anticoagulation for many decades, there are now four direct oral anticoagulants available. In three of these four, outcomes in the specific subgroup of patients with heart failure have been examined. In this review, we provide some pathophysiologic basis for the risk of stroke in heart failure. In addition, the available therapeutic options for stroke risk prevention in heart failure are described in detail including how these options are incorporated into relevant professional society guidelines. PMID:26690383

  5. How Can I Live with Heart Failure?

    MedlinePLUS

    ... High Blood Pressure Tools & Resources Stroke More How Can I Live With Heart Failure? Updated:Dec 8, ... recover. Medicine Notes: Diet Notes: Exercise Notes: How can I learn more? Call 1-800-AHA-USA1 ( ...

  6. Heart failure with preserved ejection fraction

    PubMed Central

    Gladden, James D.; Linke, Wolfgang A.

    2014-01-01

    As part of this series devoted to heart failure (HF), we review the epidemiology, diagnosis, pathophysiology, and treatment of HF with preserved ejection fraction (HFpEF). Gaps in knowledge and needed future research are discussed. PMID:24663384

  7. Recent advances in treatment of heart failure

    PubMed Central

    Kitai, Takeshi; Tang, WH Wilson

    2015-01-01

    With the total cases and economic burden of heart failure continuing to rise, there is an overwhelming need for novel therapies. Several drugs for heart failure have succeeded in preclinical and early-phase clinical trials, but most of them failed to show the real benefit in pivotal clinical trials. Meanwhile, the US Food and Drug Administration recently approved two promising new drugs to treat heart failure: ivabradine and sacubitril/valsartan. Furthermore, some of the newer agents in testing offer the potential for significant progress in addition to these drugs. Patiromer and zirconium cyclosilicate are attractive agents that are expected to prevent hyperkalemia during renin-angiotensin-aldosterone system inhibition, and serelaxin and urodilatin are promising drugs in the treatment of acute heart failure. Future clinical trials with more appropriate study designs, optimal clinical endpoints, and proper patient selection are mandatory to assess the true efficacy of these attractive compounds in clinical practice. PMID:26918130

  8. Drug Therapy for Acute Heart Failure.

    PubMed

    Di Somma, Salvatore; Magrini, Laura

    2015-08-01

    Acute heart failure is globally one of most frequent reasons for hospitalization and still represents a challenge for the choice of the best treatment to improve patient outcome. According to current international guidelines, as soon as patients with acute heart failure arrive at the emergency department, the common therapeutic approach aims to improve their signs and symptoms, correct volume overload, and ameliorate cardiac hemodynamics by increasing vital organ perfusion. Recommended treatment for the early management of acute heart failure is characterized by the use of intravenous diuretics, oxygen, and vasodilators. Although these measures ameliorate the patient's symptoms, they do not favorably impact on short- and long-term mortality. Consequently, there is a pressing need for novel agents in acute heart failure treatment with the result that research in this field is increasing worldwide. PMID:26088867

  9. Recent progress in heart failure treatment and heart transplantation.

    PubMed

    Augoustides, John G T; Riha, Hynek

    2009-10-01

    There has been significant progress in heart failure treatment; its stages are defined as a management platform for cardiovascular specialists. Surgical ventricular restoration adds no outcome advantage in ischemic heart failure over coronary artery bypass surgery alone. Novel medical therapies may include cytokine blockade and the vasodilator, relaxin. Although diastolic failure is prevalent, its clinical significance is unclear. Cardiac resynchronization reduces mortality and hospitalization. Perioperative enoximone facilitates beta-blockade for prophylaxis against myocardial ischemia. Heart failure still determines outcome in pulmonary embolism and cardiac surgery. The practice of ventricular assist devices continues to progress. A profile system based on urgency of mechanical support will guide future outcome assessment. Clinical scoring systems will guide the management of right heart failure. Device flow determines the risk of cerebral hyperperfusion and neurologic dysfunction. Regardless of device type, renal dysfunction remains an important outcome determinant. Postoperative heparinization is increasingly challenged because of the risks of bleeding and heparin-induced thrombocytopenia. The practice of heart transplantation continues to mature. The bicaval rather than the biatrial technique improves short-term outcome. Oral sildenafil is effective for pulmonary hypertension and right ventricular support. Although immunosuppression with tacrolimus is beneficial, sirolimus is less nephrotoxic and preserves coronary vasomotor function. The induction of immunosuppression may be modified as it has a weak evidence base. Psychosocial factors also continue to influence clinical outcome significantly. The future of heart failure treatment is bright with signs of active growth and progress in this vibrant subspecialty. PMID:19686962

  10. [Congestive heart failure in infancy and childhood].

    PubMed

    Schmaltz, A A

    1999-01-01

    Congestive heart failure is the inability of the heart to provide a sufficient output at a sufficient arterial pressure for the metabolic needs of the organism. Having presented the physiologic mechanisms of the contraction of the heart and its regulatory mechanisms the different aspects of classification of heart failure and its neurohormonal modulation are described. The epidemiology of heart failure in childhood is largely unknown, the causes vary considerably, symptoms are age-dependent. Main diagnostic tools for etiologic clarification are echocardiography and chest-x-ray. Focus of therapy is to eliminate the causes, but general recommendations may not be forgotten. Medical treatment of acute severe heart failure is use of catecholamines, ino- and vasodilators in the intensive care unit. Therapy of chronic heart failure is performed with diuretics, digitalis and ACE-inhibitors. Their pharmacologic effect, therapeutic trials in adults and children and peculiarities of pharmacology and side effects in childhood are reported. Low dose beta-blockers are a new therapeutic strategy still not established in children. PMID:10067211

  11. Update: Acute Heart Failure (VII): Nonpharmacological Management of Acute Heart Failure.

    PubMed

    Plcido, Rui; Mebazaa, Alexandre

    2015-09-01

    Acute heart failure is a major and growing public health problem worldwide with high morbidity, mortality, and cost. Despite recent advances in pharmacological management, the prognosis of patients with acute decompensated heart failure remains poor. Consequently, nonpharmacological approaches are being developed and increasingly used. Such techniques may include several modalities of ventilation, ultrafiltration, mechanical circulatory support, myocardial revascularization, and surgical treatment, among others. This document reviews the nonpharmacological approach in acute heart failure, indications, and prognostic implications. PMID:26169327

  12. In-hospital worsening heart failure.

    PubMed

    Butler, Javed; Gheorghiade, Mihai; Kelkar, Anita; Fonarow, Gregg C; Anker, Stefan; Greene, Stephen J; Papadimitriou, Lampros; Collins, Sean; Ruschitzka, Frank; Yancy, Clyde W; Teerlink, John R; Adams, Kirkwood; Cotter, Gadi; Ponikowski, Piotr; Felker, G Michael; Metra, Marco; Filippatos, Gerasimos

    2015-11-01

    Acute worsening heart failure (WHF) is seen in a sizable portion of patients hospitalized for heart failure, and is increasingly being recognized as an entity that is associated with an adverse in-hospital course. WHF is generally defined as worsening heart failure symptoms and signs requiring an intensification of therapy, and is reported to be seen in anywhere from 5% to 42% of heart failure admissions. It is difficult to ascertain the exact epidemiology of WHF due to varying definitions used in the literature. Studies indicate that WHF cannot be precisely predicted on the basis of baseline variables assessed at the time of admission. Recent data suggest that some experimental therapies may reduce the risk of development of WHF among hospitalized heart failure patients, and this is associated with a reduction in risk of subsequent post-discharge cardiovascular mortality. In this respect, WHF holds promise as a endpoint for acute heart failure clinical trials to better elucidate the benefit of targeted novel therapies. Better understanding of the pathophysiology and a consensus on the definition of WHF will further improve our epidemiological and clinical understanding of this entity. PMID:26235192

  13. Heart failure in sub-Saharan Africa.

    PubMed

    Bloomfield, Gerald S; Barasa, Felix A; Doll, Jacob A; Velazquez, Eric J

    2013-05-01

    The heart failure syndrome has been recognized as a significant contributor to cardiovascular disease burden in sub-Saharan African for many decades. Seminal knowledge regarding heart failure in the region came from case reports and case series of the early 20th century which identified infectious, nutritional and idiopathic causes as the most common. With increasing urbanization, changes in lifestyle habits, and ageing of the population, the spectrum of causes of HF has also expanded resulting in a significant burden of both communicable and non-communicable etiologies. Heart failure in sub-Saharan Africa is notable for the range of etiologies that concurrently exist as well as the healthcare environment marked by limited resources, weak national healthcare systems and a paucity of national level data on disease trends. With the recent publication of the first and largest multinational prospective registry of acute heart failure in sub-Saharan Africa, it is timely to review the state of knowledge to date and describe the myriad forms of heart failure in the region. This review discusses several forms of heart failure that are common in sub-Saharan Africa (e.g., rheumatic heart disease, hypertensive heart disease, pericardial disease, various dilated cardiomyopathies, HIV cardiomyopathy, hypertrophic cardiomyopathy, endomyocardial fibrosis, ischemic heart disease, cor pulmonale) and presents each form with regard to epidemiology, natural history, clinical characteristics, diagnostic considerations and therapies. Areas and approaches to fill the remaining gaps in knowledge are also offered herein highlighting the need for research that is driven by regional disease burden and needs. PMID:23597299

  14. Heart Failure in Sub-Saharan Africa

    PubMed Central

    Bloomfield, Gerald S; Barasa, Felix A; Doll, Jacob A; Velazquez, Eric J

    2013-01-01

    The heart failure syndrome has been recognized as a significant contributor to cardiovascular disease burden in sub-Saharan African for many decades. Seminal knowledge regarding heart failure in the region came from case reports and case series of the early 20th century which identified infectious, nutritional and idiopathic causes as the most common. With increasing urbanization, changes in lifestyle habits, and ageing of the population, the spectrum of causes of HF has also expanded resulting in a significant burden of both communicable and non-communicable etiologies. Heart failure in sub-Saharan Africa is notable for the range of etiologies that concurrently exist as well as the healthcare environment marked by limited resources, weak national healthcare systems and a paucity of national level data on disease trends. With the recent publication of the first and largest multinational prospective registry of acute heart failure in sub-Saharan Africa, it is timely to review the state of knowledge to date and describe the myriad forms of heart failure in the region. This review discusses several forms of heart failure that are common in sub-Saharan Africa (e.g., rheumatic heart disease, hypertensive heart disease, pericardial disease, various dilated cardiomyopathies, HIV cardiomyopathy, hypertrophic cardiomyopathy, endomyocardial fibrosis, ischemic heart disease, cor pulmonale) and presents each form with regard to epidemiology, natural history, clinical characteristics, diagnostic considerations and therapies. Areas and approaches to fill the remaining gaps in knowledge are also offered herein highlighting the need for research that is driven by regional disease burden and needs. PMID:23597299

  15. Heart failure and Starling's Law of the heart.

    PubMed

    ter Keurs, H E

    1996-10-01

    Coronary artery disease and ischemic myocardial damage form the most common cause of failure of the heart to pump enough blood for oxygenation of the body at a healthy blood pressure and at a low pressure in the veins. This paper gives an overview of the mechanisms involved in excitation-contraction coupling which are important to control of the force of the heartbeat. The inability of the heart in failure to eject a sufficient amount of blood in order to meet the needs of the body is thought to result from molecular changes in cardiac cells causing decreased active (systolic) force and impaired (diastolic) relaxation together with a greater stiffness of the remodelled ventricular wall. The failure to generate a forceful contraction is in part a consequence of derailment of the processes in the failing cardiac cells to manipulate calcium ions, despite the increased stimulus from nervous and hormone systems to enhance cardiac performance. By lack of adequate release and uptake of calcium ions, the amount of mechanical work that can be put out by the heart muscle is diminished and the heart may fail. Uptake of calcium ions by the intracellular store-the sarcoplasmic reticulum-is impaired in congestive heart failure probably as result of inadequate gene expression. In consequence, the amount of calcium that is released during each heartbeat is less than normal, thus force is reduced; in addition, the positive response of force to increased heart rate is lost. In normal heart muscle, the response of the contractile filaments to calcium ions depends strongly on sarcomere length thus explaining Starling's Law of the heart. Recent evidence suggests that this sensitivity is largely lost in congestive heart failure thereby reducing the effectiveness of stretch of cardiac cells on the mechanical output. The reduction of the maximal velocity of shortening of the cardiac sarcomere in heart failure is not well understood, but may in part be related to changes in the internal load as a result of changes in visco-elastic components of the myocardium Lastly, the effect of longstanding sympathetic drive to the heart during the development of heart failure induces a loss of sensitivity of the myocardium to catecholamines by loss of beta 1 receptors and partial uncoupling of the beta receptors from production of cyclic AMP; hence the effect of sympathetic activation is diminished and the heart has to rely more on Starling's Law. Increase of the filling pressure of the left ventricle may in part accommodate the ongoing demands of the body. However, in the case of a stenosed coronary arterial system, the increased end-diastolic pressure carries the substantial risk of aggravating pre-existent myocardial ischemia. PMID:9191498

  16. Optimization of cardiac metabolism in heart failure.

    PubMed

    Nagoshi, Tomohisa; Yoshimura, Michihiro; Rosano, Giuseppe M C; Lopaschuk, Gary D; Mochizuki, Seibu

    2011-12-01

    The derangement of the cardiac energy substrate metabolism plays a key role in the pathogenesis of heart failure. The utilization of non-carbohydrate substrates, such as fatty acids, is the predominant metabolic pathway in the normal heart, because this provides the highest energy yield per molecule of substrate metabolized. In contrast, glucose becomes an important preferential substrate for metabolism and ATP generation under specific pathological conditions, because it can provide greater efficiency in producing high energy products per oxygen consumed compared to fatty acids. Manipulations that shift energy substrate utilization away from fatty acids toward glucose can improve the cardiac function and slow the progression of heart failure. However, insulin resistance, which is highly prevalent in the heart failure population, impedes this adaptive metabolic shift. Therefore, the acceleration of the glucose metabolism, along with the restoration of insulin sensitivity, would be the ideal metabolic therapy for heart failure. This review discusses the therapeutic potential of modifying substrate utilization to optimize cardiac metabolism in heart failure. PMID:21933140

  17. Ankyrin-B Protein in Heart Failure

    PubMed Central

    Kashef, Farshid; Li, Jingdong; Wright, Patrick; Snyder, Jedidiah; Suliman, Faroug; Kilic, Ahmet; Higgins, Robert S. D.; Anderson, Mark E.; Binkley, Philip F.; Hund, Thomas J.; Mohler, Peter J.

    2012-01-01

    Ankyrins (ankyrin-R, -B, and -G) are adapter proteins linked with defects in metazoan physiology. Ankyrin-B (encoded by ANK2) loss-of-function mutations are directly associated with human cardiovascular phenotypes including sinus node disease, atrial fibrillation, ventricular tachycardia, and sudden cardiac death. Despite the link between ankyrin-B dysfunction and monogenic disease, there are no data linking ankyrin-B regulation with common forms of human heart failure. Here, we report that ankyrin-B levels are altered in both ischemic and non-ischemic human heart failure. Mechanistically, we demonstrate that cardiac ankyrin-B levels are tightly regulated downstream of reactive oxygen species, intracellular calcium, and the calcium-dependent protease calpain, all hallmarks of human myocardial injury and heart failure. Surprisingly, ?II-spectrin, previously thought to mediate ankyrin-dependent modulation in the nervous system and heart, is not coordinately regulated with ankyrin-B or its downstream partners. Finally, our data implicate ankyrin-B expression as required for vertebrate myocardial protection as hearts deficient in ankyrin-B show increased cardiac damage and impaired function relative to wild-type mouse hearts following ischemia reperfusion. In summary, our findings provide the data of ankyrin-B regulation in human heart failure, provide insight into candidate pathways for ankyrin-B regulation in acquired human cardiovascular disease, and surprisingly, implicate ankyrin-B as a molecular component for cardioprotection following ischemia. PMID:22778271

  18. [Appendicular thermal therapy for heart failure].

    PubMed

    Komamura, Kazuo

    2009-03-01

    We preliminarily assessed the utility of a steam foot bath in 4 male patients with dilated cardiomyopathy with refractory chronic congestive heart failure awaiting heart transplantation. Sublingual temperature significantly increased from 36.1 +/- 0.3 to 36.7 +/- 0.2 degrees C (p = 0.01). Blood pressure, heart rate and numbers of ventricular arrhythmia did not differ before and after two weeks of the therapy. Grade of mitral regurgitation tended to decrease (2.0 +/- 1.2 to 1.3 +/- 1.0, p = 0.06), and endothelial function measured by arterial tonometry significantly increased from 1.35 +/- 0.26 to 2.13 +/- 0.26 (p = 0.02). Thus, steam foot bath therapy may be safe and beneficial for the patients with endstage heart failure awaiting heart transplantation. PMID:19280944

  19. Metabolic and Signaling Alterations in Dystrophin-Deficient Hearts Precede Overt Cardiomyopathy

    Technology Transfer Automated Retrieval System (TEKTRAN)

    The cytoskeletal protein dystrophin has been implicated in hereditary and acquired forms of cardiomyopathy. However, much remains to be learned about the role of dystrophin in the heart. We hypothesized that the dystrophin-deficient heart displays early alterations in energy metabolism that precede ...

  20. Nebivolol for the treatment of heart failure.

    PubMed

    Dery, Allison S; Hamilton, Leslie A; Starr, Jessica A

    2011-05-15

    PURPOSE. The pharmacology, pharmacokinetics, efficacy, safety, and place in therapy of nebivolol are reviewed. SUMMARY. Nebivolol, a third-generation, highly ?(1)-specific ?-blocker, is labeled for the treatment of hypertension in the United States. In addition to its ?-blocking effects, nebivolol has been shown to increase endothelin-dependent nitric oxide, giving it a unique peripheral vasodilatory action. Nebivolol is extensively metabolized by cytochrome P-450 isoenzyme 2D6. In patients with heart failure, certain ?-blockers antagonize excessive adrenergic stimulation and can slow the progression of the disease. Clinical trials have compared nebivolol at target dosages of 5 and 10 mg once daily with placebo and, in small trials, with carvedilol in the treatment of adults with chronic heart failure. Nebivolol appears to have beneficial effects in patients with heart failure, including improvements in left ventricular ejection fraction, left ventricular volumes, and exercise capacity. In addition, the Study of the Effects of Nebivolol Intervention on Outcomes and Rehospitalisation in Seniors with Heart Failure showed a reduction in morbidity and mortality after treatment with nebivolol when compared with placebo, though this effect appeared to be less than that of other ?-blockers currently recommended for the treatment of heart failure. Nebivolol was well tolerated in all clinical trials, with the most frequently reported adverse events including bradycardia, hypotension, and dizziness. To date, no large clinical trials have compared nebivolol with currently recommended ?-blockers in patients with heart failure. CONCLUSION. Nebivolol has beneficial effects in heart failure but cannot be considered equivalent to other currently accepted therapies. PMID:21546638

  1. What Are the Signs and Symptoms of Heart Failure?

    MedlinePLUS

    ... Twitter. What Are the Signs and Symptoms of Heart Failure? The most common signs and symptoms of heart ... in your lungs. The condition requires emergency treatment. Heart Failure Signs and Symptoms The image shows the major ...

  2. Learn More about Heart Failure

    MedlinePLUS

    ... valsartan) tablets... Journal of Cardiac Failure Call for Papers: Cardio-oncology Focus Issue November 5, 2015 The ... JCF is interested in original contributions and review papers on cardio-oncology. Manuscripts... Join/Renew JCF Call ...

  3. Hemoconcentration-guided diuresis in heart failure.

    PubMed

    Vaduganathan, Muthiah; Greene, Stephen J; Fonarow, Gregg C; Voors, Adriaan A; Butler, Javed; Gheorghiade, Mihai

    2014-12-01

    One quarter of patients hospitalized for heart failure are readmitted within 30 days, perhaps related to ineffective decongestion. Limited data exist guiding the extent and duration of diuresis in patients hospitalized for heart failure. The objective of this review was to determine the prognostic value of hemoconcentration, or the relative increase in the cellular elements in blood, in patients hospitalized for heart failure and to clarify its role in guiding inpatient diuretic practices. Six post hoc retrospective studies from 2010 to 2013 were available for review. Hemoconcentration was consistently associated with markers of aggressive fluid removal, including higher diuretic dosing and reduced body weight, but increased risk of in-hospital worsening renal function. Despite this, hemoconcentration was associated with improved short-term mortality and rehospitalization. Hemoconcentration is a practical, readily available, noninvasive, economically feasible strategy to help guide diuresis and monitor congestion relief in patients hospitalized for worsening heart failure. Clinicians should strongly consider using changes in hemoglobin and hematocrit as an adjunct to other available measures of decongestion and clinical acumen in inpatient heart failure care. PMID:24937157

  4. Heart failure with preserved ejection fraction

    PubMed Central

    ElGuindy, Ahmed; Yacoub, Magdi H

    2012-01-01

    Abstract Heart failure with preserved ejection fraction (HFpEF) has recently emerged as a major cause of cardiovascular morbidity and mortality. Contrary to initial beliefs, HFpEF is now known to be as common as heart failure with reduced ejection fraction (HFrEF) and carries an unacceptably high mortality rate. With a prevalence that has been steadily rising over the past two decades, it is very likely that HFpEF will represent the dominant heart failure phenotype over the coming few years. The scarcity of trials in this semi-discrete form of heart failure and lack of unified enrolment criteria in the studies conducted to date might have contributed to the current absence of specific therapies. Understanding the epidemiological, pathophysiological and molecular differences (and similarities) between these two forms of heart failure is cornerstone to the development of targeted therapies. Carefully designed studies that adhere to unified diagnostic criteria with the recruitment of appropriate controls and adoption of practical end-points are urgently needed to help identify effective treatment strategies. PMID:25610841

  5. [Management of comorbidities in heart failure].

    PubMed

    Peperstraete, B

    2013-01-01

    We will review some diseases that interfere most with management of heart failure : anemia, chronic renal failure, chronic pulmonary diseases, diabetes, atrial fibrillation/flutter, sleep apnea, angina, systemic arterial hypertension, rheumatic disease, depression and anticancer chemotherapy. We will retain principally their therapeutic implications. Anemia can be partially corrected by administration of intravenous iron or erythropoietin. Chronic renal failure requires adaptation of the treatment, in particular for drugs of the renin-angiotensin-aldosterone system. Chronic pulmonary diseases complicate diagnosis of heart failure and may lead to sub prescription of beta-blockers. Diabetes does not alter the usual recommendations for the treatment of heart failure but some hypoglycemic medications should be prescribed with caution. In the presence of atrial fibrillation or flutter, the main purpose of the treatment is to improve the quality of live and to diminish the thromboembolic risk ; it may be obtained by rhythm or rate control. Therapeutic approach of sleep apnea is based on optimal treatment of heart failure and weight loss. In the presence of angina, systemic arterial hypertension, rheumatic disease or depression, certain drugs usually prescribed are contraindicated or must be prescribed with caution. Finally, chemotherapy can be cardiotoxic and require careful monitoring of cardiac function. PMID:23951855

  6. Mitochondrial Dynamics and Heart Failure.

    PubMed

    Knowlton, A A; Liu, T T

    2015-01-01

    Mitochondrial dynamics, fission and fusion, were first identified in yeast with investigation in heart cells beginning only in the last 5 to 7 years. In the ensuing time, it has become evident that these processes are not only required for healthy mitochondria, but also, that derangement of these processes contributes to disease. The fission and fusion proteins have a number of functions beyond the mitochondrial dynamics. Many of these functions are related to their membrane activities, such as apoptosis. However, other functions involve other areas of the mitochondria, such as OPA1's role in maintaining cristae structure and preventing cytochrome c leak, and its essential (at least a 10 kDa fragment of OPA1) role in mtDNA replication. In heart disease, changes in expression of these important proteins can have detrimental effects on mitochondrial and cellular function. © 2016 American Physiological Society. Compr Physiol 6:507-526, 2016. PMID:26756641

  7. Can complexity decrease in congestive heart failure?

    NASA Astrophysics Data System (ADS)

    Mukherjee, Sayan; Palit, Sanjay Kumar; Banerjee, Santo; Ariffin, M. R. K.; Rondoni, Lamberto; Bhattacharya, D. K.

    2015-12-01

    The complexity of a signal can be measured by the Recurrence period density entropy (RPDE) from the reconstructed phase space. We have chosen a window based RPDE method for the classification of signals, as RPDE is an average entropic measure of the whole phase space. We have observed the changes in the complexity in cardiac signals of normal healthy person (NHP) and congestive heart failure patients (CHFP). The results show that the cardiac dynamics of a healthy subject is more complex and random compare to the same for a heart failure patient, whose dynamics is more deterministic. We have constructed a general threshold to distinguish the border line between a healthy and a congestive heart failure dynamics. The results may be useful for wide range for physiological and biomedical analysis.

  8. Heart failure and Alzheimer′s disease

    PubMed Central

    Cermakova, P; Eriksdotter, M; Lund, L H; Winblad, B; Religa, P; Religa, D

    2015-01-01

    It has recently been proposed that heart failure is a risk factor for Alzheimer′s disease. Decreased cerebral blood flow and neurohormonal activation due to heart failure may contribute to the dysfunction of the neurovascular unit and cause an energy crisis in neurons. This leads to the impaired clearance of amyloid beta and hyperphosphorylation of tau protein, resulting in the formation of amyloid beta plaques and neurofibrillary tangles. In this article, we will summarize the current understanding of the relationship between heart failure and Alzheimer′s disease based on epidemiological studies, brain imaging research, pathological findings and the use of animal models. The importance of atherosclerosis, myocardial infarction, atrial fibrillation, blood pressure and valve disease as well as the effect of relevant medications will be discussed. PMID:25041352

  9. Congestive Heart Failure and Central Sleep Apnea.

    PubMed

    Sands, Scott A; Owens, Robert L

    2016-03-01

    Congestive heart failure (CHF) is among the most common causes of admission to hospitals in the United States, especially in those over age 65. Few data exist regarding the prevalence CHF of Cheyne-Stokes respiration (CSR) owing to congestive heart failure in the intensive care unit (ICU). Nevertheless, CSR is expected to be highly prevalent among those with CHF. Treatment should focus on the underlying mechanisms by which CHF increases loop gain and promotes unstable breathing. Few data are available to determine prevalence of CSR in the ICU, or how CSR might affect clinical management and weaning from mechanical ventilation. PMID:26972039

  10. Disease management for chronic congestive heart failure.

    PubMed

    Brass-Mynderse, N J

    1996-10-01

    The dilemma of the high cost of quality health care in a managed care environment for chronic disease populations has led to the development of a nurse-managed chronic care clinic that focuses on outpatient case management of chronic diseases beginning with chronic heart failure patients. The clinic provides advanced practice nurse management for heart failure patients in pharmacotherapy, education, counseling, dietary and lipid management, and exercise training via software management programs. The clinic is developing further management for comorbidity factors such as diabetes and chronic obstructive pulmonary disease. The history, development, and function of the clinic are reviewed. PMID:9069031

  11. The management of congestive heart failure.

    PubMed Central

    McAlister, F. A.; Teo, K. K.

    1997-01-01

    Despite the remarkable advances in cardiovascular therapeutics over the past four decades, little impact has been made on either the incidence or mortality rate of congestive heart failure and it remains a major clinical and public health problem. Recent practice audits have suggested that proven efficacious therapies are not maximally applied in patients with this condition. An approach to the patient with congestive heart failure is presented, emphasizing the two distinct syndromes of systolic dysfunction and diastolic dysfunction. Treatment recommendations are derived from consideration of the underlying pathophysiology and the evidence from randomised clinical trials. PMID:9156120

  12. Autonomic Regulation Therapy in Heart Failure.

    PubMed

    Buckley, Una; Shivkumar, Kalyanam; Ardell, Jeffrey L

    2015-08-01

    Autonomic regulation therapy (ART) is a rapidly emerging therapy in the management of congestive heart failure secondary to systolic dysfunction. Modulation of the cardiac neuronal hierarchy can be achieved with bioelectronics modulation of the spinal cord, cervical vagus, baroreceptor, or renal nerve ablation. This review will discuss relevant preclinical and clinical research in ART for systolic heart failure. Understanding mechanistically what is being stimulated within the autonomic nervous system by such device-based therapy and how the system reacts to such stimuli is essential for optimizing stimulation parameters and for the future development of effective ART. PMID:26054327

  13. Electron transport chain defects in heart failure.

    PubMed

    Casademont, Jordi; Mir, Oscar

    2002-04-01

    In recent years, the possibility that disorders of cardiac metabolism play a role in the mechanisms that lead to ventricular dilatation and dysfunction in heart failure has attracted much attention. Electron transport chain is constituted by a series of multimeric protein complexes, located in the inner mitochondrial membranes, whose genes are distributed over both nuclear and mitochondrial DNA. Its normal function is essential to provide the energy for cardiac function. Many studies have described abnormalities in mitochondrial DNA genes encoding for electron transport chain (ETC) in dilated cardiomyopathies. In some cases, heart failure is one more or less relevant symptom among other multisystem manifestations characteristic of mitochondrial encephalomyopathies, being heart failure imputable to a primary mitochondrial disease. In the case of idiopathic dilated cardiomyopathies (IDC), many mitochondrial abnormalities have also been described using hystological, biochemical or molecular studies. The importance of such findings is under debate. The great variability in the mitochondrial abnormalities described has prompted the proposal that mitochondrial dysfunction could be a secondary phenomenon in IDC, and not a primary one. Among other possible explanations for such findings, the presence of an increased oxidative damage due to a free radical excess has been postulated. In this setting, the dysfunction of ETC could be a consequence, but also a cause of the presence of an increased free radical damage. Independently of its origin, ETC dysfunction may contribute to the persistence and worsening of heart failure. If this hypothesis, still to be proven, was certain, the modulation of cardiac metabolism could be an interesting approach to treat IDC. The precise mechanisms that lead to ventricular dilatation and dysfunction in heart failure are still nowadays poorly understood. Circumstances such as cytotoxic insults, viral infections, immune abnormalities, contractile protein defects, ischemic factors and familial conditions have been thoroughly investigated [1]. It is possible that several mechanisms combine to produce the clinical syndrome of heart failure. In recent years the possibility that disorders of energy metabolism, either isolated or in combination with the other aforementioned factors, may play a role in the development of heart failure in susceptible patients has attracted much attention. The present paper reviews the current knowledge on mitochondrial function in the failing myocardium. We restrain our discussion to heart failure where an impaired inotropic state leads to a weakened systolic contraction (i.e. the so-called systolic heart failure). Idiopathic dilated cardiomyopathy (IDC) is the prototype of the conditions under discussion. Other circumstances where a defect in myocardial contraction is due to a chronic excessive work load (i.e., hypertension, valvular or congenital heart diseases), and states in which the principal abnormality involves impaired relaxation of the ventricle (i.e. diastolic heart failure), as well as mitochondrial defects outside the electron transport chain (i.e., defects in Krebs cycle or beta-oxidation of fatty acids) are only approached circumstantially. PMID:11988637

  14. Acute Heart Failure from Lyme Carditis

    PubMed Central

    Koene, Ryan; Boulware, David R.; Kemperman, Melissa; Konety, Suma H.; Groth, Morgan; Jessurun, Jose; Eckman, Peter M.

    2012-01-01

    Carditis can complicate Lyme disease in an estimated <5% of cases, but cardiogenic shock is rare. We report a case of severe biventricular heart failure as a manifestation of a Jarisch-Herxheimer reaction in a patient with early Lyme disease following treatment with ceftriaxone. PMID:22438525

  15. Imaging Techniques in Acute Heart Failure.

    PubMed

    Prez del Villar, Candelas; Yotti, Raquel; Bermejo, Javier

    2015-07-01

    In recent years, imaging techniques have revolutionized the diagnosis of heart failure. In patients with a clinical picture of acute decompensation, prognosis is largely determined by early implementation of general measures and treatment of the underlying cause. Given its diagnostic yield and portability, ultrasound has become an essential tool in the setting of acute heart failure, and is currently found in all medical departments involved in the care of the critically ill patient. Cardiac magnetic resonance and computed tomography allow detailed characterization of multiple aspects of cardiac structure and function that were previously unavailable. This helps guide and monitor many of the treatment decisions in the acute heart failure population in an entirely noninvasive way. This article aims to review the usefulness of the imaging techniques that are clinically relevant in the context of an episode of acute heart failure. We discuss the indications and limitations of these techniques in detail and describe the general principles for the appropriate interpretation of results. PMID:26002273

  16. Nonadherence in the Advanced Heart Failure Population.

    PubMed

    Gandhi, Jonathan; McCue, Andrew; Cole, Robert

    2016-04-01

    The number of patients living with heart failure (HF) in the USA now exceeds 5 million. Although HF is a disease readily treated by medications and lifestyle interventions, nonadherence is common, leading to worse clinical outcomes and increased healthcare costs. While adherence to medical therapy and clinician recommendations is key in the management of HF, it is perhaps more critical in patients with the most advanced disease, including those receiving home inotropic infusion, heart transplantation, or a left ventricular assist device. Yet, there is a paucity of data on the effects of nonadherence on the advanced heart failure population and little information on the most effective management strategies in these patients. Future studies of nonadherence in HF should utilize uniform definitions of adherence and, ideally, more objective measurements of adherence such as the novel "digital pill" technology. PMID:26879391

  17. Cell therapy in congestive heart failure*

    PubMed Central

    Tao, Ze-wei; Li, Long-gui

    2007-01-01

    Congestive heart failure (CHF) has emerged as a major worldwide epidemic and its main causes seem to be the aging of the population and the survival of patients with post-myocardial infarction. Cardiomyocyte dropout (necrosis and apoptosis) plays a critical role in the progress of CHF; thus treatment of CHF by exogenous cell implantation will be a promising medical approach. In the acute phase of cardiac damage cardiac stem cells (CSCs) within the heart divide symmetrically and/or asymmetrically in response to the change of heart homeostasis, and at the same time homing of bone marrow stem cells (BMCs) to injured area is thought to occur, which not only reconstitutes CSC population to normal levels but also repairs the heart by differentiation into cardiac tissue. So far, basic studies by using potential sources such as BMCs and CSCs to treat animal CHF have shown improved ventricular remodelling and heart function. Recently, however, a few of randomized, double-blind, placebo-controlled clinical trials demonstrated mixed results in heart failure with BMC therapy during acute myocardial infarction. PMID:17726746

  18. Exercise and heart failure in the elderly.

    PubMed

    Kappagoda, Tissa; Amsterdam, Ezra A

    2012-09-01

    In this review, we will examine the physiological responses to exercise in elderly populations (age>65years) with and without evidence of heart failure. Aging per se in both men and women is associated with a ~40% lower maximum oxygen consumption in sedentary subjects. In trained individuals, this value is 25-32% lower. A smaller SV accounts for nearly 50% of these age-related differences, and the remainder is explained by a lower maximal HR and reduced oxygen extraction. Exercise training is also associated with an increase in the arteriovenous O(2) difference in previously sedentary elderly men and women, which probably contributes to the overall beneficial effect of training in the elderly. However, during vigorous exercise (125W), the cardiac output in the elderly is dependent upon an age-related increase in end-diastolic volume and stroke volume, which "compensates" partially for the age-related decrease in heart rate. Hence, in elderly individuals, the stroke volume during exercise depends upon diastolic filling. The changes that occur in the heart are also associated with an overall reduction in efferent sympathetic nerve activity. Despite this decline, the metaboreflex initiated by receptors in exercising muscles remains the main determinant of sympathetic activation (to maintain blood pressure) during exercise in the elderly. It is recognized that aging is associated with the development of heart failure, particularly in women in whom its prevalence increases >twofold from age 65-69 (6.6%) to age 85years (14%). Almost half the people presenting with heart failure appear to have normal left ventricular systolic function, a phenomenon that is more common in women. Exercise training in elderly people with and without heart failure appears to have a beneficial effect in terms of enhancing the quality of life and functional capacity. Mortality benefit in the latter has not been established with certainty. PMID:22327748

  19. Remote monitoring of heart failure patients.

    PubMed

    Bhimaraj, Arvind

    2013-01-01

    "The Teledactyl (Tele, far; Dactyl, finger--from the Greek) is a future instrument by which it will be possible for us to 'feel at a distance.' This idea is not at all impossible, for the instrument can be built today with means available right now. It is simply the well known telautograph, translated into radio terms, with additional refinements. The doctor of the future, by means of this instrument, will be able to feel his patient, as it were, at a distance...The doctor manipulates his controls, which are then manipulated at the patient's room in exactly the same manner. The doctor sees what is going on in the patient's room by means of a television screen." -Hugo Gernsback, Science and Invention Magazine, February 1925 Heart failure continues to be a major burden on our health care system. As the number of patients with heart failure increases, the cost of hospitalization alone is contributing significantly to the overall cost of this disease. Readmission rate and hospital length of stay are emerging as quality markers of heart failure care along with reimbursement policies that force hospitals to optimize these outcomes. Apart from maintaining quality assurance, the disease process of heart failure per-se requires demanding and close attention to vitals, diet, and medication compliance to prevent acute decompensation episodes. Remote patient monitoring is morphing into a key disease management strategy to optimize care for heart failure. Innovative implantable technologies to monitor intracardiac hemodynamics also are evolving, which potentially could offer better and substantial parameters to monitor. PMID:23519115

  20. Remote Monitoring of Heart Failure Patients

    PubMed Central

    Bhimaraj, Arvind

    2013-01-01

    “The Teledactyl (Tele, far; Dactyl, finger — from the Greek) is a future instrument by which it will be possible for us to ‘feel at a distance.’ This idea is not at all impossible, for the instrument can be built today with means available right now. It is simply the well known telautograph, translated into radio terms, with additional refinements. The doctor of the future, by means of this instrument, will be able to feel his patient, as it were, at a distance…The doctor manipulates his controls, which are then manipulated at the patient’s room in exactly the same manner. The doctor sees what is going on in the patient’s room by means of a television screen.” —Hugo Gernsback, Science and Invention Magazine, February 1925 Heart failure continues to be a major burden on our health care system. As the number of patients with heart failure increases, the cost of hospitalization alone is contributing significantly to the overall cost of this disease. Readmission rate and hospital length of stay are emerging as quality markers of heart failure care along with reimbursement policies that force hospitals to optimize these outcomes. Apart from maintaining quality assurance, the disease process of heart failure per-se requires demanding and close attention to vitals, diet, and medication compliance to prevent acute decompensation episodes. Remote patient monitoring is morphing into a key disease management strategy to optimize care for heart failure. Innovative implantable technologies to monitor intracardiac hemodynamics also are evolving, which potentially could offer better and substantial parameters to monitor. PMID:23519115

  1. Role of cell death in the progression of heart failure.

    PubMed

    Moe, Gordon W; Marn-Garca, Jos

    2016-03-01

    All multicellular organisms develop during evolution the highly regulated and interconnected pathways of cell death. This complex network contributes to the pathogenesis of various cardiovascular disorders including ischemia/reperfusion injury, myocardial infarction, heart failure, dysrhythmias and atherosclerosis. Chronic cardiac remodeling response and transition to overt HF have been associated with modestly increased apoptosis, although the actual burden of chronic cell loss attributable to apoptosis is not clear. Central mediators of cardiomyocyte survival and death are the mitochondrial organelles. Based on its morphological characteristics, cell death can be classified into three major types: apoptosis, necrosis and autophagy. Recently, a new pathway of regulated necrosis, necroptosis, has also been reported in the failing heart. The mitochondrial (intrinsic) and the death-receptor-mediated (extrinsic) converge at mitochondria inducing release of mitochondrial apoptogens to initiate the caspase cascade and eventually degradation of the doomed cardiomyocyte. Activation of death receptors can initiate not only extrinsic apoptotic pathway, but also necrosis. On the other hand, autophagy, which is characterized by the massive formation of lysosomal-derived vesicles, containing degenerating cytoplasmic contents, is primarily a survival response to nutrient deprivation, and a selective form of autophagy, mitophagy, is also a protective mechanism that allows to eliminate damaged mitochondria and thereby to attenuate mitochondria-mediated apoptosis and necrosis in the myocardium. Further insight into the molecular mechanisms underlying cell death will increase the efficiency and repertoire of therapeutic interventions available in cardiovascular disease. PMID:26872675

  2. Heart Failure in Adult Congenital Heart Disease: Nonpharmacologic Treatment Strategies.

    PubMed

    LeMond, Lisa; Mai, Tuan; Broberg, Craig S; Muralidaran, Ashok; Burchill, Luke J

    2015-11-01

    In early stages, heart failure (HF) in adult congenital heart disease (ACHD) remains an elusive diagnosis. Many ACHD patients seem well-compensated owing to chronic physical and psychological adaptations. HF biomarkers and cardiopulmonary exercise tests are often markedly abnormal, although patients report stable health and good quality of life. Treatment differs from acquired HF. Evidence for effective drug therapy in ACHD-related HF is lacking. Residual ventricular, valvular, and vascular abnormalities contribute to HF pathophysiology, leading to an emphasis on nonpharmacologic treatment strategies. This article reviews emerging perspectives on nonpharmacologic treatment strategies, including catheter-based interventions, surgical correction, and palliative care. PMID:26471822

  3. Healthy Habits Help Reduce Risk of Heart Failure, Study Finds

    MedlinePLUS

    ... nih.gov/medlineplus/news/fullstory_156354.html Healthy Habits Help Reduce Risk of Heart Failure, Study Finds ... Dec. 22, 2015 (HealthDay News) -- Following seven healthy habits might reduce your risk of heart failure, a ...

  4. The sympathetic nervous system and heart failure.

    PubMed

    Zhang, David Y; Anderson, Allen S

    2014-02-01

    Heart failure (HF) is a syndrome characterized by upregulation of the sympathetic nervous system and abnormal responsiveness of the parasympathetic nervous system. Studies in the 1980s and 1990s demonstrated that inhibition of the renin-angiotensin-aldosterone system with angiotensin-converting enzyme inhibitors improved symptoms and mortality in HF resulting from systolic dysfunction, thus providing a framework to consider the use of ?-blockers for HF therapy, contrary to the prevailing wisdom of the time. Against this backdrop, this article reviews the contemporary understanding of the sympathetic nervous system and the failing heart. PMID:24286577

  5. Congestive heart failure revisited: new concepts in treatment.

    PubMed Central

    Haywood, L. J.

    1996-01-01

    Congestive heart failure is a major cause of morbidity and mortality as the population ages. This article reviews the progress made in treating the two major causes of heart failure--mechanical and myocardial. New approaches to relieving mitral stenosis and guidelines for the treatment of congestive heart failure are reviewed. Appropriate assessment and management leads to major improvement in prognosis. PMID:8803436

  6. [Acute heart failure - a unique challenge].

    PubMed

    Angermann, Christiane E; Ertl, Georg

    2015-03-01

    Acute heart failure (AHF) is frequent, often life threatening and followed by emergency hospitalization. Leading symptoms are dyspnea, edema and fatigue. A broad spectrum of risk factors, cardiac diseases and comorbidities predisposes to AHF. Typical triggers (e.?g. arrhythmias) modulate the individual clinical picture. Their misinterpretation may delay the diagnosis, which always needs to be ascertained by cardiac imaging (echocardiography). Rescue therapy aims at amelioration of symptoms and stabilization of vital parameters. In contrast to chronic heart failure evidence of the efficacy of available treatments is limited and in the past innovations have been sparse in this area. The clinical course is characterized by high short- and long-term mortality and repeat cardiac decompensations, but seamless multidisciplinary care and better knowledge and self-supervision on the patients' side might improve prognosis. Today, too little attention is paid to the palliative needs of patients with AHF. PMID:25774728

  7. Skeletal myoblast transplant in heart failure.

    PubMed

    Sim, Eugene K W; Jiang, Shujia; Ye, Lei; Lim, Y L; Ooi, Oon C; Haider, Khawaja H

    2003-01-01

    Despite recent advances in the prevention and treatment of ischemic heart disease (IHD), treatment of patients with heart failure secondary to myocardial infarction remains a therapeutic challenge. Heart transplantation has emerged as a viable option but is fraught with problems of supply. Mechanical assist devices are extremely expensive and dynamic cardiomyoplasty has shown only limited success in the clinical setting. Recent insights into the pathogenesis of myocardial diseases and the progress made in the field of molecular biology have resulted in the development of new strategies at molecular as well as cellular levels for cardiac muscle repair. One such strategy is to augment ventricular function by means of cellular cardiomyoplasty through intracardiac cell grafting using adult and fetal cardiomyocytes, stem cells, and autologous skeletal myoblasts. PMID:12869179

  8. Heart failure in the diabetic population pathophysiology, diagnosis and management

    PubMed Central

    Drzewoski, Jozef

    2014-01-01

    Evidence from clinical trials repeatedly confirms the association of diabetes with heart failure, independent of hypertension, atherosclerosis, coronary artery disease and valvular heart disease. However, the importance of coexistence of diabetes and heart failure is not universally recognized, despite the fact that it may significantly contribute to morbidity and mortality of the diabetic population. It seems that prevention of heart failure, early diagnosis, and appropriate management could improve the outcome. Unfortunately, the etiology of heart failure in diabetic patients is still to be elucidated. It is multifactorial in nature and several cellular, molecular and metabolic factors are implicated. Additionally, there are still no definite guidelines on either the diagnosis and treatment of heart failure in diabetic patients or on the therapy of diabetes in subjects with heart failure. This review focuses on the pathophysiology, diagnosis, and prevention of heart failure in the diabetic population as well as management of both comorbidities. PMID:25097587

  9. Cardiorenal syndrome in decompensated heart failure.

    PubMed

    Tang, W H Wilson; Mullens, Wilfried

    2010-02-01

    Worsening renal function during treatment of acute decompensated heart failure (ADHF) often complicates the treatment course of heart failure. Furthermore, the development of worsening renal function is a strong independent predictor of long-term adverse outcomes. Sometimes referred to as 'cardiorenal syndrome,' the definition varies widely, and the overall understanding of pathogenesis is limited. This is probably owing to the lack of precision and characterisation of renal compromise during treatment of heart failure. Traditionally, the predominant cause has been attributed to impairment of cardiac output and relative underfilling of arterial perfusion. Emerging data have led to a resurgence of interest in the importance of venous congestion and elevated intra-abdominal pressure rather than confining it to impaired forward cardiac output as the primary driver of renal impairment. These revived concepts may support the role of novel renal-sparing approaches to salt and water removal and renal preservation, but better ways to distinguish haemodynamic versus other nephrotoxic aetiologies are needed. PMID:19401280

  10. Chronic heart failure: contemporary diagnosis and management.

    PubMed

    Ramani, Gautam V; Uber, Patricia A; Mehra, Mandeep R

    2010-02-01

    Chronic heart failure (CHF) remains the only cardiovascular disease with an increasing hospitalization burden and an ongoing drain on health care expenditures. The prevalence of CHF increases with advancing life span, with diastolic heart failure predominating in the elderly population. Primary prevention of coronary artery disease and risk factor management via aggressive blood pressure control are central in preventing new occurrences of left ventricular dysfunction. Optimal therapy for CHF involves identification and correction of potentially reversible precipitants, target-dose titration of medical therapy, and management of hospitalizations for decompensation. The etiological phenotype, absolute decrease in left ventricular ejection fraction and a widening of QRS duration on electrocardiography, is commonly used to identify patients at increased risk of progression of heart failure and sudden death who may benefit from prophylactic implantable cardioverter-defibrillator placement with or without cardiac resynchronization therapy. Patients who transition to advanced stages of disease despite optimal traditional medical and device therapy may be candidates for hemodynamically directed approaches such as a left ventricular assist device; in selected cases, listing for cardiac transplant may be warranted. PMID:20118395

  11. Gene and Cell Therapy for Heart Failure

    PubMed Central

    2009-01-01

    Abstract Cardiac gene and cell therapy have both entered clinical trials aimed at ameliorating ventricular dysfunction in patients with chronic congestive heart failure. The transduction of myocardial cells with viral constructs encoding a specific cardiomyocyte Ca2+ pump in the sarcoplasmic reticulum (SR), SRCa2+-ATPase has been shown to correct deficient Ca2+ handling in cardiomyocytes and improvements in contractility in preclinical studies, thus leading to the first clinical trial of gene therapy for heart failure. In cell therapy, it is not clear whether beneficial effects are cell-type specific and how improvements in contractility are brought about. Despite these uncertainties, a number of clinical trials are under way, supported by safety and efficacy data from trials of cell therapy in the setting of myocardial infarction. Safety concerns for gene therapy center on inflammatory and immune responses triggered by viral constructs, and for cell therapy with myoblast cells, the major concern is increased incidence of ventricular arrhythmia after cell transplantation. Principles and mechanisms of action of gene and cell therapy for heart failure are discussed, together with the potential influence of reactive oxygen species on the efficacy of these treatments and the status of myocardial-delivery techniques for viral constructs and cells. Antioxid. Redox Signal. 11, 20252042. PMID:19416058

  12. Heart failure with normal ejection fraction: a growing pandemic.

    PubMed

    Singh, Satnam; Frenneaux, Michael

    2012-05-01

    Heart failure is a heterogeneous syndrome. Approximately 30-50% of patients with heart failure have normal or near normal left ventricle function. Several epidemiological studies confirm that the prevalence of heart failure with normal ejection fraction is increasing. Given the current trends, heart failure with normal ejection fraction will become the most common form of heart failure, for which we do not currently have an evidence-based successful treatment. This article summarizes the etiology, current recommended guidelines and management options for this clinical manifestation. PMID:22642630

  13. Mechanisms of renal hyporesponsiveness to BNP in heart failure.

    PubMed

    Egom, Emmanuel E; Feridooni, Tiam; Hotchkiss, Adam; Kruzliak, Peter; Pasumarthi, Kishore B S

    2015-06-01

    The B-type natriuretic peptide (BNP), a member of the family of vasoactive peptides, is a potent natriuretic, diuretic, and vasodilatory peptide that contributes to blood pressure and volume homeostasis. These attributes make BNP an ideal drug that could aid in diuresing a fluid-overloaded patient who had poor or worsening renal function. Despite the potential benefits of BNP, accumulating evidence suggests that simply increasing the amount of circulating BNP does not necessarily increase natriuresis in patients with heart failure (HF). Moreover, despite high BNP levels, natriuresis falls when HF progresses from a compensated to a decompensated state, suggesting the emergence of renal resistance to BNP. Although likely multifactorial, several mechanisms have been proposed to explain renal hyporesponsiveness in HF, including, but not limited to, decreased renal BNP availability, down-regulation of natriuretic peptide receptors, and altered BNP intracellular signal transduction pathways. Thus, a better understanding of renal hyporesponsiveness in HF is required to devise strategies to develop novel agents and technologies that directly restore renal BNP efficiency. It is hoped that development of these new therapeutic approaches will serve to limit sodium retention in patients with HF, which may ultimately delay the progression to overt HF. PMID:25881664

  14. Continuous ultrafiltration for congestive heart failure: the CUORE trial.

    PubMed

    Marenzi, Giancarlo; Muratori, Manuela; Cosentino, Eugenio R; Rinaldi, Elisa R; Donghi, Valeria; Milazzo, Valentina; Ferramosca, Emiliana; Borghi, Claudio; Santoro, Antonio; Agostoni, Piergiuseppe

    2014-05-01

    Background: There are limited data comparing ultrafiltration with standard medical therapy as first-line treatment in patients with severe congestive heart failure (HF). We compared ultrafiltration and conventional therapy in patients hospitalized for HF and overt fluid overload.Methods and Results: Fifty-six patients with congestive HF were randomized to receive standard medical therapy (control group; n = 29) or ultrafiltration (ultrafiltration group; = 27). The primary endpoint of the study was rehospitalizations for congestive HF during a 1-year follow-up. Despite similar body weight reduction at hospital discharge in the 2 groups (7.5 4.5 and 7.9 5.0 kg, respectively;P = .75), a lower incidence of rehospitalizations for HF was observed in the ultrafiltration-treated patients during the following year (hazard ratio 0.14, 95% confidence interval 0.04-0.48; P = .002).Ultrafiltration-induced benefit was associated with a more stable renal function, unchanged furosemide dose, and lower B-type natriuretic peptide levels. At 1 year, 7 deaths (30%) occurred in the ultrafiltration group and 11 (44%) in the control group (P = .33).Conclusions: In HF patients with severe fluid overload, first-line treatment with ultrafiltration is associated with a prolonged clinical stabilization and a greater freedom from rehospitalization for congestive HF. PMID:25089313

  15. Dilemmas in end-stage heart failure

    PubMed Central

    Chen-Scarabelli, Carol; Saravolatz, Louis; Hirsh, Benjamin; Agrawal, Pratik; Scarabelli, Tiziano M.

    2015-01-01

    Heart failure (HF), a complex clinical syndrome due to structural or functional disorder of the heart, is a major global health issue, with a prevalence of over 5.8 million in the USA alone, and over 23 million worldwide. As a leading cause of hospitalizations among patients aged 65 years or older, HF is a major consumer of healthcare resources, creating a substantial strain on the healthcare system. This paper discusses the epidemiology of HF, financial impact, and multifaceted predicaments in end-stage HF care. A search was conducted on the U.S. National Library of Medicine website (www.pubmed.gov) using keywords such as end-stage heart failure, palliative care, ethical dilemmas. Despite the poor prognosis of HF (worse than that for many cancers), many HF patients, caregivers, and clinicians are unaware of the poor prognosis. In addition, the unpredictable clinical trajectory of HF complicates the planning of end-of-life care, such as palliative care and hospice, leading to underutilization of such resources. In conclusion, ethical dilemmas in end-stage HF are numerous, embroiling not only the patient, but also the caregiver, healthcare team, and society. PMID:25678905

  16. Beta-blockers for heart failure

    PubMed Central

    Cleland, John GF; Freemantle, Nick; Eastaugh, Joanne; Young, Phillip J; Harrison, Jane

    2014-01-01

    This is the protocol for a review and there is no abstract. The objectives are as follows: Our objective is to appraise the effectiveness of beta blockers in patients with heart failure. Our protocol defined main outcome is all cause mortality. The specific a priori defined aims are to examine: the effectiveness of beta blockers in all trials of patients with heart failure, and examine the importance of the presence or absence of ischaemic cardiomyopathy in patients included in trials and vasodilator properties of beta blocking agents used. We will also examine the predictive value of left ventricular function, age, use of angiotensin converting enzyme inhibitors and New York Heart Association Class (NYHA), and the rate of discontinuation of therapy due to treatment. There are a number of important ongoing trials for which data will become available in the next few years. Thus a systematic review which may be updated regularly is required to provide an up to date synthesis of the available data in this increasingly important area. PMID:25411555

  17. Mechano-signaling in heart failure.

    PubMed

    Buyandelger, Byambajav; Mansfield, Catherine; Knöll, Ralph

    2014-06-01

    Mechanosensation and mechanotransduction are fundamental aspects of biology, but the link between physical stimuli and biological responses remains not well understood. The perception of mechanical stimuli, their conversion into biochemical signals, and the transmission of these signals are particularly important for dynamic organs such as the heart. Various concepts have been introduced to explain mechanosensation at the molecular level, including effects on signalosomes, tensegrity, or direct activation (or inactivation) of enzymes. Striated muscles, including cardiac myocytes, differ from other cells in that they contain sarcomeres which are essential for the generation of forces and which play additional roles in mechanosensation. The majority of cardiomyopathy causing candidate genes encode structural proteins among which titin probably is the most important one. Due to its elastic elements, titin is a length sensor and also plays a role as a tension sensor (i.e., stress sensation). The recent discovery of titin mutations being a major cause of dilated cardiomyopathy (DCM) also underpins the importance of mechanosensation and mechanotransduction in the pathogenesis of heart failure. Here, we focus on sarcomere-related mechanisms, discuss recent findings, and provide a link to cardiomyopathy and associated heart failure. PMID:24531746

  18. [Vasopressin receptor antagonists and heart failure].

    PubMed

    Haass, Markus

    2009-11-01

    Vasopressin plays a physiological role in regulation of blood pressure, fluid volume, and serum osmolality. In heart failure inadequate release of vasopressin may result in excess fluid retention and hyponatremia. Vasopressin receptor antagonists are a new class of orally active drugs targeted to inhibit one or more of three distinct vasopressin receptors, namely V1a- (-->vasoconstriction), V1b- (-->release of ACTH) und V2-receptors (-->inhibition of free water reabsorption in the kidney). In cardiac decompensation with fluid overload selective V2- (Lixivaptan, satavaptan and tolvaptan) and non-selective V1a/V2-receptor blockers (Conivaptan) have been shown to be superior to standard therapy, as they allow for a faster weight loss and a more rapid symptomatic improvement (i.e. reduction in dyspnea). Inhibiting free water reabsorption without affecting renal sodium excretion vasopressin receptor antagonists allow for a controlled normalisation of serum natrium in euvolemic and hypervolemic hyponatremia. Vasopressin antagonists are well tolerated and have--in contrast to diuretics--no negative influence on renal function and serum potassium. Heart rate and blood pressure are not affected by vasopressin receptor antagonists. However, despite its excellent acute clinical effects long-term treatment with tolvaptan did not result in a reduced mortality and morbidity in heart failure patients over a mean follow-up of 9.9 months in the EVEREST trial. PMID:19885790

  19. Modeling Pathologies of Diastolic and Systolic Heart Failure.

    PubMed

    Genet, M; Lee, L C; Baillargeon, B; Guccione, J M; Kuhl, E

    2016-01-01

    Chronic heart failure is a medical condition that involves structural and functional changes of the heart and a progressive reduction in cardiac output. Heart failure is classified into two categories: diastolic heart failure, a thickening of the ventricular wall associated with impaired filling; and systolic heart failure, a dilation of the ventricles associated with reduced pump function. In theory, the pathophysiology of heart failure is well understood. In practice, however, heart failure is highly sensitive to cardiac microstructure, geometry, and loading. This makes it virtually impossible to predict the time line of heart failure for a diseased individual. Here we show that computational modeling allows us to integrate knowledge from different scales to create an individualized model for cardiac growth and remodeling during chronic heart failure. Our model naturally connects molecular events of parallel and serial sarcomere deposition with cellular phenomena of myofibrillogenesis and sarcomerogenesis to whole organ function. Our simulations predict chronic alterations in wall thickness, chamber size, and cardiac geometry, which agree favorably with the clinical observations in patients with diastolic and systolic heart failure. In contrast to existing single- or bi-ventricular models, our new four-chamber model can also predict characteristic secondary effects including papillary muscle dislocation, annular dilation, regurgitant flow, and outflow obstruction. Our prototype study suggests that computational modeling provides a patient-specific window into the progression of heart failure with a view towards personalized treatment planning. PMID:26043672

  20. Multidisciplinary Approach for Patients Hospitalized With Heart Failure.

    PubMed

    Frankenstein, Lutz; Frhlich, Hanna; Cleland, John G F

    2015-10-01

    Acute heart failure describes the rapid deterioration, over minutes, days or hours, of symptoms and signs of heart failure. Its management is an interdisciplinary challenge that requires the cooperation of various specialists. While emergency providers, (interventional) cardiologists, heart surgeons, and intensive care specialists collaborate in the initial stabilization of acute heart failure patients, the involvement of nurses, discharge managers, and general practitioners in the heart failure team may facilitate the transition from inpatient care to the outpatient setting and improve acute heart failure readmission rates. This review highlights the importance of a multidisciplinary approach to acute heart failure with particular focus on the chain-of-care delivered by the various services within the healthcare system. PMID:26409892

  1. Iron deficiency anemia in heart failure.

    PubMed

    Arora, Natasha P; Ghali, Jalal K

    2013-07-01

    Anemia and iron deficiency are quite prevalent in patients with heart failure (HF) and may overlap. Both anemia and iron deficiency are associated with worse symptoms and adverse clinical outcomes. In the past few years, there has been an enormous interest in the subject of iron deficiency and its management in patients with HF. In this review, the etiology and relevance of iron deficiency, iron metabolism in the setting of HF, studies on iron supplementation in patients with HF and potential cardiovascular effects of subclinical iron overload are discussed. PMID:22948485

  2. Roadmap to inpatient heart failure management.

    PubMed

    Vaduganathan, Muthiah; Gheorghiade, Mihai

    2015-01-01

    Heart failure (HF) accounts for over 1 million primary hospitalizations in the USA each year and carries a tremendous burden on costs and patient outcomes. The clinical syndrome of HF is not a single disease, but represents the complex interplay between various cardiac and non-cardiac processes, each of which need to be individually addressed. This review provides an updated, contemporary roadmap for inpatient worsening chronic HF management with a focus on identifying and addressing initiating mechanisms, amplifying factors, and cardiac structural abnormalities. Inpatient risk stratification should guide patient education, team structuring, disposition, and post-discharge monitoring. PMID:25238886

  3. [Chronic heart failure in the elderly patient].

    PubMed

    Chivite, David; Franco, Jhonatan; Formiga, Francesc

    2015-01-01

    The prevalence and incidence of heart failure (HF) is increasing, especially in the elderly population, and is becoming a major geriatric problem. Elderly patients with HF usually show etiopathogenic, epidemiological, and even clinical characteristics significantly different from those present in younger patients. Their treatment, however, derives from clinical trials performed with only a few elderly subjects. Moreover, beyond the cardiovascular disease itself, it is essential to evaluate the patient as a whole, given the interrelationship between HF and the characteristic geriatric syndromes of the elderly patient. This review examines the peculiarities in the most prevalent "real world" HF patient. PMID:25962334

  4. Positive airway pressure therapy for heart failure

    PubMed Central

    Kato, Takao; Suda, Shoko; Kasai, Takatoshi

    2014-01-01

    Heart failure (HF) is a life-threatening disease and is a growing public health concern. Despite recent advances in pharmacological management for HF, the morbidity and mortality from HF remain high. Therefore, non-pharmacological approaches for HF are being developed. However, most non-pharmacological approaches are invasive, have limited indication and are considered only for advanced HF. Accordingly, the development of less invasive, non-pharmacological approaches that improve outcomes for patients with HF is important. One such approach may include positive airway pressure (PAP) therapy. In this review, the role of PAP therapy applied through mask interfaces in the wide spectrum of HF care is discussed. PMID:25429330

  5. Conivaptan: promise of treatment in heart failure.

    PubMed

    Hoque, Mohammad Z; Arumugham, Pradeep; Huda, Nazmul; Verma, Nitin; Afiniwala, Mitul; Karia, Darshak H

    2009-09-01

    Conivaptan, the first vasopressin receptor antagonist approved by the FDA, is available for the treatment of hyponatremia in euvolemic and hypervolemic patients. The renin-angiotensin-aldosterone system is activated in heart failure (HF) causing clinical worsening. Arginine vasopressin levels are also elevated in HF. Conivaptan is an effective and FDA approved for the treatment of euvolemic and hypervolemic hyponatremia and may offer an extra treatment option in HF by targeting V(1a) and V(2) receptors. In this article we review the physiology, preclinical studies as well as the human clinical studies on the use of conivaptan and its potential and promise in the treatment of HF. PMID:19663609

  6. Left Ventricular Wall Movement in Heart Failure

    PubMed Central

    Carson, Peter; Kanter, Lawrence

    1971-01-01

    Of 34 patients admitted to hospital with left ventricular failure seven died before echocardiograms could be repeated after treatment and in three no echocardiograms could be obtained owing to chronic obstructive lung disease. In the remaining 24 patients echocardiograms were taken soon after admission and compared with echocardiograms taken later, after clinical improvement. The results show that in most patients both anterior and posterior motion of the posterior left ventricular wall increased. The rate of backward diastolic motion was appreciably less before and after treatment of heart failure compared with that in a small group of normal younger healthy men. This technique is a quick and apparently reliable way to assess ventricular function. The rate of diastolic motion is probably a reflection of left ventricular wall compliance. Imagesp78-a PMID:5097424

  7. [Heart failure--are there gender aspects?].

    PubMed

    Regitz-Zagrosek, V; Lehmkuhl, E; Lehmkuhl, H B

    2008-04-01

    Gender differences in the syndrome of heart failure (HF) occur in etiology and pathophysiology, in the clinical presentation and course of the syndrome. In addition, gender specific treatment responses and gender associated differences in the behavior of treating physicians are found. Hypertension and diabetes play a major role as causes of HF in women and both interact in their pathophysiology with the renin angiotensin system (RAS). Modulation of the RAS by estrogens explains specific differences between pre- and postmenopausal women and men. Myocardial growth processes and myocardial calcium handling are differentially regulated in female and male myocytes. Myocardial remodeling with age and as a consequence of mechanical load differs in women and men. For yet unknown reasons, HF with preserved systolic function seems to be more frequent in women than in men and the clinical course of systolic failure is different in both genders. PMID:18301870

  8. Mechanisms of Cardiotoxicity and the Development of Heart Failure.

    PubMed

    Lee, Christopher S

    2015-12-01

    Cardiotoxicity is a broad term that refers to the negative effects of toxic substances on the heart. Cancer drugs can cause cardiotoxicity by effects on heart cells, thromboembolic events, and/or hypertension that can lead to heart failure. Rheumatoid arthritis biologics may interfere with ischemic preconditioning and cause/worsen heart failure. Long-term and heavy alcohol use can result in oxidative stress, apoptosis, and decreased contractile protein function. Cocaine use results in sympathetic nervous system stimulation of heart and smooth muscle cells and leads to cardiotoxicity and evolution of heart failure. The definition of cardiotoxicity is likely to evolve along with knowledge about detecting subclinical myocardial injury. PMID:26567492

  9. Crosstalk between the heart and peripheral organs in heart failure.

    PubMed

    Jahng, James Won Suk; Song, Erfei; Sweeney, Gary

    2016-01-01

    Mediators from peripheral tissues can influence the development and progression of heart failure (HF). For example, in obesity, an altered profile of adipokines secreted from adipose tissue increases the incidence of myocardial infarction (MI). Less appreciated is that heart remodeling releases cardiokines, which can strongly impact various peripheral tissues. Inflammation, and, in particular, activation of the nucleotide-binding oligomerization domain-like receptors with pyrin domain (NLRP3) inflammasome are likely to have a central role in cardiac remodeling and mediating crosstalk with other organs. Activation of the NLRP3 inflammasome in response to cardiac injury induces the production and secretion of the inflammatory cytokines interleukin (IL)-1β and IL-18. In addition to having local effects in the myocardium, these pro-inflammatory cytokines are released into circulation and cause remodeling in the spleen, kidney, skeletal muscle and adipose tissue. The collective effects of various cardiokines on peripheral organs depend on the degree and duration of myocardial injury, with systematic inflammation and peripheral tissue damage observed as HF progresses. In this article, we review mechanisms regulating myocardial inflammation in HF and the role of factors secreted by the heart in communication with peripheral tissues. PMID:26964833

  10. [Chronic heart failure with impaired left ventricular function (systolic heart failure)].

    PubMed

    Hőgye, Márta; Forster, Tamás

    2012-12-23

    Chronic heart failure is a common public health problem. The disease has a poor prognosis with high mortality rate and the incidence increases continuously. Prognosis of chronic systolic heart failure can be improved by several different medications as well as by special cardiac interventions based on the newly-published European and American guidelines. In case of severe systolic dysfunction, hospitalization and mortality can be reduced using angiotensin converting enzyme inhibitors, angiotensin receptor blocking drugs, beta-receptor blocking agents and aldosterone antagonists, as evidenced in multicentric studies. In selected cases different cardiac interventions, such as intracardial defibrillator and/or cardiac desynchronization device implantation can be used for supporting the failing left ventricle. In terminal stage, special devices (ventricular assist device, intra-aortic balloon pump, arteficial heart) and, finally, heart transplantation can be applied. In this paper, the authors highlight therapeutic options of chronic systolic heart failure referring to recommendations of the latest, 2012 guideline from the European Society of Cardiology. PMID:23248057

  11. Ambulatory oxygen in chronic heart failure.

    PubMed

    Restrick, L J; Davies, S W; Noone, L; Wedzicha, J A

    1992-11-14

    Ambulatory oxygen therapy may be of benefit in bicycle exercise tests. We have assessed the effects of ambulatory oxygen during walk tests in 12 patients with chronic heart failure. In 6 min walks with the patient breathing air, mean (SD) arterial oxygen saturation (SaO2) fell from 94.4 (3.7)% at rest to 90.1 (6.1)% (p = 0.014) on exercise. 21/min oxygen increased resting SaO2 from 93.7 (4.0)% (air cylinder) to 96.5 (3.0)% (p < 0.001) with no effect on minimum SaO2, distance, or breathlessness. During endurance walks, 4 l/min oxygen increased minimum SaO2 from 90.4 (5.6)% to 93.5 (4.7)% (p = 0.011) but also had no effect on breathlessness or distance. Ambulatory oxygen in currently available cylinders cannot be recommended for patients with chronic heart failure. PMID:1359262

  12. Diastolic heart failure and LV dyssynchrony.

    PubMed

    Kasner, Mario; Westermann, Dirk; Schultheiss, Heinz-Peter; Tschöpe, Carsten

    2012-10-01

    Our knowledge of diastolic heart failure (DHF) is still limited with regard to pathophysiology, diagnosis and clinical treatment. Amongst others, LV dyssynchrony was suggested to be an additional factor involved in the pathogenesis of subgroup of patients with DHF. In 20-30% of patients with DHF a systolic LV dyssynchrony could be detected and about 20% DHF patients evidenced a diastolic dyssyncrony. Both systolic and diastolic dyssynchrony may contribute to the impairment of cardiac function and clinical manifestation in DHF. Opposite to the systolic heart failure, wide QRS complex is uncommon which incriminates that dyssynchrony in DHF is rather related to regional disperse in contractility than to electromechanical coupling delay. Asynchronous LV relaxation and impairment of ventricular restoring forces may also impair the LV filing and lead to a diastolic dyssynchrony. Particularly in patients with preserved LV contractility mechanical LV dyssynchrony induces energy wastage and consequently reduces cardiac reserves. However, up to date it is not clear to what degree LV dyssynchrony is involved in the pathomechanisms of this subpopulation of DHF. PMID:22280429

  13. Insulin Resistance and Heart Failure: Molecular Mechanisms

    PubMed Central

    Aroor, Annayya R.; Mandavia, Chirag H.; Sowers, James R.

    2012-01-01

    Insulin resistance and associated reductions in cardiac insulin metabolic signaling is emerging as a major factor for the development of heart failure and assumes more importance because of an epidemic increase in obesity and the cardiorenal metabolic syndrome and our aging population. Major factors contributing to the development of cardiac insulin resistance are oxidative stress, hyperglycemia, hyperlipidemia, dysregulated secretion of adipokines/cytokines and inappropriate activation of renin-angiotensin II-aldosterone system (RAAS) and the sympathetic nervous system. The effects of cardiac insulin resistance are exacerbated by metabolic, endocrine and cytokine alterations associated with systemic insulin resistance. The aggregate of these various alterations leads to an insulin resistant phenotype with metabolic inflexibility, impaired calcium handling, mitochondrial dysfunction and oxidative stress, dysregulated myocardial-endothelial interactions resulting in energy deficiency, impaired diastolic dysfunction, myocardial cell death and cardiac fibrosis. Therefore, understanding the molecular mechanisms linking insulin resistance and heart failure may help to design new and more effective mechanism-based drugs to improve myocardial and systemic insulin resistance. PMID:22999243

  14. Prospective memory and chronic heart failure

    PubMed Central

    2013-01-01

    Background Patients with chronic heart failure (CHF) experience a number of debilitating symptoms, which impact on activities of daily living and result in poor quality of life. Prospective memory, which is defined as memory to carry out future intentions, has not been investigated in this group. However, emerging evidence suggests CHF patients have difficulties with cognitive processes related to prospective memory. Self-care, which partly relies on prospective memory, is essential in symptom management and preventing acute clinical deterioration. This study aims to measure prospective memory in CHF patients, and examine the relationship between prospective memory and CHF self-care. Methods/Design A comprehensive neuropsychological assessment will be conducted to assess a range of cognitive functions and psychopathology. The primary focus will be an assessment of prospective memory using a well-established behavioral measure; Virtual Week. Thirty CHF patients attending a nurse-led management program will be recruited from three hospital sites in Melbourne, Australia and their self-care behaviors will be assessed using the Self-care Chronic Heart Failure Index (SCHFI), a validated self-report tool. An additional 30 healthy controls, matched on age, gender, and IQ will be recruited from the general community. Discussion This is a group comparison study that will provide an evaluation of the prospective memory abilities of CHF patients. The findings of this research will provide insight into whether prospective memory may be hindering patients ability to perform adequate self-care. PMID:23984757

  15. Exploring the Microbiome in Heart Failure.

    PubMed

    Kitai, Takeshi; Kirsop, Jennifer; Tang, W H Wilson

    2016-04-01

    Recent years have brought interesting insights into the human gut microbiota and have highlighted its increasingly recognized impact on cardiovascular (CV) diseases, including heart failure (HF). Changes in composition of gut microbiota, called dysbiosis, can trigger systemic inflammation, which is known to be involved in the pathophysiology of HF. Trimethylamine N-oxide (TMAO), which is derived from gut microbiota metabolites of specific dietary nutrients, has emerged as a key contributor to cardiovascular disease pathogenesis. Elevated TMAO levels have been reported to be associated with poor outcomes in patients with both HF and chronic kidney disease (CKD). Dysbiosis of gut microbiota can contribute to higher levels of TMAO and the generation of uremic toxins, progressing to both HF and CKD. Therefore, this bidirectional relationship between HF and CKD through gut microbiota may be a novel therapeutic target for the cardiorenal syndrome. However, the mechanisms by which gut microbiota could influence the development of heart failure are still unknown, and there are still some questions regarding the causative effects of TMAO and the underlying mechanistic link that explains how TMAO might directly or indirectly promote CV diseases including HF. Further studies are warranted to clarify the function of TMAO on the pathophysiology of cardiorenal syndrome and the handling of TMAO levels by the kidneys. PMID:26886380

  16. Novel Therapeutic Strategies for Reducing Right Heart Failure Associated Mortality in Fibrotic Lung Diseases

    PubMed Central

    Adegunsoye, Ayodeji; Levy, Matthew; Oyenuga, Olusegun

    2015-01-01

    Fibrotic lung diseases carry a significant mortality burden worldwide. A large proportion of these deaths are due to right heart failure and pulmonary hypertension. Underlying contributory factors which appear to play a role in the mechanism of progression of right heart dysfunction include chronic hypoxia, defective calcium handling, hyperaldosteronism, pulmonary vascular alterations, cyclic strain of pressure and volume changes, elevation of circulating TGF-β, and elevated systemic NO levels. Specific therapies targeting pulmonary hypertension include calcium channel blockers, endothelin (ET-1) receptor antagonists, prostacyclin analogs, phosphodiesterase type 5 (PDE5) inhibitors, and rho-kinase (ROCK) inhibitors. Newer antifibrotic and anti-inflammatory agents may exert beneficial effects on heart failure in idiopathic pulmonary fibrosis. Furthermore, right ventricle-targeted therapies, aimed at mitigating the effects of functional right ventricular failure, include β-adrenoceptor (β-AR) blockers, angiotensin-converting enzyme (ACE) inhibitors, antioxidants, modulators of metabolism, and 5-hydroxytryptamine-2B (5-HT2B) receptor antagonists. Newer nonpharmacologic modalities for right ventricular support are increasingly being implemented. Early, effective, and individualized therapy may prevent overt right heart failure in fibrotic lung disease leading to improved outcomes and quality of life. PMID:26583148

  17. Neuregulin in heart failure : reverse translation from cancer cardiotoxicity to new heart failure therapy.

    TOXLINE Toxicology Bibliographic Information

    Geisberg CA; Lenihan DJ

    2011-06-01

    Trastuzumab is a monoclonal antibody to the ErbB2 (Her2nue) receptor over-expressed in Her2(+) breast cancer. Trastuzumab-related cardiotoxicity has revealed the importance of ErbB2 signaling in the heart. Neuregulin (NRG-1) is an important stress-mediated paracrine growth factor that signals through the family of ErbB receptors to promote cardioprotection (myocyte cell survival, proliferation, differentiation, hypertrophy, and angiogenesis). Animal models with disrupted NRG/ErbB signaling fail to develop normally or result in impaired cardiac function post-natally. Pre-clinical animal studies and early-phase human studies suggest that recombinant NRG-1 holds promise as a new therapy for the treatment of various forms of heart failure. Much work is needed to further understand the exact mechanisms of cardiac repair and to find a safe mode of application for recombinant NRG-1 in heart failure.

  18. Neuregulin in heart failure : reverse translation from cancer cardiotoxicity to new heart failure therapy.

    PubMed

    Geisberg, C A; Lenihan, D J

    2011-06-01

    Trastuzumab is a monoclonal antibody to the ErbB2 (Her2nue) receptor over-expressed in Her2(+) breast cancer. Trastuzumab-related cardiotoxicity has revealed the importance of ErbB2 signaling in the heart. Neuregulin (NRG-1) is an important stress-mediated paracrine growth factor that signals through the family of ErbB receptors to promote cardioprotection (myocyte cell survival, proliferation, differentiation, hypertrophy, and angiogenesis). Animal models with disrupted NRG/ErbB signaling fail to develop normally or result in impaired cardiac function post-natally. Pre-clinical animal studies and early-phase human studies suggest that recombinant NRG-1 holds promise as a new therapy for the treatment of various forms of heart failure. Much work is needed to further understand the exact mechanisms of cardiac repair and to find a safe mode of application for recombinant NRG-1 in heart failure. PMID:21633805

  19. Khat Use: History and Heart Failure

    PubMed Central

    El-Menyar, Ayman; Mekkodathil, Ahammed; Al-Thani, Hassan; Al-Motarreb, Ahmed

    2015-01-01

    Recent reports suggest that 20 million people worldwide are regularly using khat as a stimulant, even though the habit of chewing khat is known to cause serious health issues. Historical evidence suggests khat use has existed since the 13th century in Ethiopia and the southwestern Arabian regions even before the cultivation and use of coffee. In the past three decades, its availability and use spread all over the world including the United States and Europe. Most of the consumers in the Western world are immigrant groups from Eastern Africa or the Middle East. The global transport and availability of khat has been enhanced by the development of synthetic forms of its active component. The World Health Organization considers khat a drug of abuse since it causes a range of health problems. However, it remains lawful in some countries. Khat use has long been a part of Yemeni culture and is used in virtually every social occasion. The main component of khat is cathinone, which is structurally and functionally similar to amphetamine and cocaine. Several studies have demonstrated that khat chewing has unfavorable cardiovascular effects. The effect on the myocardium could be explained by its effect on the heart rate, blood pressure, its vasomotor effect on the coronary vessels, and its amphetamine–like effects. However, its direct effect on the myocardium needs further elaboration. To date, there are few articles that contribute death among khat chewers to khat-induced heart failure. Further studies are needed to address the risk factors in khat chewers that may explain khat-induced cardiotoxicity, cardiomyopathy, and heart failure. PMID:25960830

  20. Khat use: history and heart failure.

    PubMed

    El-Menyar, Ayman; Mekkodathil, Ahammed; Al-Thani, Hassan; Al-Motarreb, Ahmed

    2015-03-01

    Recent reports suggest that 20 million people worldwide are regularly using khat as a stimulant, even though the habit of chewing khat is known to cause serious health issues. Historical evidence suggests khat use has existed since the 13th century in Ethiopia and the southwestern Arabian regions even before the cultivation and use of coffee. In the past three decades, its availability and use spread all over the world including the United States and Europe. Most of the consumers in the Western world are immigrant groups from Eastern Africa or the Middle East. The global transport and availability of khat has been enhanced by the development of synthetic forms of its active component. The World Health Organization considers khat a drug of abuse since it causes a range of health problems. However, it remains lawful in some countries. Khat use has long been a part of Yemeni culture and is used in virtually every social occasion. The main component of khat is cathinone, which is structurally and functionally similar to amphetamine and cocaine. Several studies have demonstrated that khat chewing has unfavorable cardiovascular effects. The effect on the myocardium could be explained by its effect on the heart rate, blood pressure, its vasomotor effect on the coronary vessels, and its amphetamine-like effects. However, its direct effect on the myocardium needs further elaboration. To date, there are few articles that contribute death among khat chewers to khat-induced heart failure. Further studies are needed to address the risk factors in khat chewers that may explain khat-induced cardiotoxicity, cardiomyopathy, and heart failure. PMID:25960830

  1. Serelaxin: new investigational treatment in acute heart failure.

    PubMed

    Said, Sarmad; Mukherjee, Debabrata

    2013-09-01

    Over the last decade several pharmacological approaches for acute heart failure have been introduced, however, no drastic change in the medical management apart from device-dependent therapy was observed. Essentially vasodilators and diuretics as primary therapy in acute heart failure was discussed and encouraged in the guidelines but no breakthrough in the treatment of acute heart failure was achieved. More recently, clinical trials of relaxin and its recombinant form, i.e., serelaxin in patients with acute heart failure demonstrated a significant clinical improvement with favorable safety and tolerability profile in symptomatic heart failure patients. This report reviews the potential beneficial effects and role of serelaxin in the setting of acute heart failure. PMID:24289727

  2. [Roles of cytokines in the pathogenesis of heart failure].

    PubMed

    Matsumori, Akira

    2003-05-01

    Cytokines are being increasingly recognized as important factors in the pathogenesis and pathophysiology of heart failure. Elevated levels of circulating cytokines have been reported in patients with heart failure, and various cytokines have been shown to depress myocardial contractility in vitro and in vivo. Our recent study showed that the various drugs for heart failure modulated the production of cytokines, and some of these drugs inhibited activation of NF-kappa B. Cytokine gene therapy which inhibits inflammatory response by viral IL-10 and IL-1 receptor antagonist has been shown to be effective in the animal models of heart failure. Mast cells have been shown to play important role in the pathogenesis of heart failure due to viral myocarditis, and transition from compensated hypertrophy to heart failure. PMID:12754997

  3. Advanced Congestive Heart Failure Associated With Disseminated Intravascular Coagulopathy

    PubMed Central

    Sarcon, Annahita; Liu, Xiaoli; Ton, David; Haywood, James; Hitchcock, Todd

    2015-01-01

    Background. Disseminated intravascular coagulopathy (DIC) is a complication of an underlying disease and not a primary illness. It is most commonly associated with sepsis, trauma, obstetrical complications, and malignancies. There are very few cases in the literature illustrating the association between DIC and congestive heart failure. Findings. In this report, we present a case of severe congestive heart failure, leading to biventricular thrombi and subsequently DIC. Conclusion. We suggest that the association between congestive heart failure and DIC is an underrecognized one. Congestive heart failure continues to remain a major cause of morbidity and mortality despite advances in medical therapies. Thus far, the precise role of coagulation factors in congestive heart failure is unknown. Further investigations are needed to elucidate the pathophysiology of congestive heart failure and coagulation factors.

  4. Advanced Congestive Heart Failure Associated With Disseminated Intravascular Coagulopathy.

    PubMed

    Sarcon, Annahita; Liu, Xiaoli; Ton, David; Haywood, James; Hitchcock, Todd

    2015-01-01

    Background. Disseminated intravascular coagulopathy (DIC) is a complication of an underlying disease and not a primary illness. It is most commonly associated with sepsis, trauma, obstetrical complications, and malignancies. There are very few cases in the literature illustrating the association between DIC and congestive heart failure. Findings. In this report, we present a case of severe congestive heart failure, leading to biventricular thrombi and subsequently DIC. Conclusion. We suggest that the association between congestive heart failure and DIC is an underrecognized one. Congestive heart failure continues to remain a major cause of morbidity and mortality despite advances in medical therapies. Thus far, the precise role of coagulation factors in congestive heart failure is unknown. Further investigations are needed to elucidate the pathophysiology of congestive heart failure and coagulation factors. PMID:26788528

  5. Statins in heart failure: do we need another trial?

    PubMed Central

    Bonsu, Kwadwo Osei; Kadirvelu, Amudha; Reidpath, Daniel Diamond

    2013-01-01

    Statins lower serum cholesterol and are employed for primary and secondary prevention of cardiovascular events. Clinical evidence from observational studies, retrospective data, and post hoc analyses of data from large statin trials in various cardiovascular conditions, as well as small scale randomized trials, suggest survival and other outcome benefits for heart failure. Two recent large randomized controlled trials, however, appear to suggest statins do not have beneficial effects in heart failure. In addition to lowering cholesterol, statins are believed to have many pleotropic effects which could possibly influence the pathophysiology of heart failure. Following the two large trials, evidence from recent studies appears to support the use of statins in heart failure. This review discusses the role of statins in the pathophysiology of heart failure, current evidence for statin use in heart failure, and suggests directions for future research. PMID:23807852

  6. Novel biomarkers in heart failure with preserved ejection fraction.

    PubMed

    Shah, Kevin S; Maisel, Alan S

    2014-07-01

    Heart failure with preserved ejection fraction (HFPEF) is a common subtype of heart failure with morbidity and mortality similar to that of heart failure with systolic dysfunction. This article discusses the numerous biomarkers that promise to play a substantial role in terms of our ability to understand the mechanisms of HFPEF and discern possible phenotypes that respond to targeted therapies: natriuretic peptides, high-sensitivity troponins, galectin-3, soluble ST2, neutrophil gelatinase-associated lipocalin, and cystatin C. PMID:24975910

  7. British Society of Heart Failure 2009 meeting report.

    PubMed

    McDonagh, Theresa; Guha, Kaushik

    2010-04-01

    The 12th Annual Meeting of the British Society of Heart Failure was held in London (UK). As heart failure has evolved into an accredited subspecialty in its own right, the conference has become increasingly well attended. This year there were over 400 delegates from around the world. As per clinical practice, there were large numbers of multidisciplinary members including a strong representation from the heart failure specialist nurse division. PMID:20397823

  8. Congestive heart failure: what should be the initial therapy and why?

    PubMed

    Chatterjee, Kanu

    2002-01-01

    Left ventricular systolic dysfunction is associated with neurohormonal activation which contributes to progressive ventricular remodeling and worsening clinical heart failure. Renin-angiotensin-aldosterone and sympathetic nervous systems are activated, not only in patients with clinically overt heart failure, but also in patients with asymptomatic or minimally symptomatic left ventricular systolic dysfunction. Activation of the angiotensin and adrenergic systems produces deleterious effects on systemic and coronary hemodynamics, promotes myocyte hypertrophy and fibroblast growth, and myocyte necrosis and apoptosis. Thus, therapy of heart failure should consist of pharmacologic agents not only to relieve symptoms but also to prevent and attenuate ventricular remodeling and progressive heart failure, thereby improving prognosis. In patients who are symptomatic, ACE inhibitors along with digitalis and diuretics as initial therapy (triple therapy) have the greater potential to improve exercise tolerance and decrease the incidence of treatment failure compared with diuretics alone or a combination of diuretics and digitalis. Diuretics alone should not be considered for long-term therapy as plasma renin activity, angiotensin II, aldosterone, norepinephrine and vasopressin levels may increase. ACE inhibitors decrease mortality in patients with heart failure resulting from left ventricular systolic dysfunction. The results of presently available studies indicate that angiotensin II receptor blockers (ARBs) do not provide any advantage over ACE inhibitors regarding survival benefit but may be better tolerated. Long-term adrenergic inhibition with the use of ss-adrenoceptor antagonists added to ACE inhibitors is associated with attenuation of ventricular remodeling, improvement in ventricular function and clinical class and survival of patients with symptomatic systolic left ventricular failure. Thus, initial pharmacotherapy for systolic heart failure should consist of: maximal tolerated dosages of ACE inhibitors;ARBs if ACE inhibitors are not tolerated because of intractable cough or angioedema;adequate dosages of hydralazine and isosorbide dinitrate if ACE inhibitors or ARBs are not tolerated; relatively low dosages of digoxin (serum concentrations of < or = 1.0 ng/dl) if not contraindicated; and diuretics to relieve congestive symptoms. Addition of spironolactone to ACE inhibitors can result in a significant reduction in the risk of sudden death in patients with symptomatic severe heart failure. Myocardial infarction resulting from ischemic heart disease is the most common cause of systolic left ventricular failure and the therapeutic modalities with potential to reduce the risks of myocardial infraction, such as risk factor modification, adequate control of diabetes and hypertension, antiplatelet agents and lipid-lowering agents, should also be included in the initial therapy. PMID:14727993

  9. New pharmacological strategies for the treatment of heart failure.

    PubMed

    Chin, B S; Lip, G Y

    2001-07-01

    Heart failure still carries a high morbidity and mortality, necessitating new approaches for its management. Greater understanding of the pathophysiology of heart failure has opened the way for novel therapeutic approaches, including analogs of natriuretic peptides and drugs that modulate endothelin, cytokine release and endothelial vasoconstriction. Other drugs are undergoing laboratory and clinical trials that will eventually supersede or complement less optimal heart failure treatments. Clinical trials will ascertain if these new strategies in the treatment of heart failure will ultimately be successful in the management of these patients. PMID:11757792

  10. [The role of uric acid in heart failure].

    PubMed

    Alcano, Hernn; Greig, Douglas; Castro, Pablo; Verdejo, Hugo; Mellado, Rosemarie; Garca, Lorena; Daz-Araya, Guillermo; Quiroga, Clara; Chiong, Mario; Lavandero, Sergio

    2011-04-01

    Complications and mortality of heart failure are high, despite the availability of several forms of treatment. Uric acid, the end product of purine metabolism would actively participate in the pathophysiology of heart failure. However, there is no consensus about its action in cardiovascular disease. Serum uric acid would have a protective antioxidant activity. This action could help to reduce or counteract the processes that cause or appear as a result of heart failure. However, these protective properties would vanish in the intracellular environment or in highly hydrophobic areas such as atherosclerotic plaques and adipose tissue. This review discusses the paradoxical action of uric acid in the pathophysiology of heart failure. PMID:21879191

  11. Prognostic Value of Galectin-3 in Patients with Heart Failure

    PubMed Central

    Bonjak, Ivica; Selthofer-Relati?, Kristina; V?ev, Aleksandar

    2015-01-01

    Galectins are a family of soluble ?-galactoside-binding lectins that have important role in inflammation, immunity, and cancer. Galectin-3 as a part of this lectin family plays a very important role in development of heart failure. According to recent papers, galectin-3 plasma level correlates with heart failure outcome, primarily with rehospitalisation and death from heart failure. This paper summarizes the most recent advances in galectin-3 research, with the accent on the role of galectin-3 in pathophysiology of myocardial remodelling and heart failure developmentwith preserved and reduced ejection fraction, and some implication on development of new disease modifying drugs. PMID:25960597

  12. Clinical service organisation for heart failure

    PubMed Central

    Taylor, Stephanie JC; Bestall, Janine C; Cotter, Sarah; Falshaw, Margaret; Hood, Sonja G; Parsons, Suzanne; Wood, Lesley; Underwood, Martin

    2014-01-01

    Background Chronic heart failure (CHF) is a serious, common condition associated with frequent hospitalisation. Several different disease management interventions (clinical service organisation interventions) for patients with CHF have been proposed. Objectives To assess the effectiveness of disease management interventions for patients with CHF. Search methods We searched: Cochrane CENTRAL Register of Controlled Trials (to June 2003); MEDLINE (January 1966 to July 2003); EMBASE (January 1980 to July 2003); CINAHL (January 1982 to July 2003); AMED (January 1985 to July 2003); Science Citation Index Expanded (searched January 1981 to March 2001); SIGLE (January 1980 to July 2003); DARE (July 2003); National Research Register (July 2003); NHS Economic Evaluations Database (March 2001); reference lists of articles and asked experts in the field. Selection criteria Randomised controlled trials comparing disease management interventions specifically directed at patients with CHF to usual care. Data collection and analysis At least two reviewers independently extracted data information and assessed study quality. Study authors were contacted for further information where necessary. Main results Sixteen trials involving 1,627 people were included. We classified the interventions into three models: multidisciplinary interventions (a holistic approach bridging the gap between hospital admission and discharge home delivered by a team); case management interventions (intense monitoring of patients following discharge often involving telephone follow up and home visits); and clinic interventions (follow up in a CHF clinic). There was considerable overlap within these categories, however the components, intensity and duration of the interventions varied. Case management interventions tended to be associated with reduced all cause mortality but these findings were not statistically significant (odds ratio 0.86, 95% confidence interval 0.67 to 1.10, P = 0.23), although the evidence was stronger when analysis was limited to the better quality studies (odds ratio 0.68, 95% confidence interval 0.46 to 0.98, P = 0.04). There was weak evidence that case management interventions may be associated with a reduction in admissions for heart failure. It is unclear what the effective components of the case management interventions are. The single RCT of a multidisciplinary intervention showed reduced heart-failure related re-admissions in the short term. At present there is little available evidence to support clinic based interventions. Authors’ conclusions The data from this review are insufficient for forming recommendations. Further research should include adequately powered, multicentre studies. Future studies should also investigate the effect of interventions on patients’ and carers’ quality of life, their satisfaction with the interventions and cost effectiveness. PMID:15846638

  13. Excess Weight Helps Women with Heart Failure, Hurts Men

    MedlinePLUS

    ... Excess Weight Helps Women With Heart Failure, Hurts Men: Study This isn't an excuse for females ... failure may live significantly longer than similarly heavy men with the progressive disease, a new study suggests. ...

  14. Heart Failure With Preserved Ejection Fraction.

    PubMed

    Reddy, Yogesh N V; Borlaug, Barry A

    2016-04-01

    Heart failure (HF) is one of the largest drivers of morbidity and health care expenditure in the world and continues to increase in prevalence at an alarming rate. Most of this increasing burden is related to the rapidly expanding population of HF with preserved ejection fraction (HFpEF), largely driven by the increasing rates of obesity, hypertension, and metabolic syndrome in western countries. In the last 3 decades, there have been tremendous advances in treating patients with HF with reduced ejection fraction (HFrEF), with essentially no change in outcomes for HFpEF. The lack of efficacy for established HFrEF therapies in HFpEF underscores the fundamental differences between both these phenotypically distinct forms of HF. In this review, we will summarize the current understanding of the pathophysiology of HFpEF, discuss diagnostic and therapeutic strategies, and provide future avenues to direct clinical investigation. PMID:26952248

  15. Metabolic remodeling in chronic heart failure.

    PubMed

    Wang, Jing; Guo, Tao

    2013-08-01

    Although the management of chronic heart failure (CHF) has made enormous progress over the past decades, CHF is still a tremendous medical and societal burden. Metabolic remodeling might play a crucial role in the pathophysiology of CHF. The characteristics and mechanisms of metabolic remodeling remained unclear, and the main hypothesis might include the changes in the availability of metabolic substrate and the decline of metabolic capability. In the early phases of the disease, metabolism shifts toward carbohydrate utilization from fatty acids (FAs) oxidation. Along with the progress of the disease, the increasing level of the hyperadrenergic state and insulin resistance cause the changes that shift back to a greater FA uptake and oxidation. In addition, a growing body of experimental and clinical evidence suggests that the improvement in the metabolic capability is likely to be more significant than the selection of the substrate. PMID:23897787

  16. Cognitive impairment in heart failure patients

    PubMed Central

    Leto, Laura; Feola, Mauro

    2014-01-01

    Cognitive damage in heart failure (HF) involves different domains thus interfering with the ability for single patient to self-care and to cope with treatment regimens, modifying symptoms and health behaviours. Many cerebral and functional changes were detected in brain imaging, involving areas of both grey and white matter deputed to cognition. Although various instruments are available to explore cognition, no consensus was obtained on better tools to be used in HF population. Reduction in cerebral blood flow, decreased cardiac output, alterations of cerebrovascular reactivity and modification of blood pressure levels are the main features involved in the etiopathogenetic mechanisms of cognitive deficit. Several cardiac variables, laboratory parameters, demographic and clinical elements were studied for their possible relation with cognition and should be properly evaluated to define patients at increased risk of impairment. The present review gathers available data pointing out assured information and discussing possible areas of research development. PMID:25593581

  17. The pathophysiology of hypertensive acute heart failure.

    PubMed

    Viau, David M; Sala-Mercado, Javier A; Spranger, Marty D; O'Leary, Donal S; Levy, Phillip D

    2015-12-01

    While acute heart failure (AHF) is often regarded as a single disorder, an evolving understanding recognises the existence of multiple phenotypes with varied pathophysiological alterations. Herein we discuss hypertensive AHF and provide insight into a mechanism where acute fluid redistribution is caused by a disturbance in the ventricular-vascular coupling relationship. In this relationship, acute alterations in vascular elasticity, vasoconstriction and reflected pulse waves lead to increases in cardiac work and contribute to decompensated LV function with associated subendocardial ischaemia and end-organ damage. Chronic predisposing factors (neurohormonal activity, nitric oxide insensitivity, arterial stiffening) and physiological stressors (sympathetic surge, volume overload, physical exertion) that are causally linked to acute symptom onset are discussed. Lastly, we review treatment options including both nitrovasodilators and promising novel therapeutics, and discuss future directions in the management of this phenotypic variant. PMID:26123135

  18. Treatment options for hyponatremia in heart failure.

    PubMed

    Goldsmith, Steven R

    2010-07-01

    Hyponatremia is independently associated with adverse outcomes in patients with congestive heart failure (CHF). The primary cause of hyponatremia in CHF is the inappropriate secretion of the antidiuretic hormone arginine vasopressin (AVP). The binding of AVP to V(2) receptors in the renal collecting duct promotes water retention, a process that can lead to dilutional hyponatremia as well as increased ventricular preload. Conventional treatment of hyponatremia in CHF is largely based on water restriction, which is neither effective nor well-tolerated. V(2)- and dual V(1a)/V(2)-receptor antagonists offer physiologically based treatment for dilutional hyponatremia. Clinical trials in patients with hyponatremia including those with CHF using both selective and nonselective vasopressin antagonists have demonstrated the effectiveness and safety of these agents in correcting this common electrolyte abnormality. PMID:20653706

  19. Preventing Heart Failure in Inflammatory and Immune Disorders

    PubMed Central

    Serhal, Maya; Longenecker, Chris T.

    2014-01-01

    Patients with chronic inflammatory diseases are at increased risk for heart failure due to ischemic heart disease and other causes including heart failure with preserved ejection fraction. Using rheumatoid arthritis and treated HIV infection as two prototypical examples, we review the epidemiology and potential therapies to prevent heart failure in these populations. Particular focus is given to anti-inflammatory therapies including statins and biologic disease modifying drugs. There is also limited evidence for lifestyle changes and blockade of the renin-angiotensin-aldosterone system. We conclude by proposing how a strategy for heart failure prevention, such as the model tested in the Screening To Prevent Heart Failure (STOP-HF) trial, may be adapted to chronic inflammatory disease. PMID:26316924

  20. Rural Patients Knowledge about Heart Failure

    PubMed Central

    Dracup, Kathleen; Moser, Debra; Pelter, Michele M.; Nesbitt, Thomas; Southard, Jeffrey; Paul, Steven M.; Robinson, Susan; Zgre Hemsey, Jessica; Cooper, Lawton

    2015-01-01

    Background Heart failure (HF) is a potentially disabling condition requiring significant patient knowledge to manage the requirements of self-care. The need for self-care is important for all patients, but particularly for those living in rural areas that are geographically remote from health care services. Objective To identify the level of knowledge of rural patients with HF and the clinical and demographic characteristics associated with low levels of HF knowledge Methods Baseline data from 612 patients with HF enrolled in the REMOTE-HF trial were analyzed using the Heart Failure Knowledge Scale, the Short Test of Functional Health literacy in Adults, and the anxiety subscale of the Brief Symptom Inventory. Multiple linear regression was used to explore the contribution of sociodemographic and clinical variables to levels of HF knowledge. Results Mean age was 6613 years; 59% were male, and 50.5% had an ejection fraction (EF) <40%. Mean percent correct on the HF Knowledge Scale was 69.513 (range 25 to 100) percent, with the most frequent incorrect items related to symptoms of HF and the need for daily weights. Males and older patients scored significantly lower in HF knowledge than females and younger patients (p = 0.002 and 0.011 respectively). Patients with preserved systolic function also scored significantly lower than those with systolic HF (p=0.030). Conclusion Patients can be identified who are at risk for poor self-care because of low levels of HF knowledge. Older patients, males and patients with HF with preserved systolic function may require special educational strategies to gain the knowledge required for effective self-care. PMID:23839575

  1. Rethinking Phase II Clinical Trial Design in Heart Failure

    PubMed Central

    Lavine, Kory J.; Mann, Douglas L.

    2014-01-01

    The incidence and economic burden of heart failure continue to rise worldwide, despite implementation of a number of effective heart failure therapies. Although there have been a number phase III studies of potential novel heart failure therapies over the past decade, none of these new compounds have been successful in phase III clinical trials. While there are likely a number of reasons for this failure, one of the problems that has become increasingly apparent is the inability of phase II trials to correctly identify novel therapies that will be successful in phase III clinical trials. In the following review, we will discuss the some of the problems inherent with current phase II heart failure clinical trials, as well as discuss possible ways to rethink phase II development of new therapies for heart failure. PMID:25343020

  2. Soluble ST2 in heart failure.

    PubMed

    Dieplinger, Benjamin; Mueller, Thomas

    2015-03-30

    In addition to routine clinical laboratory tests (including natriuretic peptides and cardiac troponins), other biomarkers are gaining attention for their utility in heart failure (HF) management. Among them, soluble ST2 (sST2) a novel biomarker integrating inflammation, fibrosis, and cardiac stress has been included in the 2013 ACCF/AHA guideline for additive risk stratification of patients with acute and chronic HF. sST2 is an interleukin-1 (IL-1) receptor family member, is secreted into the circulation and functions as a "decoy" receptor for IL-33, inhibiting IL-33/ST2 signaling. Blood concentrations of sST2 are increased in various diseases such as inflammatory diseases and heart diseases and are considered a valuable prognostic marker in both conditions. sST2 lacks disease specificity and, therefore, is not a valuable marker for the diagnosis of HF. In acute and chronic HF, however, sST2 is strongly associated with measures of HF severity and poor outcome. Several studies in patients with HF indicate that serial measurement of sST2 has prognostic value and could have a potential role in future biomarker-directed therapy. In this review, the role of sST2 as a HF biomarker will be discussed, specifically addressing analytical considerations of measuring sST2 as well as the clinical applications of measurement of sST2 for the diagnosis, prognosis and monitoring of acute and chronic HF. PMID:25269091

  3. The kidney in heart failure: an update.

    PubMed

    Damman, Kevin; Testani, Jeffrey M

    2015-06-14

    Heart and kidney are closely related in the clinical syndrome of heart failure (HF). It is now sufficiently clear that renal dysfunction occurs frequently in all phenotypes of HF, and when present, it is associated with higher mortality and morbidity. While the pathophysiology is multifactorial, the most important factors are a reduced renal perfusion and venous congestion. Recent interest has focused on worsening renal function (WRF), a situation strongly related to mortality, but seemingly only when HF status deteriorates. Unfortunately, to date clinicians are unable to identify specifically those patients with a grim prognosis following WRF. Although much has been learned on cardiorenal interaction in HF, still more questions have been left unanswered. The coming decade should provide us with more dedicated epidemiologic, mechanistic, and controlled trials in HF patients with reduced renal function. An updated classification of the cardiorenal syndrome that incorporates recent evidence and points towards areas of interest and uncertainties, and areas where progress is needed could facilitate this process. Ultimately, this should lead to preventive and treatment strategies that can preserve renal function and associated outcome in patients with HF. PMID:25838436

  4. Nutritional assessment in heart failure patients.

    PubMed

    Lee, John H; Jarreau, Tara; Prasad, Amit; Lavie, Carl; O'Keefe, James; Ventura, Hector

    2011-01-01

    Heart failure (HF) is a growing epidemic worldwide with a particularly large presence in the United States. Nutritional assessment and supplementation is an area that can be studied to potentially improve the outcomes of these chronically ill patients. There have been many studies reporting the effect of various nutrients on HF patients, often with mixed results. Amino acids such as taurine, which is involved in calcium exchange, has been reported to improve heart function. Coenzyme Q10, a key component in the electron transport chain, is vital for energy production. l-carnitine, an amino acid derivative, is responsible for transport of fatty acids into the mitochondria along with modulating glucose metabolism. Thiamine and the other B vitamins, which serve as vital cofactors, can often be deficient in HF patients. Omega-3 fatty acid supplementation has been demonstrated to benefit HF patients potentially through anti-arrhythmic and anti-inflammatory mechanisms. Vitamin D supplementation can potentially benefit HF patients by way of modulating the renin-angiotensin system, smooth muscle proliferation, inflammation, and calcium homeostasis. Although supplementation of all of the above nutrients has the potential to benefit patients with HF, more studies are needed to solidify these recommendations. PMID:21790970

  5. Apoptosis predominates in nonmyocytes in heart failure.

    PubMed

    Park, Misun; Shen, You-Tang; Gaussin, Vinciane; Heyndrickx, Guy R; Bartunek, Jozef; Resuello, Ranillo R G; Natividad, Filipinas F; Kitsis, Richard N; Vatner, Dorothy E; Vatner, Stephen F

    2009-08-01

    The goal of this investigation was to determine the distribution of myocardial apoptosis in myocytes and nonmyocytes in primates and patients with heart failure (HF). Almost all clinical cardiologists and cardiovascular investigators believe that myocyte apoptosis is considered to be a cardinal sign of HF and a major factor in its pathogenesis. However, with the knowledge that 75% of the number of cells in the heart are nonmyocytes, it is important to determine whether the apoptosis in HF is occurring in myocytes or in nonmyocytes. We studied both a nonhuman primate model of chronic HF, induced by rapid pacing 2-6 mo after myocardial infarction (MI), and biopsies from patients with ischemic cardiomyopathy. Dual labeling with a cardiac muscle marker was used to discriminate apoptosis in myocytes versus nonmyocytes. Left ventricular ejection fraction decreased following MI (from 78% to 60%) and further with HF (35%, P < 0.05). As expected, total apoptosis was increased in the myocardium following recovery from MI (0.62 cells/mm(2)) and increased further with the development of HF (1.91 cells/mm(2)). Surprisingly, the majority of apoptotic cells in MI and MI + HF, and in both the adjacent and remote areas, were nonmyocytes. This was also observed in myocardial biopsies from patients with ischemic cardiomyopathy. We found that macrophages contributed the largest fraction of apoptotic nonmyocytes (41% vs. 18% neutrophils, 16% fibroblast, and 25% endothelial and other cells). Although HF in the failing human and monkey heart is characterized by significant apoptosis, in contrast to current concepts, the apoptosis in nonmyocytes was eight- to ninefold greater than in myocytes. PMID:19465551

  6. Comprehensive rehabilitation in chronic heart failure.

    PubMed

    Gąsiorowski, Adam; Dutkiewicz, Jacek

    2013-01-01

    Chronic heart failure (CHF) is a complex disease process connected with cardiovascular system as well as other organs and skeletal muscles. In connection with the above, cardiac rehabilitation, consisting of exercise training and diet supplementation, aims at recovery of physical, social and psychic function and removing risk factors influencing the occurrence of circulatory system diseases. Evidence has shown that exercise training in CHF patients, both aerobic and resistance, can increase peak oxygen consumption and exercise capacity, improve NYHA (New York Heart Association) functional class, reduce mortality and improve the quality of life. Evidence suggests that most improvement is due to the effects of training on the peripheral circulation and skeletal muscle, rather than on the heart itself. Exercise training can improve skeletal muscle metabolism, increase blood flow within the active skeletal muscles, increase capillary density, promote the synthesis and release of nitric oxide, improve angiogenesis, and decrease oxidative stress. Physical effort reduces sympathetic arousal and increases parasympathetic arousal, thus reducing cardiac dysrythmia and ischemia. Mitochondria start working harder, as the demand for energy is higher and electron flow provides energy in the form of ATP. Studies have consistently demonstrated that exercise training is safe and has no deleterious effect on central haemodynamics, left ventricular remodeling, systolic or diastolic function, or myocardial metabolism. Taking several supplements that have documented roles in medical therapy, including vitamins B, C and E, coenzyme Q10, alpha-lipoic acid, chromium, omega-3 polyunsaturated fatty acids, L-carnitine, and quercetin, has beneficiary effect on many diseases, including CHF. In our experience, 19 patients with CHF who undertook resistance (weight) training and food supplementation, returned to their normal activities after 4 months, without any complaints. PMID:24069873

  7. Paediatric heart failure research: role of the National Heart, Lung, and Blood Institute.

    PubMed

    Burns, Kristin M

    2015-08-01

    The National Heart, Lung, and Blood Institute, of the National Institutes of Health, is committed to supporting research in paediatric heart failure. The Institute's support of paediatric heart failure research includes both investigator-initiated grants and Institute initiatives. There were 107 funded grants in paediatric heart failure over the past 20 years in basic, translational and clinical research, technology development, and support of registries. Such research includes a broad diversity of scientific topics and approaches. The Institute also supports several initiatives for paediatric heart failure, including the Pediatric Circulatory Support Program, the Pumps for Kids, Infants, and Neonates (PumpKIN) Program, PediMACS, and the Pediatric Heart Network. This review article describes the National Heart, Lung, and Blood Institute's past, present, and future efforts to promote a better understanding of paediatric heart failure, with the ultimate goal of improving outcomes. PMID:26377724

  8. The Alberta Heart Failure Etiology and Analysis Research Team (HEART) study

    PubMed Central

    2014-01-01

    Background Nationally, symptomatic heart failure affects 1.5-2% of Canadians, incurs $3 billion in hospital costs annually and the global burden is expected to double in the next 1–2 decades. The current one-year mortality rate after diagnosis of heart failure remains high at >25%. Consequently, new therapeutic strategies need to be developed for this debilitating condition. Methods/Design The objective of the Alberta HEART program (http://albertaheartresearch.ca) is to develop novel diagnostic, therapeutic and prognostic approaches to patients with heart failure with preserved ejection fraction. We hypothesize that novel imaging techniques and biomarkers will aid in describing heart failure with preserved ejection fraction. Furthermore, the development of new diagnostic criteria will allow us to: 1) better define risk factors associated with heart failure with preserved ejection fraction; 2) elucidate clinical, cellular and molecular mechanisms involved with the development and progression of heart failure with preserved ejection fraction; 3) design and test new therapeutic strategies for patients with heart failure with preserved ejection fraction. Additionally, Alberta HEART provides training and education for enhancing translational medicine, knowledge translation and clinical practice in heart failure. This is a prospective observational cohort study of patients with, or at risk for, heart failure. Patients will have sequential testing including quality of life and clinical outcomes over 12 months. After that time, study participants will be passively followed via linkage to external administrative databases. Clinical outcomes of interest include death, hospitalization, emergency department visits, physician resource use and/or heart transplant. Patients will be followed for a total of 5 years. Discussion Alberta HEART has the primary objective to define new diagnostic criteria for patients with heart failure with preserved ejection fraction. New criteria will allow for targeted therapies, diagnostic tests and further understanding of the patients, both at-risk for and with heart failure. Trial registration ClinicalTrials.gov NCT02052804. PMID:25063541

  9. Patient Safety Coalition: A Focus on Heart Failure.

    PubMed

    Kitchens, Jennifer; Kingery, Joanna; Fuller, James H; Nazir, Arif

    2015-12-01

    Indianapolis Coalition for Patient Safety, Inc engaged a citywide effort to reduce hospital readmissions of patients diagnosed with heart failure within 30days of discharge. An innovative collaboration among interdisciplinary representatives of hospitals, skilled nursing facilities, and home care agencies resulted in reduction in readmissions for patients with heart failure. PMID:26567496

  10. Heart failure with preserved ejection fraction: A clinical crisis.

    PubMed

    Banerjee, Prithwish

    2016-02-01

    A previously less known form of heart failure (Heart Failure with Preserved Ejection Fraction, HFPEF) is on the rise. This article discusses the threat this poses and what could be done including a call for dedicated HFPEF clinics run jointly by cardiologists and geriatricians. PMID:26670172

  11. DIASTOLIC DYSFUNCTION: A LINK BETWEEN HYPERTENSION AND HEART FAILURE

    PubMed Central

    Lalande, Sophie; Johnson, Bruce D.

    2009-01-01

    Summary Diastolic heart failure is characterized by the symptoms and signs of heart failure, a preserved ejection fraction and abnormal left ventricular (LV) diastolic function caused by a decreased LV compliance and relaxation. The signs and symptoms of diastolic heart failure are indistinguishable from those of heart failure related to systolic dysfunction; therefore, the diagnosis of diastolic heart failure is often one of exclusion. The majority of patients with heart failure and preserved ejection fraction have a history of hypertension. Hypertension induces a compensatory thickening of the ventricular wall in an attempt to normalize wall stress, which results in LV concentric hypertrophy, which in turn decreases LV compliance and LV diastolic filling. There is an abnormal accumulation of fibrillar collagen accompanying the hypertension-induced LV hypertrophy, which is also associated with decreased compliance and LV diastolic dysfunction. There are no specific guidelines for treating diastolic heart failure, but pharmacological treatment should be directed at normalizing blood pressure, promoting regression of LV hypertrophy, preventing tachycardia and treating symptoms of congestion. Preventive strategies directed toward an early and aggressive blood pressure control are likely to offer the greatest promise for reducing the incidence of diastolic heart failure. PMID:18806901

  12. Genetics and Heart Failure: A Concise Guide for the Clinician

    PubMed Central

    Skrzynia, Cécile; Berg, Jonathan S; Willis, Monte S; Jensen, Brian C

    2015-01-01

    The pathogenesis of heart failure involves a complex interaction between genetic and environmental factors. Genetic factors may influence the susceptibility to the underlying etiology of heart failure, the rapidity of disease progression, or the response to pharmacologic therapy. The genetic contribution to heart failure is relatively minor in most multifactorial cases, but more direct and profound in the case of familial dilated cardiomyopathy. Early studies of genetic risk for heart failure focused on polymorphisms in genes integral to the adrenergic and renin-angiotensin-aldosterone system. Some of these variants were found to increase the risk of developing heart failure, and others appeared to affect the therapeutic response to neurohormonal antagonists. Regardless, each variant individually confers a relatively modest increase in risk and likely requires complex interaction with other variants and the environment for heart failure to develop. Dilated cardiomyopathy frequently leads to heart failure, and a genetic etiology increasingly has been recognized in cases previously considered to be “idiopathic”. Up to 50% of dilated cardiomyopathy cases without other cause likely are due to a heritable genetic mutation. Such mutations typically are found in genes encoding sarcomeric proteins and are inherited in an autosomal dominant fashion. In recent years, rapid advances in sequencing technology have improved our ability to diagnose familial dilated cardiomyopathy and those diagnostic tests are available widely. Optimal care for the expanding population of patients with heritable heart failure involves counselors and physicians with specialized training in genetics, but numerous online genetics resources are available to practicing clinicians. PMID:24251456

  13. Diagnosis and management of heart failure in the fetus

    PubMed Central

    DAVEY, B.; SZWAST, A.; RYCHIK, J.

    2015-01-01

    Heart failure can be defined as the inability of the heart to sufficiently support the circulation. In the fetus, heart failure can be caused by a myriad of factors that include fetal shunting abnormalities, genetic cardiomyopathies, extracardiac malformations, arrhythmias and structural congenital heart disease. With advances in ultrasound has come the ability to characterize many complex conditions, previously poorly understood. Fetal echocardiography provides the tools necessary to evaluate and understand the various physiologies that contribute to heart failure in the fetus. In this review, we will explore the different mechanisms of heart failure in this unique patient population and highlight the role of fetal echocardiography in the current management of these conditions PMID:22992530

  14. Using galectin-3 to reduce heart failure rehospitalization.

    PubMed

    Xue, Yang; Maisel, Alan; Peacock, W Frank

    2014-03-01

    Increasing attention is being paid towards reducing short-term heart failure readmissions in recent years. Biomarkers such as galectin-3 are likely to play pivotal roles in future heart failure management strategies as they can provide objective information on various pathophysiologic processes involved in heart failure. Galectin-3 is a biomarker of inflammation and fibrosis, which is strongly associated with adverse remodeling of the myocardium and subsequent left ventricular dysfunction. Clinically, elevated galectin-3 levels are associated with increased risk for short- and long-term risk for mortality and heart failure readmission. Galectin-3 can provide incremental predictive value for adverse events over natriuretic peptides. Although significant work is still required to further define the role of galectin-3, it has the potential to become an important part of future heart failure management algorithms by helping to provide an individualized risk profile, which can be used to optimize resource allocation and improve treatment outcomes. PMID:24762249

  15. Respiratory sleep disorders in patients with congestive heart failure

    PubMed Central

    2015-01-01

    Respiratory sleep disorders (RSD) occur in about 40-50% of patients with symptomatic congestive heart failure (CHF). Obstructive sleep apnea (OSA) is considered a cause of CHF, whereas central sleep apnea (CSA) is considered a response to heart failure, perhaps even compensatory. In the setting of heart failure, continuous positive airway pressure (CPAP) has a definite role in treating OSA with improvements in cardiac parameters expected. However in CSA, CPAP is an adjunctive therapy to other standard therapies directed towards the heart failure (pharmacological, device and surgical options). Whether adaptive servo controlled ventilatory support, a variant of CPAP, is beneficial is yet to be proven. Supplemental oxygen therapy should be used with caution in heart failure, in particular, by avoiding hyperoxia as indicated by SpO2 values >95%. PMID:26380758

  16. ?-adrenoceptor blockers in chronic heart failurea review

    PubMed Central

    Krum, Henry

    1997-01-01

    There are now considerable clinical trial data to support the use of ?-adrenoceptor blockers in patients with chronic heart failure due to systolic left ventricular dysfunction. Increases in ejection fraction, improved well-being as judged by both patient and physician and reduced progression of ventricular dysfunction have been demonstrated. From meta-analyses of available trial data, a mortality reduction of approximately 30% is obtained when these drugs are added to standard heart failure therapies. Furthermore, reductions in cardiovascular morbidity associated with decreased hospitalization rates suggest pharmacoeconomic benefits with these agents. This review addresses the following issues regarding ?-adrenoceptor blockers in chronic heart failure: the known adverse effects of chronic sympathetic activation in heart failure, the theoretical benefits of blockade of this neurohormonal system, the current clinical database of ?-adrenoceptor blockers in heart failure and practical issues regarding the administration of these agents to these patients. PMID:9278193

  17. New Targets in the Drug Treatment of Heart Failure.

    PubMed

    Iwaz, James A; Lee, Elizabeth; Aramin, Hermineh; Romero, Danilo; Iqbal, Navaid; Kawahara, Matt; Khusro, Fatima; Knight, Brian; Patel, Minal V; Sharma, Sumita; Maisel, Alan S

    2016-02-01

    Heart failure is a complex syndrome that has been a major contributor to readmissions into hospitals in the USA. Currently, a large number of medications are being used to treat the symptoms of the disease-digoxin, diuretics, renin-angiotensin-aldosterone system inhibitors, ?-blockers, and vasodilators. There is no doubt that the given pharmaceutical therapy has been effective in lowering hospital readmission rates and prolonging life in individual chronic heart failure patients. Despite this, admission rates following heart failure hospitalization remain high, resulting in a substantial financial strain on healthcare institutions. Clearly, there is much room for improvement in heart failure therapy and management in reducing readmission rates. In this review, we address the unmet needs in the current drug treatment of chronic heart failure and describe novel drug targets that are currently under investigation. PMID:26659475

  18. Sarcomere gene mutations in hypertrophy and heart failure.

    PubMed

    Morita, Hiroyuki; Nagai, Ryozo; Seidman, J G; Seidman, Christine E

    2010-08-01

    Despite considerable progress in identifying and modifying risk factors that cause cardiovascular disease, heart failure has emerged as an important medical and socioeconomic problem. Hypertrophic remodeling, a common response to many cardiovascular disorders, increases the risk of heart failure. Discovery of the genetic basis of hypertrophic cardiomyopathy has allowed consideration of whether these genes also contribute to pathologic remodeling that occurs in the context of common acquired cardiovascular disorders. Evidence supporting a shared etiology has emerged from the recent identification of sarcomere protein mutations and sequence variants in community-based populations with hypertrophy and heart failure. These findings imply that harnessing genetic testing for hypertrophic mutations may help define patients at risk for heart failure. In the future, mechanistic insights into hypertrophic remodeling, combined with strategies to prevent this pathology, are expected to reduce the burden of heart failure. PMID:20559778

  19. Ivabradine in Management of Heart Failure: a Critical Appraisal.

    PubMed

    Orasanu, Gabriela; Al-Kindi, Sadeer G; Oliveira, Guilherme H

    2016-02-01

    Elevated resting heart rate has been linked to poor outcomes in patients with chronic systolic heart failure. Blockade of funny current channel with ivabradine reduces heart rate without inotropic effects. Ivabradine was recently approved by US Food and Drug Administration for patients with stable, symptomatic chronic heart failure (HF) with left ventricular ejection fraction (LVEF) ?35%, who are in sinus rhythm with resting heart rate (HR)???70bpm and either are on maximally tolerated doses of beta-blockers, or have a contraindication to beta-blockers. This article will review and evaluate the data supporting the use of ivabradine in patients with HF and explore its mechanisms and physiologic effects. PMID:26797824

  20. Left ventricular heart failure and pulmonary hypertension†

    PubMed Central

    Rosenkranz, Stephan; Gibbs, J. Simon R.; Wachter, Rolf; De Marco, Teresa; Vonk-Noordegraaf, Anton; Vachiéry, Jean-Luc

    2016-01-01

    In patients with left ventricular heart failure (HF), the development of pulmonary hypertension (PH) and right ventricular (RV) dysfunction are frequent and have important impact on disease progression, morbidity, and mortality, and therefore warrant clinical attention. Pulmonary hypertension related to left heart disease (LHD) by far represents the most common form of PH, accounting for 65–80% of cases. The proper distinction between pulmonary arterial hypertension and PH-LHD may be challenging, yet it has direct therapeutic consequences. Despite recent advances in the pathophysiological understanding and clinical assessment, and adjustments in the haemodynamic definitions and classification of PH-LHD, the haemodynamic interrelations in combined post- and pre-capillary PH are complex, definitions and prognostic significance of haemodynamic variables characterizing the degree of pre-capillary PH in LHD remain suboptimal, and there are currently no evidence-based recommendations for the management of PH-LHD. Here, we highlight the prevalence and significance of PH and RV dysfunction in patients with both HF with reduced ejection fraction (HFrEF) and HF with preserved ejection fraction (HFpEF), and provide insights into the complex pathophysiology of cardiopulmonary interaction in LHD, which may lead to the evolution from a ‘left ventricular phenotype’ to a ‘right ventricular phenotype’ across the natural history of HF. Furthermore, we propose to better define the individual phenotype of PH by integrating the clinical context, non-invasive assessment, and invasive haemodynamic variables in a structured diagnostic work-up. Finally, we challenge current definitions and diagnostic short falls, and discuss gaps in evidence, therapeutic options and the necessity for future developments in this context.

  1. Nutrient Intake in Heart Failure Patients

    PubMed Central

    Grossniklaus, Daurice A.; OBrien, Marian C.; Clark, Patricia C.; Dunbar, Sandra B.

    2009-01-01

    Background and Research Objective Approximately 50% of heart failure (HF) patients are thought to be malnourished, and macronutrient and micronutrient deficiencies may potentially aggravate HF symptoms. Thus, concerns have been raised about the overall nutrient composition of diets in HF populations. The purpose of this study was to examine the macronutrient and micronutrient intake by caloric adequacy among community-dwelling adults with HF. Participants and Methods A secondary analysis of baseline data of participants in an HF lifestyle intervention study was conducted. Participants (n = 45) were predominantly male (55.6%), white, and non-Hispanic (64.4%); had a mean age of 61 years (SD, 11 years) and mean body mass index of 31.2 kg/m2 (SD, 7.3 kg/m2); were of New York Heart Association functional classes II and III (77.8%); and had a mean ejection fraction of 31.9% (SD,13.2%); and 69% had a college or higher level of education. The Block Food Habits Questionnaire was used to assess the intake of macronutrients and micronutrients. Analysis included descriptive statistics and Mann-Whitney U tests. Results and Conclusions Individuals reporting inadequate daily caloric intake reported a lower intake of macronutrients and micronutrients as well as other differences in dietary patterns compared with individuals reporting adequate daily caloric intake. More than half of the individuals reporting adequate caloric intake did not meet the recommended dietary allowance for magnesium and vitamin E. Interventions aimed at increasing overall intake and nutrient density are suggested. Further research is needed to better understand the relationship between dietary factors and outcomes in HF. PMID:18596500

  2. Most Heart Failure Patients Die from Pump Failure: Implications for Therapy.

    PubMed

    Pereira-Barretto, Antonio Carlos; Bacal, Fernando; de Albuquerque, Denilson Campos

    2015-12-01

    Careful review of the literature of the last 20years since the appearance of the first positive trials in heart failure indicates an evolution in the mode of death moving from sudden death to a predominance of pump failure death (i.e., death due to progression of heart failure). Pump failure is becoming a leading cause of mortality in a range of patient profiles, including patients with newly diagnosed or severe heart failure, patients with devices, and patients with heart failure associated with Chagas' disease. Indeed, the evidence suggests that modern management strategies, such as beta-blockers and devices, are successful in preventing sudden death. However, this means that optimally treated patients are at greater risk for the consequences of pump failure (death, hospitalization, and reduced quality of life). This highlights a new important unmet need in heart failure, and a priority for current research should be therapies that reduce pump failure death and hospitalization for more cost-effective management of the disease. Insofar as one-third of heart failure patients do not survive more than 3 years after diagnosis, properly addressing pump failure is an essential target in heart failure. PMID:26239259

  3. Acute heart failure: Epidemiology, risk factors, and prevention.

    PubMed

    Farmakis, Dimitrios; Parissis, John; Lekakis, John; Filippatos, Gerasimos

    2015-03-01

    Acute heart failure represents the first cause of hospitalization in elderly persons and is the main determinant of the huge healthcare expenditure related to heart failure. Despite therapeutic advances, the prognosis of acute heart failure is poor, with in-hospital mortality ranging from 4% to 7%, 60- to 90-day mortality ranging from 7% to 11%, and 60- to 90-day rehospitalization from 25% to 30%. Several factors including cardiovascular and noncardiovascular conditions as well as patient-related and iatrogenic factors may precipitate the rapid development or deterioration of signs and symptoms of heart failure, thus leading to an acute heart failure episode that usually requires patient hospitalization. The primary prevention of acute heart failure mainly concerns the prevention, early diagnosis, and treatment of cardiovascular risk factors and heart disease, including coronary artery disease, while the secondary prevention of a new episode of decompensation requires the optimization of heart failure therapy, patient education, and the development of an effective transition and follow-up plan. PMID:25659507

  4. The war against heart failure: the Lancet lecture.

    PubMed

    Braunwald, Eugene

    2015-02-28

    Heart failure is a global problem with an estimated prevalence of 38 million patients worldwide, a number that is increasing with the ageing of the population. It is the most common diagnosis in patients aged 65 years or older admitted to hospital and in high-income nations. Despite some progress, the prognosis of heart failure is worse than that of most cancers. Because of the seriousness of the condition, a declaration of war on five fronts has been proposed for heart failure. Efforts are underway to treat heart failure by enhancing myofilament sensitivity to Ca(2+); transfer of the gene for SERCA2a, the protein that pumps calcium into the sarcoplasmic reticulum of the cardiomyocyte, seems promising in a phase 2 trial. Several other abnormal calcium-handling proteins in the failing heart are candidates for gene therapy; many short, non-coding RNAs--ie, microRNAs (miRNAs)--block gene expression and protein translation. These molecules are crucial to calcium cycling and ventricular hypertrophy. The actions of miRNAs can be blocked by a new class of drugs, antagomirs, some of which have been shown to improve cardiac function in animal models of heart failure; cell therapy, with autologous bone marrow derived mononuclear cells, or autogenous mesenchymal cells, which can be administered as cryopreserved off the shelf products, seem to be promising in both preclinical and early clinical heart failure trials; and long-term ventricular assistance devices are now used increasingly as a destination therapy in patients with advanced heart failure. In selected patients, left ventricular assistance can lead to myocardial recovery and explantation of the device. The approaches to the treatment of heart failure described, when used alone or in combination, could become important weapons in the war against heart failure. PMID:25467564

  5. New medical therapies for heart failure.

    PubMed

    von Lueder, Thomas G; Krum, Henry

    2015-12-01

    Heart failure (HF) can rightfully be called the epidemic of the 21(st) century. Historically, the only available medical treatment options for HF have been diuretics and digoxin, but the capacity of these agents to alter outcomes has been brought into question by the scrutiny of modern clinical trials. In the past 4 decades, neurohormonal blockers have been introduced into clinical practice, leading to marked reductions in morbidity and mortality in chronic HF with reduced left ventricular ejection fraction (LVEF). Despite these major advances in pharmacotherapy, our understanding of the underlying disease mechanisms of HF from epidemiological, clinical, pathophysiological, molecular, and genetic standpoints remains incomplete. This knowledge gap is particularly evident with respect to acute decompensated HF and HF with normal (preserved) LVEF. For these clinical phenotypes, no drug has been shown to reduce long-term clinical event rates substantially. Ongoing developments in the pharmacotherapy of HF are likely to challenge our current best-practice algorithms. Novel agents for HF therapy include dual-acting neurohormonal modulators, contractility-enhancing agents, vasoactive and anti-inflammatory peptides, and myocardial protectants. These novel compounds have the potential to enhance our armamentarium of HF therapeutics. PMID:26416006

  6. Blood flow dynamics in heart failure

    NASA Technical Reports Server (NTRS)

    Shoemaker, J. K.; Naylor, H. L.; Hogeman, C. S.; Sinoway, L. I.

    1999-01-01

    BACKGROUND: Exercise intolerance in heart failure (HF) may be due to inadequate vasodilation, augmented vasoconstriction, and/or altered muscle metabolic responses that lead to fatigue. METHODS AND RESULTS: Vascular and metabolic responses to rhythmic forearm exercise were tested in 9 HF patients and 9 control subjects (CTL) during 2 protocols designed to examine the effect of HF on the time course of oxygen delivery versus uptake (protocol 1) and on vasoconstriction during exercise with 50 mm Hg pressure about the forearm to evoke a metaboreflex (protocol 2). In protocol 1, venous lactate and H+ were greater at 4 minutes of exercise in HF versus CTL (P<0.05) despite similar blood flow and oxygen uptake responses. In protocol 2, mean arterial pressure increased similarly in each group during ischemic exercise. In CTL, forearm blood flow and vascular conductance were similar at the end of ischemic and ambient exercise. In HF, forearm blood flow and vascular conductance were reduced during ischemic exercise compared with the ambient trial. CONCLUSIONS: Intrinsic differences in skeletal muscle metabolism, not vasodilatory dynamics, must account for the augmented glycolytic metabolic responses to moderate-intensity exercise in class II and III HF. The inability to increase forearm vascular conductance during ischemic handgrip exercise, despite a normal pressor response, suggests that enhanced vasoconstriction of strenuously exercising skeletal muscle contributes to exertional fatigue in HF.

  7. Prognostic Role of Hypothyroidism in Heart Failure

    PubMed Central

    Ning, Ning; Gao, Dengfeng; Triggiani, Vincenzo; Iacoviello, Massimo; Mitchell, Judith E.; Ma, Rui; Zhang, Yan; Kou, Huijuan

    2015-01-01

    Abstract Hypothyroidism is a risk factor of heart failure (HF) in the general population. However, the relationship between hypothyroidism and clinical outcomes in patients with established HF is still inconclusive. We conducted a systematic review and meta-analysis to clarify the association of hypothyroidism and all-cause mortality as well as cardiac death and/or hospitalization in patients with HF. We searched MEDLINE via PubMed, EMBASE, and Scopus databases for studies of hypothyroidism and clinical outcomes in patients with HF published up to the end of January 2015. Random-effects models were used to estimate summary relative risk (RR) statistics. We included 13 articles that reported RR estimates and 95% confidence intervals (95% CIs) for hypothyroidism with outcomes in patients with HF. For the association of hypothyroidism with all-cause mortality and with cardiac death and/or hospitalization, the pooled RR was 1.44 (95% CI: 1.291.61) and 1.37 (95% CI: 1.221.55), respectively. However, the association disappeared on adjustment for B-type natriuretic protein level (RR 1.17, 95% CI: 0.901.52) and in studies of patients with mean age <65 years (RR 1.23, 95% CI: 0.881.76). We found hypothyroidism associated with increased all-cause mortality as well as cardiac death and/or hospitalization in patients with HF. Further diagnostic and therapeutic procedures for hypothyroidism may be needed for patients with HF. PMID:26222845

  8. Heart failure with preserved ejection fraction

    PubMed Central

    Rigolli, Marzia; Whalley, Gillian A

    2013-01-01

    Progressive aging of the population and prolongation of life expectancy have led to the rising prevalence of heart failure (HF). Despite the improvements in medical therapy, the mortality rate of this condition has remained unacceptably high, becoming the primary cause of death in the elderly population. Almost half of patients with signs and symptoms of HF are found to have a nearly normal ejection fraction, which delineates a distinct clinical syndrome, known as HF with preserved ejection fraction (HF-PEF). While early research focused on the importance of diastolic dysfunction, more recent studies reported the pathophysiological complexity of the disease with multiple cardiovascular abnormalities contributing to its development and progression. HF-PEF is a challenging major health problem with yet no solution as there is no evidence-based treatment which improves clinical outcomes. This review summarizes the state of current knowledge on diagnosis, prognosis and treatment of HF-PEF, with particular insights on the pathological characteristics in the elderly population. PMID:24454331

  9. MODELS OF INSULIN RESISTANCE AND HEART FAILURE

    PubMed Central

    Velez, Mauricio; Kohli, Smita; Sabbah, Hani N.

    2013-01-01

    The incidence of heart failure (HF) and diabetes mellitus is rapidly increasing and is associated with poor prognosis. In spite of the advances in therapy, HF remains a major health problem with high morbidity and mortality. When HF and diabetes coexist, clinical outcomes are significantly worse. The relationship between these two conditions has been studied in various experimental models. However, the mechanisms for this interrelationship are complex, incompletely understood, and have become a matter of considerable clinical and research interest. There are only few animal models that manifest both HF and diabetes. However, the translation of results from these models to human disease is limited and new models are needed to expand our current understanding of this clinical interaction. In this review, we discuss mechanisms of insulin signaling and insulin resistance, the clinical association between insulin resistance and HF and its proposed pathophysiologic mechanisms. Finally, we discuss available animal models of insulin resistance and HF and propose requirements for future new models. PMID:23456447

  10. Comorbidity of atrial fibrillation and heart failure.

    PubMed

    Ling, Liang-Han; Kistler, Peter M; Kalman, Jonathan M; Schilling, Richard J; Hunter, Ross J

    2016-03-01

    Atrial fibrillation (AF) and heart failure (HF) are evolving epidemics, together responsible for substantial human suffering and health-care expenditure. Ageing, improved cardiovascular survival, and epidemiological transition form the basis for their increasing global prevalence. Although we now have a clear picture of how HF promotes AF, gaps remain in our knowledge of how AF exacerbates or even causes HF, and how the development of HF affects the outcome of patients with AF. New data regarding HF with preserved ejection fraction and its unique relationship with AF suggest a possible role for AF in its aetiology, possibly as a trigger for ventricular fibrosis. Deciding on optimal treatment strategies for patients with both AF and HF is increasingly difficult, given that results from trials of pharmacological rhythm control are arguably obsolete in the age of catheter ablation. Restoring sinus rhythm by catheter ablation seems successful in the medium term and improves HF symptoms, functional capacity, and left ventricular function. Long-term studies to examine the effect on rates of stroke and death are ongoing. Guidelines continue to evolve to keep pace with this rapidly changing field. PMID:26658575

  11. Treatment options for hyponatremia in heart failure.

    PubMed

    Goldsmith, Steven R

    2009-06-01

    Hyponatremia is independently associated with adverse outcomes in patients with congestive heart failure (CHF). The primary cause of hyponatremia in CHF is the inappropriate secretion of the antidiuretic hormone, arginine vasopressin (AVP). The binding of AVP to V(2) receptors in the renal collecting duct promotes water retention, a process that can lead to dilutional hyponatremia as well as increased ventricular preload. AVP could also exacerbate the course of CHF by interacting with V(1A) receptors on vascular smooth muscle cells and myocytes. Conventional treatment of hyponatremia in CHF is based largely on water restriction, which is neither effective nor well tolerated. Current research is exploring V(2)- and dual V(1A)/V(2)-receptor antagonism for the treatment of hyponatremia, as well as for the congestion and edema associated with CHF, since AVP-receptor antagonists may offer benefits in comparison to conventional loop diuretics. Clinical trials in patients with hyponatremia and CHF using both selective and nonselective vasopressin antagonists have demonstrated the effectiveness of these agents in correcting this common electrolyte abnormality. PMID:18777208

  12. Heart failure patients utilizing an electric home monitor: What effects does heart failure have on their quality of life?

    NASA Astrophysics Data System (ADS)

    Simuel, Gloria J.

    Heart Failure continues to be a major public health problem associated with high mortality and morbidity. Heart Failure is the leading cause of hospitalization for persons older than 65 years, has a poor prognosis and is associated with poor quality of life. More than 5.3 million American adults are living with heart failure. Despite maximum medical therapy and frequent hospitalizations to stabilize their condition, one in five heart failure patients die within the first year of diagnosis. Several disease-management programs have been proposed and tested to improve the quality of heart failure care. Studies have shown that hospital admissions and emergency room visits decrease with increased nursing interventions in the home and community setting. An alternative strategy for promoting self-management of heart failure is the use of electronic home monitoring. The purpose of this study was to examine what effects heart failure has on patient's quality of life that had been monitoring on an electronic home monitor longer than 2 months. Twenty-one questionnaires were given to patients utilizing an electronic home monitor by their home health agency nurse. Eleven patients completed the questionnaire. The findings showed that there is some deterioration in quality of life with more association with the physical aspects of life than with the emotional aspects of life, which probably was due to the small sample size. There was no significant difference in readmission rates in patients utilizing an electronic home monitor. Further research is needed with a larger population of patients with chronic heart failure and other chronic diseases which may provide more data, and address issues such as patient compliance with self-care, impact of heart failure on patient's quality of life, functional capacity, and heart failure patient's utilization of the emergency rooms and hospital. Telemonitoring holds promise for improving the self-care abilities of persons with HF.

  13. Clinical treatment regimens for chronic heart failure: a review.

    PubMed

    Gould, Paul A; Kaye, David M

    2002-11-01

    Chronic heart failure (CHF) is increasing in prevalence worldwide, particularly in the elderly. Accordingly, this epidemic is likely to translate into a major increase in healthcare costs. Systolic heart failure is the most common cause of CHF presentations. Although the causes vary, the most common single aetiological factor is ischaemic heart disease, which accounts for approximately 50% of heart failure presentations. Research into CHF pharmacotherapy has been copious, with the focus principally centred on systolic heart failure. The evidence base for pharmacotherapy in CHF is amongst the largest currently in clinical medicine. There have been multiple trials establishing the mortality and morbidity benefits of pharmacotherapy. Amongst these, large scale trials of angiotensin-converting enzyme inhibitors, beta-blockers and spironolactone have provided a sound basis for evidence-based treatment approaches to the CHF patient. Recently research interest has increased in biomedical engineering with studies being performed in biventricular pacing and mechanical hearts. Early data with biventricular pacing or cardiac resynchronisation therapy is encouraging. Diastolic heart failure alone accounts for at least 20 - 40% of CHF presentations and whilst it may occur in isolation, is most commonly seen in association with systolic heart failure. In this study, we present a broad overview of the current therapeutic modalities for the management of CHF, with particular emphasis on pharmacotherapy. PMID:12437491

  14. Management of Patients Admitted with Acute Decompensated Heart Failure

    PubMed Central

    Krim, Selim R.; Campbell, Patrick T.; Desai, Sapna; Mandras, Stacy; Patel, Hamang; Eiswirth, Clement; Ventura, Hector O.

    2015-01-01

    Background Hospital admission for the treatment of acute decompensated heart failure is an unfortunate certainty in the vast majority of patients with heart failure. Regardless of the etiology, inpatient treatment for acute decompensated heart failure portends a worsening prognosis. Methods This review identifies patients with heart failure who need inpatient therapy and provides an overview of recommended therapies and management of these patients in the hospital setting. Results Inpatient therapy for patients with acute decompensated heart failure should be directed at decongestion and symptom improvement. Clinicians should also treat possible precipitating events, identify comorbid conditions that may exacerbate heart failure, evaluate and update current guideline-directed medical therapy, and perform risk stratification for all patients. Finally, efforts should be made to educate patients about the importance of restricting salt and fluid, monitoring daily weights, and adhering to a graded exercise program. Conclusion Early discharge follow-up and continued optimization of guideline-directed medical therapy are key to preventing future heart failure readmissions. PMID:26413005

  15. Atrial natriuretic factor binding sites in experimental congestive heart failure

    SciTech Connect

    Bianchi, C.; Thibault, G.; Wrobel-Konrad, E.; De Lean, A.; Genest, J.; Cantin, M. )

    1989-10-01

    A quantitative in vitro autoradiographic study was performed on the aorta, renal glomeruli, and adrenal cortex of cardiomyopathic hamsters in various stages of heart failure and correlated, in some instances, with in vivo autoradiography. The results indicate virtually no correlation between the degree of congestive heart failure and the density of 125I-labeled atrial natriuretic factor ((Ser99, Tyr126)ANF) binding sites (Bmax) in the tissues examined. Whereas the Bmax was increased in the thoracic aorta in moderate and severe heart failure, there were no significant changes in the zona glomerulosa. The renal glomeruli Bmax was lower in mild and moderate heart failure compared with control and severe heart failure. The proportion of ANF B- and C-receptors was also evaluated in sections of the aorta, adrenal, and kidney of control and cardiomyopathic hamsters with severe heart failure. (Arg102, Cys121)ANF (des-(Gln113, Ser114, Gly115, Leu116, Gly117) NH2) (C-ANF) at 10(-6) M displaced approximately 505 of (Ser99, Tyr126)125I-ANF bound in the aorta and renal glomeruli and approximately 20% in the adrenal zona glomerulosa in both series of animals. These results suggest that ANF may exert a buffering effect on the vasoconstriction of heart failure and to a certain extent may inhibit aldosterone secretion. The impairment of renal sodium excretion does not appear to be related to glomerular ANF binding sites at any stage of the disease.

  16. Heart failure among Indigenous Australians: a systematic review

    PubMed Central

    2012-01-01

    Background Cardiovascular diseases contribute substantially to the poor health and reduced life expectancy of Indigenous Australians. Heart failure is a common, disabling, progressive and costly complication of these disorders. The epidemiology of heart failure and the adequacy of relevant health service provision in Indigenous Australians are not well delineated. Methods A systematic search of the electronic databases PubMed, Embase, Web of Science, Cinahl Plus, Informit and Google Scholar was undertaken in April 2012 for peer-reviewed journal articles relevant to the topic of heart failure in Indigenous Australians. Additionally, a website search was done to identify other pertinent publications, particularly government reports. Results There was a paucity of relevant peer-reviewed research, and government reports dominated the results. Ten journal articles, 1 published conference abstract and 10 reports were eligible for inclusion. Indigenous Australians reportedly have higher morbidity and mortality from heart failure than their non-Indigenous counterparts (age-standardised prevalence ratio 1.7; age-standardised hospital separation ratio ≥3; crude per capita hospital expenditure ratio 1.58; age-adjusted mortality ratio >2). Despite the evident disproportionate burden of heart failure in Indigenous Australians, the accuracy of estimation from administrative data is limited by poor indigenous identification, inadequate case ascertainment and exclusion of younger subjects from mortality statistics. A recent journal article specifically documented a high prevalence of heart failure in Central Australian Aboriginal adults (5.3%), noting frequent undiagnosed disease. One study examined barriers to health service provision for Indigenous Australians in the context of heart failure. Conclusions Despite the shortcomings of available published data, it is clear that Indigenous Australians have an excess burden of heart failure. Emerging data suggest that undiagnosed cases may be common in this population. In order to optimise management and to inform policy, high quality research on heart failure in Indigenous Australians is required to delineate accurate epidemiological indicators and to appraise health service provision. PMID:23116367

  17. Present and future pharmacotherapy for heart failure.

    PubMed

    Doggrell, Sheila A; Brown, Lindsay

    2002-07-01

    The pharmacotherapy currently recommended by the American College of Cardiology and the American Heart Association for heart failure (HF) is a diuretic, an angiotensin-converting enzyme inhibitor (ACEI), a beta-adrenoceptor antagonist and (usually) digitalis. This current treatment of HF may be improved by optimising the dose of ACEI used, as increasing the dose of lisinopril increases its benefits in HF. Selective angiotensin receptor-1 (AT(1)) antagonists are effective alternatives for those who cannot tolerate ACEIs. AT(1) antagonists may also be used in combination with ACEIs, as some studies have shown cumulative benefits for the combination. In addition to being used in Stage IV HF patients, in whom it has a marked benefit, spironolactone should be studied in less severe HF and in the presence of beta-blockers. The use of carvedilol, extended-release metoprolol and bisoprolol should be extended to severe HF patients as these agents have been shown to decrease mortality in this group. The ancillary properties of carvedilol, particularly antagonism at prejunctional beta -adrenoceptors, may give it additional benefits to selective beta(1)-adrenoceptor antagonists. Celiprolol and bucindolol are not the beta-blockers of choice in HF, as they do not decrease mortality. Although digitalis does not reduce mortality, it remains the only option for a long-term positive inotropic effect, as the long-term use of the phosphodiesterase inhibitors is associated with increased mortality. The calcium sensitising drug levosimendan may be useful in the hospital treatment of decompensated HF to increase cardiac output and improve dyspnoea and fatigue. The antiarrhythmic drug amiodarone should probably be used in patients at high risk of arrhythmic or sudden death, although this treatment may soon be superseded by the more expensive implanted cardioverter defibrillators, which are probably more effective and have fewer side effects. The natriuretic peptide nesiritide has recently been introduced for the hospital treatment of decompensated HF. Novel drugs that may be beneficial in the treatment of HF include the vasopeptidase inhibitors and the selective endothelin-A receptor antagonists but these require much more investigation. However, disappointing results have been obtained in a large clinical trial of the tumour necrosis factor alpha antagonist etanercept, where no likelihood of a difference between placebo and etanercept was observed. Small clinical trials with recombinant growth hormone to thicken ventricles in dilated cardiomyopathy have given variable results. PMID:12083991

  18. Incorporating Common Biomarkers into the Clinical Management of Heart Failure

    PubMed Central

    Halkar, Meghana

    2013-01-01

    Heart failure is a prevalent and costly disease, and its management with polypharmacy is complex. Commonly available biomarkers primarily help to 1) establish or refute the diagnosis of heart failure; 2) help to determine the disease severity; and 3) identify adverse consequences of treatment. Although several of them are commonly ordered (such as electrolytes, renal and liver function), their use is primarily based on broad clinical experience rather than established evidence. The availability of cardiac-specific natriuretic peptide testing has provided an evidence-based breakthrough in our abilities to establish the diagnosis and severity of heart failure, yet the appropriate boundaries to guide management are still in refinement. PMID:24085636

  19. Prospects for gene transfer for clinical heart failure

    PubMed Central

    Tang, T; Gao, MH; Hammond, H Kirk

    2013-01-01

    Congestive heart failure is an inexorable disease associated with unacceptably high morbidity and mortality. Preclinical results indicate that gene transfer using various proteins is a safe and effective approach for increasing function of the failing heart. In the current review, we provide a summary of cardiac gene transfer in general and summarize findings using adenylyl cyclase 6 as therapeutic gene in the failing heart. We also discuss the potential usefulness of a new treatment for congestive heart failure, paracrine-based gene transfer. PMID:22534469

  20. Optimized Treatment and Heart Rate Reduction in Chronic Heart Failure

    PubMed Central

    Moreno, Irineu Blanco; Del Carlo, Carlos Henrique; Pereira-Barretto, Antnio Carlos

    2013-01-01

    Background Heart failure (HF) is a syndrome that leads to poor outcome in advanced forms. The neurohormonal blockade modifies this natural history; however, it is often suboptimal. Objective The aim of this study is to assess at what percentage cardiologists used to treating HF can prescribe target doses of drugs of proven efficacy. Methods A total of 104 outpatients with systolic dysfunction were consecutively enrolled, all under stabilized treatment. Demographic and treatment data were evaluated and the doses achieved were verified. The findings are shown as percentages and correlations are made between different variables. Results The mean age of patients was 64.1 14.2 years, with SBP =115.4 15.3, HR = 67.8 9.4 bpm, weight = 76.0 17.0 kg and sinus rhythm (90.4%). As for treatment, 93.3% received a RAS blocker (ACEI 52.9%), all received beta-blockers (BB), the most often prescribed being carvedilol (92.3%). As for the doses: 97.1% of those receiving an ARB were below the optimal dose and of those who received ACEI, 52.7% received an optimized dose. As for the BB, target doses were prescribed to 76.0% of them. In this group of patients, most with BB target dose, it can be seen that 36.5% had HR ? 70 bpm in sinus rhythm. Conclusion Cardiologists used to treating HF can prescribe target doses of ACEI and BB to most patients. Even though they receive the recommended doses, about one third of patients persists with HR > 70 bpm and should have their treatment optimized. PMID:24100693

  1. ZINC AND THE PROOXIDANT HEART FAILURE PHENOTYPE

    PubMed Central

    Efeovbokhan, Nephertiti; Bhattacharya, Syamal K.; Ahokas, Robert A.; Sun, Yao; Guntaka, Ramareddy V.; Gerling, Ivan C.; Weber, Karl T.

    2014-01-01

    Neurohormonal activation with attendant aldosteronism contributes to the clinical appearance of congestive heart failure (CHF). Aldosteronism is intrinsically coupled to Zn2+ and Ca2+ dyshomeostasis, in which consequent hypozincemia compromises Zn2+ homeostasis and Zn2+-based antioxidant defenses that contribute to the CHF prooxidant phenotype. Ionized hypocalcemia leads to secondary hyperparathyroidism with parathyroid hormone-mediated Ca2+ overloading of diverse cells, including cardiomyocytes. When mitochondrial Ca2+ overload exceeds a threshold, myocyte necrosis follows. The reciprocal regulation involving cytosolic free [Zn2+]i as antioxidant and [Ca2+]i as prooxidant that can be uncoupled in favor of Zn2+-based antioxidant defenses. Increased [Zn2+]i acts as a multifaceted antioxidant by: i) inhibiting Ca2+ entry via L-type channels and hence cardioprotectant from the Ca2+-driven mitochondriocentric signal-transducer-effector pathway to nonischemic necrosis; ii) serving as catalytic regulator of Cu/Zn-superoxide dismutase; and iii) activating its cytosolic sensor, metal-responsive transcription factor that regulates the expression of relevant antioxidant defense genes. Albeit present in subnanomolar range, increased cytosolic free [Zn2+]i enhances antioxidant capacity that confers cardioprotection. It can be achieved exogenously by ZnSO4 supplementation or endogenously, using a β3 receptor agonist, (e.g., nebivolol) that enhances NO generation to release inactive cytosolic Zn2+ bound to metallothionein. By recognizing the pathophysiologic relevance of Zn2+ dyshomeostasis in the prooxidant CHF phenotype and by exploiting the pharmacophysiologic potential of [Zn2+]i as antioxidant, vulnerable cardiomyocytes under assault from neurohormonal activation can be protected and the myocardium spared from adverse structural remodeling. PMID:25291496

  2. Soluble epoxide hydrolase inhibitors and heart failure.

    PubMed

    Qiu, Hong; Li, Ning; Liu, Jun-Yan; Harris, Todd R; Hammock, Bruce D; Chiamvimonvat, Nipavan

    2011-04-01

    Cardiovascular disease remains one of the leading causes of death in the Western societies. Heart failure (HF) is due primarily to progressive myocardial dysfunction accompanied by myocardial remodeling. Once HF develops, the condition is, in most cases, irreversible and is associated with a very high mortality rate. Soluble epoxide hydrolase (sEH) is an enzyme that catalyzes the hydrolysis of epoxyeicosatrienoic acids (EETs), which are lipid mediators derived from arachidonic acid through the cytochrome P450 epoxygenase pathway. EETs have been shown to have vasodilatory, antiinflammatory, and cardioprotective effects. When EETs are hydrolyzed by sEH to corresponding dihydroxyeicosatrienoic acids, their cardioprotective activities become less pronounced. In line with the recent genetic study that has identified sEH as a susceptibility gene for HF, the sEH enzyme has received considerable attention as an attractive therapeutic target for cardiovascular diseases. Indeed, sEH inhibition has been demonstrated to have antihypertensive and antiinflammatory actions, presumably due to the increased bioavailability of endogenous EETs and other epoxylipids, and several potent sEH inhibitors have been developed and tested in animal models of cardiovascular disease including hypertension, cardiac hypertrophy, and ischemia/reperfusion injury. sEH inhibitor treatment has been shown to effectively prevent pressure overload- and angiotensin II-induced cardiac hypertrophy and reverse the pre-established cardiac hypertrophy caused by chronic pressure overload. Application of sEH inhibitors in several cardiac ischemia/reperfusion injury models reduced infarct size and prevented the progressive cardiac remodeling. Moreover, the use of sEH inhibitors prevented the development of electrical remodeling and ventricular arrhythmias associated with cardiac hypertrophy and ischemia/reperfusion injury. The data published to date support the notion that sEH inhibitors may represent a promising therapeutic approach for combating detrimental cardiac remodeling and HF. PMID:20433684

  3. CONGESTIVE HEART FAILURE: WHERE HOMEOSTASIS BEGETS DYSHOMEOSTASIS

    PubMed Central

    Kamalov, German; Bhattacharya, Syamal K.; Weber, Karl T.

    2010-01-01

    Despite today’s standard of care, aimed at containing homeostatic neurohormonal activation, 1 in every 5 patients recently hospitalized with congestive heart failure (CHF) will be readmitted within 30 days of discharge because of a recurrence of their symptoms and signs. In light of recent pathophysiologic insights, it is now propitious to revisit CHF with a view toward complementary and evolving management strategies. CHF is a progressive systemic illness. Its features include: oxidative stress in diverse tissues; an immunostimulatory state with circulating proinflammatory cytokines; a wasting of soft tissues; and a resorption of bone. Its origins are rooted in homeostatic mechanisms gone awry to beget dyshomeostasis. For example, marked excretory losses of Ca2+ and Mg2+ accompany renin-angiotensin-aldosterone system (RAAS) activation, causing ionized hypocalcemia and hypomagnesemia that lead to secondary hyperparathyroidism (SHPT) with consequent bone resorption and a propensity to atraumatic fractures. Parathyroid hormone (PTH) accounts for paradoxical intracellular Ca2+ overloading in diverse tissues and consequent systemic induction of oxidative stress. In cardiac myocytes and mitochondria these events orchestrate opening of the mitochondrial membrane permeability transition pore (mPTP) with an ensuing osmotic-based destruction of these organelles and resultant cardiomyocyte necrosis with myocardial scarring. Contemporaneous with Ca2+ and Mg2+ dyshomeostasis is hypozincemia and hyposelenemia, which compromise metalloenzyme-based antioxidant defenses while hypovitaminosis D threatens Ca2+ stores needed to prevent SHPT. An intrinsically coupled dyshomeostasis of intracellular Ca2+ and Zn2+, representing prooxidant and antioxidant, respectively, is integral to regulating mitochondrial redox state; it can be uncoupled by a Zn2+ supplement in favor of antioxidant defenses. Hence, the complementary use of nutriceuticals to nullify dyshomeostatic responses involving macro- and micronutrients should be considered. Evolving strategies with mitochondria-targeted interventions interfering with their uptake of Ca2+ or serving as selective antioxidant or mPTP inhibitor may also prove efficacious in the overall management of CHF. PMID:20588190

  4. Diaphragm strength in chronic heart failure.

    PubMed

    Hughes, P D; Polkey, M I; Harrus, M L; Coats, A J; Moxham, J; Green, M

    1999-08-01

    Reduced respiratory muscle strength has been reported in chronic heart failure (CHF) in several studies. The data supporting this conclusion come almost exclusively from static inspiratory and expiratory mouth pressure maneuvers (MIP, MEP), which many subjects find difficult to perform. We therefore performed a study using measurements that are less dependent on patient aptitude and also provide specific data on diaphragm strength. In 20 male patients and 15 control subjects we measured MIP and MEP as well as esophageal and transdiaphragmatic pressure during maximal sniffs (Sn Pes, Sn Pdi) and cervical magnetic phrenic nerve stimulation (Tw Pdi). In a subgroup the response to paired phrenic nerve stimulation (pTw Pdi) at interpulse intervals from 10 to 200 ms (5 to 100 Hz) was also determined. As expected, MIP was significantly reduced in the CHF group (CHF, 69.5 cm H(2)O; control, 96.7 cm H(2)O; p = 0.01), but differences were much less marked for Sn Pes (CHF, 95.2 cm H(2)O; control, 104.8 cm H(2)O; p = 0.20) and MEP (CHF, 109.1 cm H(2)O; control, 135.7 cm H(2)O; p = 0.09). Diaphragm strength was significantly reduced (Sn Pdi: CHF, 123.8 cm H(2)O; control 143.5 cm H(2)O; p = 0.04. Tw Pdi: CHF, 21.4 cm H(2)O; control, 28.5 cm H(2)O; p = 0.0005). Paired phrenic nerve stimulation suggested a trend to increased twitch summation at 5 to 20 Hz in CHF, although this did not reach significance. We conclude that mild reduction in diaphragm strength occurs in CHF, possibly because of an increased proportion of slow fibers, but overall strength of the respiratory muscles remains well preserved. PMID:10430724

  5. Inflammatory cytokines as biomarkers in heart failure.

    PubMed

    Ueland, Thor; Gullestad, Lars; Nymo, Ståle H; Yndestad, Arne; Aukrust, Pål; Askevold, Erik T

    2015-03-30

    Inflammation has been implicated in the pathogenesis of heart failure (HF). In addition to their direct involvement as mediators in the pathogenesis of HF, inflammatory cytokines and related mediators could also be suitable markers for risk stratification and prognostication in HF patients. Many reports have suggested that inflammatory cytokines may predict adverse outcome in these patients. However, most studies have been limited in sample size and lacking full adjustment with the most recent and strongest biochemical predictor such as NT-proBNP and high sensitivity troponins. Furthermore, a number of pre-analytical and analytical aspects of cytokine measurements may limit their use as biomarkers. This review focuses on technical, informative and practical considerations concerning the clinical use of inflammatory cytokines as prognostic biomarkers in HF. We focus on the predictive value of tumor necrosis factor (TNF) α, the TNF family receptors sTNFR1 and osteoprotegerin, interleukin (IL)-6 and its receptor gp130, the chemokines MCP-1, IL-8, CXCL16 and CCL21 and the pentraxin PTX-3 in larger prospective fully adjusted studies. No single inflammatory cytokine provides sufficient discrimination to justify the transition to everyday clinical use as a prognosticator in HF. However, while subjecting potential new HF markers to rigorous comparisons with "gold-standard" markers, such as NT-proBNP, using receiver operating characteristics (ROCs) and HF risk models, makes sense from a clinical standpoint, it may pose a threat to a broadening of mechanistic insight if the new markers are dismissed solely on account of lower statistical power. PMID:25199849

  6. Use of pimobendan in the management of heart failure.

    PubMed

    Fuentes, Virginia Luis

    2004-09-01

    Pimobendan is an oral inodilator compound available in many countries for use in canine heart failure. It combines calcium-sensitizing effects with PDE III inhibition, resulting in positive inotropic effects and veno- and ergic signal transduction pathway in the failing heart, the calcium-sensitizing effects may assume greater importance in patients with heart failure. Clinical studies in human patients have shown sustained improvement in hemodynamics and exercise tolerance, with favorable neurohormonal effects. One study showed a nonsignificant trend toward increased mortality [20], but proarrhythmic effects have not ben observed. Studies in naturally occurring canine heart failure suggest that pimobendan's effects are at least comparable to those of ACE inhibitors, if not superior. Pimobendan is likely to play an increasing role in the future in the treatment of canine heart disease. PMID:15325474

  7. Comorbid Heart Failure and Renal Impairment: Epidemiology and Management

    PubMed Central

    Iyngkaran, Pupalan; Thomas, Merlin; Majoni, William; Anavekar, Nagesh S.; Ronco, Claudio

    2012-01-01

    Heart failure mortality is significantly increased in patients with baseline renal impairment and those with underlying heart failure who subsequently develop renal dysfunction. This accelerated progression occurs independent of the cause or grade of renal dysfunction and baseline risk factors. Recent large prospective databases have highlighted the depth of the current problem, while longitudinal population studies support an increasing disease burden. We have extensively reviewed the epidemiological and therapeutic data among these patients. The evidence points to a progression of heart failure early in renal impairment, even in the albuminuric stage. The data also support poor prescription of prognostic therapies. As renal function is the most important prognostic factor in heart failure, it is important to establish the current understanding of the disease burden and the therapeutic implications. PMID:23381594

  8. Common Heart Failure Drugs May Harm More Than Help

    MedlinePLUS

    ... mg) to 120 mg -- or to take a placebo. The patients suffered from heart failure with so- ... the nitrate regardless of dose, compared with the placebo. And as the dose of isosorbide mononitrate increased, ...

  9. Postinfarct Left Ventricular Remodelling: A Prevailing Cause of Heart Failure

    PubMed Central

    Galli, Alessio; Lombardi, Federico

    2016-01-01

    Heart failure is a chronic disease with high morbidity and mortality, which represents a growing challenge in medicine. A major risk factor for heart failure with reduced ejection fraction is a history of myocardial infarction. The expansion of a large infarct scar and subsequent regional ventricular dilatation can cause postinfarct remodelling, leading to significant enlargement of the left ventricular chamber. It has a negative prognostic value, because it precedes the clinical manifestations of heart failure. The characteristics of the infarcted myocardium predicting postinfarct remodelling can be studied with cardiac magnetic resonance and experimental imaging modalities such as diffusion tensor imaging can identify the changes in the architecture of myocardial fibers. This review discusses all the aspects related to postinfarct left ventricular remodelling: definition, pathogenesis, diagnosis, consequences, and available therapies, together with experimental interventions that show promising results against postinfarct remodelling and heart failure. PMID:26989555

  10. Diastolic heart failure: a clinical challenge early recognition & timely intervention is the need of the hour.

    PubMed

    Chopra, H K

    2009-01-01

    Diastolic Heart failure (DHF) is the major cause of morbidity and mortality all over the world. It is responsible for more than 50% of the heart failure cases. New onset of symptomatic DHF is a lethal disease with a 5-yr mortality of approximately 50%. DHF is also referred to as heart failure (HF) with normal left ventricular ejection fraction (LVEF)-HFNLVEF. The diagnosis of DHF requires the following criteria: (i) signs and symptoms of heart failure (ii) normal or mildly abnormal systolic left ventricular (LV) function (iii) evidence of LV diastolic dysfunction. Diagnostic evidence of LV diastolic dysfunction can be obtained invasively (LV end-diastolic pressure > 16 mmHg or mean pulmonary capillary wedge pressure > 12 mmHg) or non-invasively by tissue Doppler imaging (TDI) (E/E' > 15). If TDI yields an E/E' ratio suggestive of LV diastolic dysfunction (15 > E/E' > 8), then additional echo variables are required for diagnostic evidence of LV diastolic dysfunction, which include Doppler flow profile of mitral valve or pulmonary veins, measurement of LV mass index (LVMi) or left atrium volume index (LAVi), electrocardiographic evidence of atrial fibrillation or high levels of B-natreuretic peptide. Echo-Doppler techniques using LV filling pressures and tissue Doppler imaging of the mitral annulus help in identifying and classifying the degree of LV diastolic dysfunction. However, clinically this is more relevant to advanced overt disease. Therefore early recognition of DHF in relatively asymptomatic or less symptomatic patients with occult LV diastolic dysfunction is a real challenge. Recently it has been shown that reduction in left atrial strain and strain rate and increase in left atrial (LA) stiffness index has a high predictive value for detection of occult LV diastolic dysfunction. Thus early recognition of occult DHF and timely therapeutic intervention may help in prognostic stratification in DHF. PMID:20039498

  11. Iron Deficiency in Heart Failure: Looking Beyond Anaemia.

    PubMed

    Wong, Christopher C Y; Ng, Austin C C; Kritharides, Leonard; Sindone, Andrew P

    2016-03-01

    Iron is an essential micronutrient in many cellular processes. Iron deficiency, with or without anaemia, is common in patients with chronic heart failure. Observational studies have shown iron deficiency to be associated with worse clinical outcomes and mortality. The treatment of iron deficiency in chronic heart failure patients using intravenous iron alone has shown promise in several clinical trials, although further studies which include larger populations and longer follow-up times are needed. PMID:26669811

  12. Nesiritide for heart failure: impact on costs and complications.

    PubMed

    Hunter, Claire B; Ndemo, Francis; Lenz, Thomas L; Maciejewski, Stephanie; Hilleman, Daniel E

    2005-02-01

    Decompensated heart failure accounts for approximately 1 million hospitalizations in the USA each year with an estimated cost of US$11,000 per hospitalization. Despite this prevalence and cost burden, relatively few therapies for decompensated heart failure have been developed over the past 30 years. Although once the mainstay of treatment of decompensated heart failure, the use of positive inotropic agents has fallen into disfavor. Although these agents improve hemodynamics and ejection fraction, there is evidence that the positive inotropes increase the risk of adverse clinical outcomes and mortality. Nesiritide is a naturetic peptide that produces balance vasodilation, inhibits sympathetic nervous system activity, and promotes diuresis and naturesis. At the time the drug received Food and Drug Administration approval for marketing in the USA, it had been shown to produce hemodynamic improvements to an extent greater than placebo or nitroglycerin. However, evidence of benefit in terms of clinical improvement and other outcomes was lacking. Recent trials have found that nesiritide reduces hospital length of stay (although not statistically significant in all trials) and healthcare resource utilization in patients admitted to hospital with decompensated heart failure. In a randomized, controlled trial, nesiritide given in the emergency room reduced hospital admissions for heart failure compared with placebo/usual care. Preliminary data from an outpatient intermittent infusion trial of nesiritide found that patients receiving nesiritide had fewer hospital admissions than patients randomized to standard care. There is currently little objective evidence that therapies used routinely in the management of patients with decompensated heart failure are associated with improved outcomes. Data with positive inotropic agents suggest that they do more harm than good. There is a growing body of evidence that nesiritide is associated with improvements in clinical outcomes in decompensated heart failure including fewer complications, less healthcare resource utilization, and lower costs when compared with standard therapy. Despite this evidence, larger, prospective trials demonstrating the impact of nesiritide on the costs and complications in decompensated heart failure are needed. PMID:19807556

  13. Pathogenesis and clinical presentation of acute heart failure.

    PubMed

    Ponikowski, Piotr; Jankowska, Ewa A

    2015-04-01

    Acute heart failure constitutes a heterogeneous clinical syndrome, whose pathophysiology is complex and not completely understood. Given the diversity of clinical presentations, several different pathophysiological mechanisms along with factors triggering circulatory decompensation are involved. This article discusses the available evidence on the pathophysiological phenomena attributed or/and associated with episodes of acute heart failure and describes different clinical profiles, which, from a clinical perspective, constitute a key element for therapeutic decision-making. PMID:25743769

  14. High-output heart failure secondary to arteriovenous fistula.

    PubMed

    Stern, Adam B; Klemmer, Philip J

    2011-01-01

    In the hemodialysis patient population, a surgically created arteriovenous fistula is the preferred vascular access option. Development of high-output heart failure may be an underappreciated complication in patients who have undergone this procedure. When a large proportion of arterial blood is shunted from the left-sided circulation to the right-sided circulation via the fistula, the increase in preload can lead to increased cardiac output. Over time, the demands of an increased workload may lead to cardiac hypertrophy and eventual heart failure. Patients may present with the usual signs of high-output heart failure including tachycardia, elevated pulse pressure, hyperkinetic precordium, and jugular venous distension. Typically, the AV fistula is quite large and is likely located in the upper arm, more proximal to the heart. Routine access flow monitoring should demonstrate blood flows (Qa) >2000 ML/min. Echocardiogram may reveal either a low or high left ventricular ejection fraction, and right-heart catheterization demonstrates an elevated cardiac output with a low to normal systemic vascular resistance. When addressing the problem of high-output heart failure, the nephrologist is faced with the dilemma of preventing progression of heart failure at the expense of loss of vascular access. Nevertheless, treatment should be directed at correcting the underlying problem by surgical banding or ligation of the fistula. PMID:21223485

  15. Heart Failure Management: The Present and the Future

    PubMed Central

    Jameel, Mohammad N.

    2009-01-01

    Abstract Clinical heart failure has been defined for a long time as a clinical syndrome with symptoms and signs including shortness of breath, cyanosis, ascites, and edema. However, in recent years, with the thought of promoting early diagnosis and heart-failure prevention, the concept of heart failure has often been defined simply as a subject with severe LV dysfunction and a dilated left ventricle, or by some, defined by evidence of increased circulating levels of molecular markers of cardiac dysfunction, such as ANP and BNP. Heart failure has been considered an irreversible clinical end point. Current medical management for heart failure only relieves symptoms, slows deterioration, and prolongs life modestly. However, in the recent years, rejuvenation of the failing myocardium began to seem possible as the accumulating preclinical studies demonstrated that rejuvenating the myocardium at the molecular and cellular level can be achieved by gene therapy or stem cell transplantation. Here, we review selected novel modalities that have been shown in preclinical studies to exert beneficial effects in animal models of severe LV dysfunction and seem to have the potential to make an impact in the clinical practice of heart-failure management. Antioxid. Redox Signal. 11, 19892010. PMID:19203220

  16. Self-care behaviour of patients with heart failure.

    PubMed

    Jaarsma, T; Abu-Saad, H H; Dracup, K; Halfens, R

    2000-01-01

    Heart failure-related self-care behaviour is important to optimize outcomes for patients with heart failure. Such behaviours include adherence to medication, diet and exercise, but self-care also refers to such things as seeking assistance when symptoms occur, and daily weighing. The study aim was to describe heart failure-related self-care behaviour, to test the effect of education and support on self-care behaviour and to discuss limitations. Data were collected from 128 heart failure patients during their hospital stay and at 1-, 3-, and 9-month follow-ups. Concepts from Orem's general theory of nursing were used to describe heart failure-related self-care behaviour and its limitations. The effects of intensive systematized and planned education from a nurse in hospital and at home were evaluated in an experimental design. Results showed that education enhanced self-care behaviour significantly at 1 and 3 months after discharge. Despite intensive education and support, patients did not manifest all self-care behaviours that might be expected. Patients in both the intervention and control groups described limitations in knowledge, judgement/decision-making and skills. It can be concluded that supportive-educative intervention is effective in enhancing heart failure-related self-care behaviour early after discharge. To optimize such intervention, more emphasis must be placed on behavioural strategies (e.g. self-medication), social support (e.g. from family members) and reinforcement (e.g. home visits). PMID:12035274

  17. Angiotensin II, sympathetic nerve activity and chronic heart failure.

    PubMed

    Wang, Yutang; Seto, Sai-Wang; Golledge, Jonathan

    2014-03-01

    Sympathetic nerve activity has been reported to be increased in both humans and animals with chronic heart failure. One of the mechanisms believed to be responsible for this phenomenon is increased systemic and cerebral angiotensin II signaling. Plasma angiotensin II is increased in humans and animals with chronic heart failure. The increase in angiotensin II signaling enhances sympathetic nerve activity through actions on both central and peripheral sites during chronic heart failure. Angiotensin II signaling is enhanced in different brain sites such as the paraventricular nucleus, the rostral ventrolateral medulla and the area postrema. Blocking angiotensin II type 1 receptors decreases sympathetic nerve activity and cardiac sympathetic afferent reflex when therapy is administered to the paraventricular nucleus. Injection of an angiotensin receptor blocker into the area postrema activates the sympathoinhibitory baroreflex. In peripheral regions, angiotensin II elevates both norepinephrine release and synthesis and inhibits norepinephrine uptake at nerve endings, which may contribute to the increase in sympathetic nerve activity seen in chronic heart failure. Increased circulating angiotensin II during chronic heart failure may enhance the sympathoexcitatory chemoreflex and inhibit the sympathoinhibitory baroreflex. In addition, increased circulating angiotensin II can directly act on the central nervous system via the subfornical organ and the area postrema to increase sympathetic outflow. Inhibition of angiotensin II formation and its type 1 receptor has been shown to have beneficial effects in chronic heart failure patients. PMID:23225134

  18. Ventricular arrhythmia in congestive heart failure.

    PubMed

    Podrid, P J; Fogel, R I; Fuchs, T T

    1992-06-01

    The importance of ventricular arrhythmia is based on its association with sudden death. In certain groups of patients, ventricular arrhythmia--primarily runs of nonsustained ventricular tachycardia (NSVT)--is associated with an increased risk for sudden death. Although this relationship has been most often reported in patients with recent myocardial infarction, it has also been recognized in patients with dilated cardiomyopathy, regardless of etiology. Therefore, ventricular arrhythmia is common in patients with CHF due to cardiomyopathy. A number of studies have reported that 70-95% of patients with cardiomyopathy and congestive heart failure (CHF) have frequent ventricular premature beats, and 40-80% will manifest runs of NSVT. Many factors are responsible for ventricular arrhythmia in such patients, including structural abnormalities, electrolyte imbalance, hemodynamic impairment, activation of neurohormonal mechanisms, and pharmacologic therapy. Many studies have reported a high yearly mortality in patients with cardiomyopathy and CHF; greater than 40% of deaths are sudden, most often the result of sustained ventricular tachyarrhythmia. Most studies have noted an association between presence (and frequency) of NSVT and risk of sudden cardiac death in these patients. Unfortunately, other techniques--such as the signal-averaged electrocardiogram and electrophysiologic testing--are not helpful in identifying the individual at risk. Although several drug interventions will reduce mortality from progressive CHF, these drugs have not been shown to reduce sudden death and, indeed, have a variable effect on ventricular arrhythmia. Although NSVT is a marker for increased risk for sudden death, it is uncertain if antiarrhythmic drugs will prevent this outcome. Antiarrhythmic drugs have not been shown to be effective for preventing sudden death, although there are as yet no well-controlled randomized trials. Several studies suggest that amiodarone and beta blockers are beneficial, but this requires confirmation. For patients who have been resuscitated following an episode of sudden death due to a sustained ventricular tachyarrhythmia, antiarrhythmic therapy guided by invasive and noninvasive techniques appears to reduce risk of recurrent arrhythmia. However, the response rate to antiarrhythmic agents is low and side effects are common in patients with CHF. Especially important is the increased risk of precipitating CHF and aggravating the arrhythmia being treated. For many such patients who have had serious ventricular tachyarrhythmia, the automatic implantable cardioverter defibrillator may prove a better option. Other drugs used for management of CHF reduce overall mortality, but not risk of sudden death. PMID:1626494

  19. Heart rate variability in left ventricular dysfunction and heart failure: effects and implications of drug treatment.

    PubMed Central

    Tuininga, Y S; van Veldhuisen, D J; Brouwer, J; Haaksma, J; Crijns, H J; Man in't Veld, A J; Lie, K I

    1994-01-01

    OBJECTIVE--To review the importance of heart rate variability analysis in left ventricular dysfunction and heart failure and to assess the effects of drug treatment. In patients with left ventricular dysfunction or heart failure, a low heart rate variability is a strong predictor of a low probability of survival. Because drug treatment in these patients has rapidly changed over the past two decades, the effect of these drugs on heart rate variability needs special attention. DESIGN--A study of published reports to give an overview of heart rate variability in patients with left ventricular dysfunction or heart failure and how it is affected by drug treatment. RESULTS--Analysis of heart rate variability provides an easily obtained early marker for progression of disease. It seems to be more closely related to the degree of neurohumoral activation than to haemodynamic variables. Cardiovascular drugs may either stimulate or inhibit the degree of neurohumoral activation, and the effects of pharmacological intervention can be closely monitored with this method. CONCLUSIONS--The analysis of heart rate variability, including spectral analysis, is a novel non-invasive way to obtain potentially useful clinical information in patients with reduced left ventricular function. The effects of drug treatment on heart rate variability are in general consistent with their long-term effects in left ventricular dysfunction and heart failure. PMID:7857731

  20. Use of pimobendan in feline congenital heart failure.

    PubMed

    Wainberg, Shannon

    2013-12-01

    A 6-month-old domestic shorthair cat was referred for evaluation of sudden lethargy and tachypnea following ovariohysterectomy. Upon failure of improvement with supportive care, a cardiologist identified congenital tricuspid dysplasia with signs of heart failure. Furosemide, enalapril, and pimobendan were used to reduce clinical signs and improve length and quality of life. PMID:24293678

  1. Gene Transfer for Congestive Heart Failure: Update 2013

    PubMed Central

    Tang, Tong; Hammond, H. Kirk

    2013-01-01

    Congestive heart failure is a major cause of morbidity and mortality with increasing social and economic costs. There have been no new high impact therapeutic agents for this devastating disease for more than a decade. However, many pivotal regulators of cardiac function have been identified using cardiac-directed transgene expression and gene deletion in preclinical studies. Some of these increase function of the failing heart. Altering the expression of these pivotal regulators using gene transfer is now either being tested in clinical gene transfer trials, or soon will be. In this review, we summarize recent progress in cardiac gene transfer for clinical congestive heart failure. PMID:23261978

  2. Cardiac Autonomic Nerve Stimulation in the Treatment of Heart Failure

    PubMed Central

    Kobayashi, Mariko; Massiello, Alex; Karimov, Jamshid H.; Van Wagoner, David R.; Fukamachi, Kiyotaka

    2014-01-01

    Research on the therapeutic modulation of cardiac autonomic tone by electrical stimulation has yielded encouraging early clinical results. Vagus nerve stimulation has reduced the rates of morbidity and sudden death from heart failure, but therapeutic vagus nerve stimulation is limited by side effects of hypotension and bradycardia. Sympathetic nerve stimulation that has been implemented in the experiment may exacerbate the sympathetic-dominated autonomic imbalance. In contrast, concurrent stimulation of both sympathetic and parasympathetic cardiac nerves increases myocardial contractility without increasing heart rate. This review assesses the current state of electrical stimulation of the cardiac autonomic nervous system to treat heart failure. PMID:23747176

  3. Dietary Salt Restriction in Heart Failure: Where Is the Evidence?

    PubMed

    DiNicolantonio, James J; Chatterjee, Subhankar; O'Keefe, James H

    2016-01-01

    Several dietary guidelines, health organizations and government policies recommend population-wide sodium restriction to prevent hypertension and related comorbidities like heart failure (HF). The current European Society of Cardiology and American College of Cardiology/American Heart Association Heart Failure guidelines recommend restricting sodium in HF patients. However, these recommendations are based on expert opinion (level C), leading to wide variability in application and lack of consensus among providers pertaining to dietary salt restriction. To evaluate the strength of current evidences to recommend dietary salt restriction among HF patients, we performed a comprehensive literature review and explored the safety and efficacy of such recommendations. PMID:26721179

  4. Clinical Issues and Controversies in Heart Failure and Transplantation.

    PubMed

    Rossano, Joseph W; Hoffman, Timothy M; Jefferies, John L; Lorts, Angela; Kirsch, Roxanne E; Thiagarajan, Ravi R

    2016-01-01

    Heart failure is a common problem among children admitted in the intensive care unit and is associated with significant morbidity and mortality. As such, the 2014 meeting of the Pediatric Cardiac Intensive Care Society included a session on Clinical Controversies in Heart Failure and Transplantation. This review contains the summaries of the podium presentations of this session and will cover some of the challenging aspects of caring for these patients including medical and mechanical support, fluid overload states, high-risk populations including those after heart transplantation, and end-of-life considerations. PMID:26714996

  5. Hemodynamic support with percutaneous devices in patients with heart failure.

    PubMed

    Kapur, Navin K; Esposito, Michele

    2015-04-01

    The use of surgically implanted durable mechanical circulatory support (MCS) in high-risk patients with heart failure is declining and short-term, nondurable MCS device use is growing. Percutaneously delivered MCS options for advanced heart failure include the intra-aortic balloon pump, Impella axial flow catheter, TandemHeart centrifugal pump, and venoarterial extracorporeal membrane oxygenation. Nondurable MCS devices have unique implantation characteristics and hemodynamic effects. Algorithms and guidelines for optimal nondurable MCS device selection do not exist. Emerging technologies and applications will address the need for improved left ventricular unloading using lower-profile devices, longer-term ambulatory support, and the potential for myocardial recovery. PMID:25834971

  6. The multi-biomarker approach for heart failure in patients with hypertension.

    PubMed

    Bielecka-Dabrowa, Agata; Gluba-Brzzka, Anna; Michalska-Kasiczak, Marta; Misztal, Ma?gorzata; Rysz, Jacek; Banach, Maciej

    2015-01-01

    We assessed the predictive ability of selected biomarkers using N-terminal pro-brain natriuretic peptide (NT-proBNP) as the benchmark and tried to establish a multi-biomarker approach to heart failure (HF) in hypertensive patients. In 120 hypertensive patients with or without overt heart failure, the incremental predictive value of the following biomarkers was investigated: Collagen III N-terminal propeptide (PIIINP), cystatin C (CysC), lipocalin-2/NGAL, syndecan-4, tumor necrosis factor-? (TNF-?), interleukin 1 receptor type I (IL1R1), galectin-3, cardiotrophin-1 (CT-1), transforming growth factor ? (TGF-?) and N-terminal pro-brain natriuretic peptide (NT-proBNP). The highest discriminative value for HF was observed for NT-proBNP (area under the receiver operating characteristic curve (AUC)=0.873) and TGF-? (AUC=0.878). On the basis of ROC curve analysis we found that CT-1>152 pg/mL, TGF-?<7.7 ng/mL, syndecan>2.3 ng/mL, NT-proBNP>332.5 pg/mL, CysC>1 mg/L and NGAL>39.9 ng/mL were significant predictors of overt HF. There was only a small improvement in predictive ability of the multi-biomarker panel including the four biomarkers with the best performance in the detection of HF-NT-proBNP, TGF-?, CT-1, CysC-compared to the panel with NT-proBNP, TGF-? and CT-1 only. Biomarkers with different pathophysiological backgrounds (NT-proBNP, TGF-?, CT-1, CysC) give additive prognostic value for incident HF in hypertensive patients compared to NT-proBNP alone. PMID:25984599

  7. Diastolic and systolic heart failure: different stages or distinct phenotypes of the heart failure syndrome?

    PubMed

    Bronzwaer, Jean G F; Paulus, Walter J

    2009-12-01

    It remains uncertain if diastolic heart failure (DHF) is a distinct HF phenotype or a precursor stage of systolic HF (SHF). The unimodal distribution of left ventricular ejection fraction (LVEF) in HF, depressed LV long-axis shortening in DHF, and progression to eccentric LV remodeling in hypertension favor DHF and SHF as successive stages. These arguments are countered by the bimodal distribution of LVEF after correction for gender, by the preserved LV twist in DHF and by the low incidence of eccentric LV remodeling in hypertension. Clinical features, LV anatomy and histology, cardiomyocyte stiffness, myocardial effects of diabetes, and the response to HF therapy support DHF and SHF as distinct phenotypes. Comparison of the myocardial signal transduction cascades that drive LV remodeling in DHF and SHF may solve the controversy. This review analyzes arguments supporting DHF and SHF as successive stages or distinct phenotypes of the HF syndrome. PMID:19948097

  8. Pacemaker-induced transient asynchrony suppresses heart failure progression.

    PubMed

    Kirk, Jonathan A; Chakir, Khalid; Lee, Kyoung Hwan; Karst, Edward; Holewinski, Ronald J; Pironti, Gianluigi; Tunin, Richard S; Pozios, Iraklis; Abraham, Theodore P; de Tombe, Pieter; Rockman, Howard A; Van Eyk, Jennifer E; Craig, Roger; Farazi, Taraneh G; Kass, David A

    2015-12-23

    Uncoordinated contraction from electromechanical delay worsens heart failure pathophysiology and prognosis, but restoring coordination with biventricular pacing, known as cardiac resynchronization therapy (CRT), improves both. However, not every patient qualifies for CRT. We show that heart failure with synchronous contraction is improved by inducing dyssynchrony for 6 hours daily by right ventricular pacing using an intracardiac pacing device, in a process we call pacemaker-induced transient asynchrony (PITA). In dogs with heart failure induced by 6 weeks of atrial tachypacing, PITA (starting on week 3) suppressed progressive cardiac dilation as well as chamber and myocyte dysfunction. PITA enhanced β-adrenergic responsiveness in vivo and normalized it in myocytes. Myofilament calcium response declined in dogs with synchronous heart failure, which was accompanied by sarcomere disarray and generation of myofibers with severely reduced function, and these changes were absent in PITA-treated hearts. The benefits of PITA were not replicated when the same number of right ventricular paced beats was randomly distributed throughout the day, indicating that continuity of dyssynchrony exposure is necessary to trigger the beneficial biological response upon resynchronization. These results suggest that PITA could bring the benefits of CRT to the many heart failure patients with synchronous contraction who are not CRT candidates. PMID:26702095

  9. A reappraisal of loop diuretic choice in heart failure patients.

    PubMed

    Buggey, Jonathan; Mentz, Robert J; Pitt, Bertram; Eisenstein, Eric L; Anstrom, Kevin J; Velazquez, Eric J; O'Connor, Christopher M

    2015-03-01

    The health and economic burden of heart failure is significant and continues to grow each year. Loop diuretics are an integral part of symptom management in heart failure. Furosemide is used disproportionately compared with other loop diuretics, and there is currently no guidance for physicians regarding which agent to choose. However, there exist pharmacologic differences as well as other mechanistic differences that appear to favor torsemide use over furosemide. Compared with furosemide, torsemide improves surrogate markers of heart failure severity such as left ventricular function, plasma brain natriuretic peptide levels, and New York Heart Association functional class and may also reduce hospitalizations, readmissions, and mortality. Data suggest that these benefits could be mediated through torsemide's ability to positively affect the renin-angiotensin-aldosterone system. Specifically, torsemide has been shown to inhibit aldosterone secretion, synthesis, and receptor binding in vitro, as well as decrease transcardiac extraction of aldosterone, myocardial collagen production, and cardiac fibrosis in patients with heart failure. We identified pertinent literature using keyword MEDLINE searches and cross-referencing prior bibliographies. We summarize the available data suggesting potential benefits with torsemide over furosemide, and call attention to the need for a reappraisal of diuretic use in heart failure patients and also for a well-powered, randomized control trial assessing torsemide versus furosemide use. PMID:25728721

  10. A reappraisal of loop diuretic choice in heart failure patients

    PubMed Central

    Buggey, Jonathan; Mentz, Robert J.; Pitt, Bertram; Eisenstein, Eric L.; Anstrom, Kevin J.; Velazquez, Eric J.; O’Connor, Christopher M.

    2015-01-01

    The health and economic burden of heart failure is significant, and continues to grow each year. Loop diuretics are an integral part of symptom management in heart failure. Furosemide is used disproportionately compared to other loop diuretics and there is currently no guidance for physicians regarding which agent to choose. However, there exist pharmacologic differences as well as other mechanistic differences that appear to favor torsemide use over furosemide. Compared to furosemide, torsemide improves surrogate markers of heart failure severity such as left ventricular function, plasma brain natriuretic peptide levels, and New York Heart Association functional class and may also reduce hospitalizations, readmissions, and mortality. Data suggest these benefits could be mediated through torsemide’s ability to positively affect the renin-angiotensin-aldosterone system. Specifically, torsemide has been shown to inhibit aldosterone secretion, synthesis, and receptor binding in vitro, as well as decrease transcardiac extraction of aldosterone, myocardial collagen production and cardiac fibrosis in patients with heart failure. We identified pertinent literature using keyword MEDLINE searches and cross-referencing prior bibliographies. We summarize the available data suggesting potential benefits with torsemide over furosemide, and call attention to the need for a reappraisal of diuretic use in heart failure patients and also for a well powered, randomized control trial assessing torsemide versus furosemide use. PMID:25728721

  11. [Converting enzyme inhibitors in acute myocardial infarct and heart failure].

    PubMed

    Arslanagi?, A; Raljevi?, E

    1999-01-01

    Inhibitors of angiotensin converting enzyme (ACE inhibitors) have been introduced more than fifteen years ago into the treatment of hypertension, congestive heart failure, myocardial infarction and diabetic nephropathy. The therapeutic success is related to their action in reduction of plasma and tissue angiotensin II concentrations and potentiation of endogenous kinins. They are able to improve myocardium metabolic status, prevent cardiac hypertrophy, limit myocardial infarct size, and thus prevent heart failure. Since 1987 ACE inhibitors are introduced in the clinical practice in our clinic. We introduced the therapy with lisinopril (Lopril), in 70% of patients among 2855 patients that were admitted in Coronary Care Unit in 1997 and 1998. Lisinopril was introduced as soon as the patient was admitted, together with fibrinolitic, Heparin and Aspirin therapy. Since that time we noticed decrease in postinfarction heart failure in comparison to previous years. We recommend permanent therapy with a small doses of ACE inhibitors in patients with heart infarction. PMID:10356928

  12. New Insights in the Diagnosis and Treatment of Heart Failure

    PubMed Central

    Agnetti, Giulio; Piepoli, Massimo F.; Siniscalchi, Giuseppe; Nicolini, Francesco

    2015-01-01

    Cardiovascular disease is the leading cause of mortality in the US and in westernized countries with ischemic heart disease accounting for the majority of these deaths. Paradoxically, the improvements in the medical and surgical treatments of acute coronary syndrome are leading to an increasing number of “survivors” who are then developing heart failure. Despite considerable advances in its management, the gold standard for the treatment of end-stage heart failure patients remains heart transplantation. Nevertheless, this procedure can be offered only to a small percentage of patients who could benefit from a new heart due to the limited availability of donor organs. The aim of this review is to evaluate the safety and efficacy of innovative approaches in the diagnosis and treatment of patients refractory to standard medical therapy and excluded from cardiac transplantation lists. PMID:26634204

  13. Healing the orphaned heart: heart failure in a patient with glucose-6-phosphate dehydrogenase deficiency.

    PubMed

    Balderia, Percy Guanzon; Wongrakpanich, Supakanya; Patel, Monil; Stanek, Marjorie

    2015-01-01

    Patients with glucose-6-phosphate dehydrogenase (G6PD) deficiency are not represented in clinical trials for heart failure. Moreover, many of the recommended medications can cause haemolysis in this group of patients. We present the case of a 71-year-old woman with G6PD deficiency admitted for acute non-ischemic heart failure with reduced ejection fraction. Our experience showed that a combination of ethacrynic acid and spironolactone is safe and effective for relief of volume overload in this group of patients. Studies are needed to determine whether the morbidity and mortality benefits of established heart failure regimens extend to patients with G6PD deficiency. PMID:25743872

  14. Iron deficiency: an emerging therapeutic target in heart failure.

    PubMed

    Cohen-Solal, Alain; Leclercq, Christophe; Deray, Gilbert; Lasocki, Sigismond; Zambrowski, Jean-Jacques; Mebazaa, Alexandre; de Groote, Pascal; Damy, Thibaud; Galinier, Michel

    2014-09-15

    In patients with heart failure, iron deficiency is frequent but overlooked, with a prevalence of 30%-50%. Since it contributes to cardiac and peripheral muscle dysfunction, iron deficiency is associated with poorer clinical outcomes and a greater risk of death, independent of haemoglobin level. Therefore, iron deficiency emerges as a new comorbidity and a therapeutic target of chronic heart failure in addition to chronic renal insufficiency, anaemia and diabetes. In a series of placebo-controlled, randomised studies in patients with heart failure and iron deficiency, intravenous iron had a favourable effect on exercise capacity, functional class, LVEF, renal function and quality of life. These clinical studies were performed in the context of a renewed interest in iron metabolism. During the past 10 years, knowledge about the transport, storage and homeostasis of iron has improved dramatically, and new molecules involved in iron metabolism have been described (eg, hepcidin, ferroportin, divalent metal transporter 1). Recent European guidelines recommend the monitoring of iron parameters (ie, serum ferritin, transferrin saturation) for all patients with heart failure. Ongoing clinical trials will explore the benefits of iron deficiency correction on various heart failure parameters. PMID:24957529

  15. Beta-adrenergic blocker mortality trials in congestive heart failure.

    PubMed

    Teerlink, J R; Massie, B M

    1999-11-01

    Many of the current discussions of beta-adrenergic blocker therapy in patients with congestive heart failure have used fairy tales to describe the evolution of this treatment from contraindication to standard of care. This article reviews the early studies that initiated this revolution in heart failure therapy and discusses the major mortality trials that have demonstrated that these agents improve survival and limit the progression of congestive heart failure. These major trials have used 1 of 4 beta blockers (metoprolol, bisoprolol, carvedilol, or bucindolol) in varying study designs with different patient populations. Each trial had different objectives and limitations, and these are described in the context of their impact on proving a survival benefit. In addition, the specific effect of beta-blocker therapy on sudden death in patients with heart failure is briefly discussed. The weight of these trials suggests that beta-adrenergic blocker therapy can save 1 life of every 35 patients treated in patients with mild-to-moderate heart failure. The data are compelling and the techniques for "starting low and going slow" with titrations have been well documented. PMID:10568667

  16. Needs of caregivers in heart failure management: A qualitative study

    PubMed Central

    Frost, Julia; Britten, Nicky; Jolly, Kate; Greaves, Colin; Abraham, Charles; Dalal, Hayes

    2015-01-01

    Objectives To identify the needs of caregivers supporting a person with heart failure and to inform the development of a caregiver resource to be used as part of a home-based self-management programme. Methods A qualitative study informed by thematic analysis involving 26 caregivers in individual interviews or a focus group. Results Three distinct aspects of caregiver support in heart failure management were identified. Firstly, caregivers identified needs about supporting management of heart failure including: coping with the variability of heart failure symptoms, what to do in an emergency, understanding and managing medicines, providing emotional support, promoting exercise and physical activity, providing personal care, living with a cardiac device and supporting depression management. Secondly, as they make the transition to becoming a caregiver, they need to develop skills to undertake difficult discussions about the role; communicate with health professionals; manage their own mental health, well-being and sleep; and manage home and work. Thirdly, caregivers require skills to engage social support, and voluntary and formal services while recognising that the long-term future is uncertain. Discussion The identification of the needs of caregiver has been used to inform the development of a home-based heart failure intervention facilitated by a trained health care practitioner. PMID:25795144

  17. Use of Inotropic Agents in Treatment of Systolic Heart Failure.

    PubMed

    Tariq, Sohaib; Aronow, Wilbert S

    2015-01-01

    The most common use of inotropes is among hospitalized patients with acute decompensated heart failure, with reduced left ventricular ejection fraction and with signs of end-organ dysfunction in the setting of a low cardiac output. Inotropes can be used in patients with severe systolic heart failure awaiting heart transplant to maintain hemodynamic stability or as a bridge to decision. In cases where patients are unable to be weaned off inotropes, these agents can be used until a definite or escalated supportive therapy is planned, which can include coronary revascularization or mechanical circulatory support (intra-aortic balloon pump, extracorporeal membrane oxygenation, impella, left ventricular assist device, etc.). Use of inotropic drugs is associated with risks and adverse events. This review will discuss the use of the inotropes digoxin, dopamine, dobutamine, norepinephrine, milrinone, levosimendan, and omecamtiv mecarbil. Long-term inotropic therapy should be offered in selected patients. A detailed conversation with the patient and family shall be held, including a discussion on the risks and benefits of use of inotropes. Chronic heart failure patients awaiting heart transplants are candidates for intravenous inotropic support until the donor heart becomes available. This helps to maintain hemodynamic stability and keep the fluid status and pulmonary pressures optimized prior to the surgery. On the other hand, in patients with severe heart failure who are not candidates for advanced heart failure therapies, such as transplant and mechanical circulatory support, inotropic agents can be used for palliative therapy. Inotropes can help reduce frequency of hospitalizations and improve symptoms in these patients. PMID:26690127

  18. Use of Inotropic Agents in Treatment of Systolic Heart Failure

    PubMed Central

    Tariq, Sohaib; Aronow, Wilbert S.

    2015-01-01

    The most common use of inotropes is among hospitalized patients with acute decompensated heart failure, with reduced left ventricular ejection fraction and with signs of end-organ dysfunction in the setting of a low cardiac output. Inotropes can be used in patients with severe systolic heart failure awaiting heart transplant to maintain hemodynamic stability or as a bridge to decision. In cases where patients are unable to be weaned off inotropes, these agents can be used until a definite or escalated supportive therapy is planned, which can include coronary revascularization or mechanical circulatory support (intra-aortic balloon pump, extracorporeal membrane oxygenation, impella, left ventricular assist device, etc.). Use of inotropic drugs is associated with risks and adverse events. This review will discuss the use of the inotropes digoxin, dopamine, dobutamine, norepinephrine, milrinone, levosimendan, and omecamtiv mecarbil. Long-term inotropic therapy should be offered in selected patients. A detailed conversation with the patient and family shall be held, including a discussion on the risks and benefits of use of inotropes. Chronic heart failure patients awaiting heart transplants are candidates for intravenous inotropic support until the donor heart becomes available. This helps to maintain hemodynamic stability and keep the fluid status and pulmonary pressures optimized prior to the surgery. On the other hand, in patients with severe heart failure who are not candidates for advanced heart failure therapies, such as transplant and mechanical circulatory support, inotropic agents can be used for palliative therapy. Inotropes can help reduce frequency of hospitalizations and improve symptoms in these patients. PMID:26690127

  19. Ivabradine, coronary artery disease, and heart failure: beyond rhythm control

    PubMed Central

    Scicchitano, Pietro; Cortese, Francesca; Ricci, Gabriella; Carbonara, Santa; Moncelli, Michele; Iacoviello, Massimo; Cecere, Annagrazia; Gesualdo, Michele; Zito, Annapaola; Caldarola, Pasquale; Scrutinio, Domenico; Lagioia, Rocco; Riccioni, Graziano; Ciccone, Marco Matteo

    2014-01-01

    Elevated heart rate could negatively influence cardiovascular risk in the general population. It can induce and promote the atherosclerotic process by means of several mechanisms involving endothelial shear stress and biochemical activities. Furthermore, elevated heart rate can directly increase heart ischemic conditions because of its skill in unbalancing demand/supply of oxygen and decreasing the diastolic period. Thus, many pharmacological treatments have been proposed in order to reduce heart rate and ameliorate the cardiovascular risk profile of individuals, especially those suffering from coronary artery diseases (CAD) and chronic heart failure (CHF). Ivabradine is the first pure heart rate reductive drug approved and currently used in humans, created in order to selectively reduce sinus node function and to overcome the many side effects of similar pharmacological tools (ie, ?-blockers or calcium channel antagonists). The aim of our review is to evaluate the role and the safety of this molecule on CAD and CHF therapeutic strategies. PMID:24940047

  20. Effect of Yoga Therapy on Heart Rate, Blood Pressure and Cardiac Autonomic Function in Heart Failure

    PubMed Central

    Krishna, Bandi Hari; Pal, Pravati; G.K., Pal; J., Balachander; E., Jayasettiaseelon; Y, Sreekanth; M.G., Sridhar; G.S., Gaur

    2014-01-01

    Background and Objective: It is well known that a hall mark of heart failure is adverse changes in autonomic function. Elevated blood pressure is a powerful predictor of congestive heart failure and other Cardiovascular Disease (CVD) outcomes. In this study, we planned to examine the effects of a 12 week yoga therapy on blood pressure, heart rate, heart rate variability, and rate pressure product (RPP). Methods: Out of 130 heart failure patients recruited for the study, 65 patients were randomly selected to receive 12 week yoga therapy along with standard medical therapy (yoga group). Other patients (n=65) received only standard medical therapy (control group). Heart rate, blood pressure, cardiac autonomic function (by short-term heart-rate variability analysis) and myocardial oxygen consumption (by RPP) were assessed before and after 12 weeks. In the yoga group, 44 patients and in the control group, 48 patients completed the study. Results: There was a significant decrease in heart rate, blood pressure and RPP in yoga group compared to control group. Also, LFnu and LF-HF ratio decreased significantly and HFnu increased significantly in yoga group compared to control group. Conclusion: Twelve-week yoga therapy significantly improved the parasympathetic activity and decreased the sympathetic activity in heart failure patients (NYHA I&II) PMID:24596712

  1. Digoxin remains useful in the management of chronic heart failure.

    PubMed

    Dec, G William

    2003-03-01

    Despite the introduction of a variety of new classes of drugs for the management of heart failure, digoxin continues to have an important role in long-term outpatient management. A wide variety of placebo-controlled clinical trials have unequivocally shown that treatment with digoxin can improve symptoms, quality of life, and exercise tolerance in patients with mild, moderate, or severe heart failure. These benefits are evident regardless of the underlying rhythm (normal sinus rhythm or atrial fibrillation), etiology of the heart failure, or concomitant therapy (eg. ACE inhibitors). Unlike other agents with positive inotropic properties, digoxin does not increase all-cause mortality and has a substantial benefit in reducing heart failure hospitalizations. Consensus guidelines have recently been published by the Heart Failure Society of America and the American College of Cardiology/American Heart Association, and they contain the following recommendations for digoxin treatment: 1. Digoxin should be considered for the outpatient treatment of all patients who have persistent symptoms of heart failure (NYHA class II-IV) despite conventional pharmacologic therapy with diuretics, ACE inhibitors, and a beta-blocker when the heart failure is caused by systolic dysfunction (the strength of evidence = A for NYHA class II and III; strength of evidence = C for NYHA class IV). 2. Digoxin is not indicated as primary treatment for the stabilization of patients with acutely decompensated heart failure. (Strength of evidence = B). Digoxin may be initiated after emergent treatment of heart failure has been completed in an effort to establish a long-term treatment strategy. 3. Digoxin should not be administered to patients who have significant sinus or atrioventricular block, unless the block has been treated with a permanent pacemaker (strength of evidence = B). The drug should be used cautiously in patients who receive other agents known to depress sinus or atrioventricular nodal function (such as amiodarone or a beta-blocker) (strength of evidence = B). 4. The dosage of digoxin should be 0.125-0.25 mg daily in the majority of patients (strength of evidence = C). The lower dose should be used in patients over 70 years of age, those with impaired renal function, or those with a low lean body mass. Higher doses (eg, digoxin 0.375-0.50 mg daily) are rarely needed. Loading doses of digoxin are not necessary during initiation of therapy for patients with chronic heart failure. 5. Serial assessment of serum digoxin levels is unnecessary in most patients. The radioimmunoassay was developed to assist in the evaluation of toxicity, not the efficacy of the drug. There appears to be little relationship between serum digoxin concentration and the drug's therapeutic effects. 6. Digoxin toxicity is commonly associated with serum levels >2 ng/mL but may occur with lower digoxin levels if hypokalemia, hypomagnesemia, or hypothyroidism coexist. Likewise, the concomitant use of agents such as quinidine, verapamil, spironolactone, flecainide, and amiodarone can increase serum digoxin levels and increase the likelihood of digoxin toxicity. 7. For patients with heart failure and atrial fibrillation with a rapid ventricular response, the administration of high doses of digoxin (>0.25 mg daily) for the purpose of rate control is not recommended. When necessary, additional rate control should be achieved by the addition of beta-blocker therapy or amiodarone (strength of evidence = C). If amiodarone is added, the dose of digoxin should be reduced. Digitalis preparations are now entering their fourth century of clinical use for the treatment of chronic heart failure symptoms. Its clinical efficacy can no longer be doubted and its safety has been verified by the multicenter DIG trial. Future advances in pharmacogenetics should facilitate identification of those patients most likely to benefit from its pharmacologic effects. PMID:12693728

  2. Vasodilator treatment for acute and chronic heart failure.

    PubMed Central

    Chatterjee, K; Parmley, W W

    1977-01-01

    The current status of the use of vasodilator drugs in the treatment of acute and chronic heart failure has been reviewed. It is apparent that vasodilator treatment can be used effectively in some patients with heart failure with a beneficial haemodynamics response, and that vasodilator agents are likely to find an important place in the management of such patients. Vasodilator treatment may be associated with complications and must be used with care. Though several nonparenteral vasodilator agents have been investigated, no ideal drug is yet available for the treatment of chronic heart failure. Nevertheless, it is probable that suitable drugs will emerge and find an important place in the management of such patients. Images PMID:884021

  3. Patient Characteristics Predicting Readmission Among Individuals Hospitalized for Heart Failure.

    PubMed

    O'Connor, Melissa; Murtaugh, Christopher M; Shah, Shivani; Barrn-Vaya, Yolanda; Bowles, Kathryn H; Peng, Timothy R; Zhu, Carolyn W; Feldman, Penny H

    2016-02-01

    Heart failure is difficult to manage and increasingly common with many individuals experiencing frequent hospitalizations. Little is known about patient factors consistently associated with hospital readmission. A literature review was conducted to identify heart failure patient characteristics, measured before discharge, that contribute to variation in hospital readmission rates. Database searches yielded 950 potential articles, of which 34 studies met inclusion criteria. Patient characteristics generally have a very modest effect on all-cause or heart failure-related readmission within 7 to 180 days of index hospital discharge. A range of cardiac diseases and other comorbidities only minimally increase readmission rates. No single patient characteristic stands out as a key contributor across multiple studies underscoring the challenge of developing successful interventions to reduce readmissions. Interventions may need to be general in design with the specific intervention depending on each patient's unique clinical profile. PMID:26180045

  4. Beta-adrenergic blockers for chronic heart failure.

    PubMed

    Javed, Usman; Deedwania, Prakash C

    2009-01-01

    Systolic dysfunction and heart failure are major public health problems associated with a significant risk of morbidity and mortality. During the past 2 decades, considerable progress has been made in defining the underlying pathophysiology and the appropriate therapies in heart failure. In patients with chronic heart failure (CHF), sustained sympathetic overactivation leads to down-regulation of beta receptors and uncoupling of the receptors from adenylate cyclase. The clear understanding of the pivotal role of sympathetic overactivation in CHF has led to the evaluation of beta- blocker therapy in CHF. A number of large randomized clinical trials have been conducted with a variety of beta-blockers, and although most of them have shown benefit, there have been differing findings with different molecules. beta-blockers are now considered part of the standard therapy for all patients with symptomatic CHF. Despite the strong evidence supporting their use, beta-blockers continue to be underutilized in CHF. PMID:19829179

  5. Subclinical Myocardial Disease in Heart Failure Detected by CMR

    PubMed Central

    Ohyama, Yoshiaki; Volpe, Gustavo J.

    2014-01-01

    Noninvasive cardiac imaging plays a central role in the assessment of patients with heart failure at all stages of disease. Moreover, this role can be even more important for individuals with asymptomatic cardiac functional or structural abnormalities—subclinical myocardial disease — because they could have benefits from early interventions before the onset of clinical heart failure. In this sense, cardiac magnetic resonance offers not only precise global cardiac function and cardiac structure, but also more detailed regional function and tissue characterization by recent developing methods. In this section, some of the main methods available for subclinical myocardial disease detection are reviewed in terms of what they can provide and how they can improve heart failure assessment. PMID:25132911

  6. SUBSTANCE P IN HEART FAILURE: THE GOOD AND THE BAD

    PubMed Central

    Dehlin, Heather M.; Levick, Scott P.

    2015-01-01

    The tachykinin, substance P, is found primarily in sensory nerves. In the heart, substance P-containing nerve fibers are often found surrounding coronary vessels, making them ideally situated to sense changes in the myocardial environment. Recent studies in rodents have identified substance P as having dual roles in the heart, depending on disease etiology and/or timing. Thus far, these studies indicate that substance P may be protective acutely following ischemia-reperfusion, but damaging long-term in non-ischemic induced remodeling and heart failure. Sensory nerves may be at the apex of the cascade of events leading to heart failure, therefore, they make a promising potential therapeutic target that warrants increased investigation. PMID:24286592

  7. Chronic heart failure: Ca(2+), catabolism, and catastrophic cell death.

    PubMed

    Cho, Geoffrey W; Altamirano, Francisco; Hill, Joseph A

    2016-04-01

    Robust successes have been achieved in recent years in conquering the acutely lethal manifestations of heart disease. Many patients who previously would have died now survive to enjoy happy and productive lives. Nevertheless, the devastating impact of heart disease continues unabated, as the spectrum of disease has evolved with new manifestations. In light of this ever-evolving challenge, insights that culminate in novel therapeutic targets are urgently needed. Here, we review fundamental mechanisms of heart failure, both with reduced (HFrEF) and preserved (HFpEF) ejection fraction. We discuss pathways that regulate cardiomyocyte remodeling and turnover, focusing on Ca(2+) signaling, autophagy, and apoptosis. In particular, we highlight recent insights pointing to novel connections among these events. We also explore mechanisms whereby potential therapeutic approaches targeting these processes may improve morbidity and mortality in the devastating syndrome of heart failure. PMID:26775029

  8. Nitric Oxide Synthases in Heart Failure

    PubMed Central

    Carnicer, Ricardo; Crabtree, Mark J.; Sivakumaran, Vidhya

    2013-01-01

    Abstract Significance: The regulation of myocardial function by constitutive nitric oxide synthases (NOS) is important for the maintenance of myocardial Ca2+ homeostasis, relaxation and distensibility, and protection from arrhythmia and abnormal stress stimuli. However, sustained insults such as diabetes, hypertension, hemodynamic overload, and atrial fibrillation lead to dysfunctional NOS activity with superoxide produced instead of NO and worse pathophysiology. Recent Advances: Major strides in understanding the role of normal and abnormal constitutive NOS in the heart have revealed molecular targets by which NO modulates myocyte function and morphology, the role and nature of post-translational modifications of NOS, and factors controlling nitroso-redox balance. Localized and differential signaling from NOS1 (neuronal) versus NOS3 (endothelial) isoforms are being identified, as are methods to restore NOS function in heart disease. Critical Issues: Abnormal NOS signaling plays a key role in many cardiac disorders, while targeted modulation may potentially reverse this pathogenic source of oxidative stress. Future Directions: Improvements in the clinical translation of potent modulators of NOS function/dysfunction may ultimately provide a powerful new treatment for many hearts diseases that are fueled by nitroso-redox imbalance. Antioxid. Redox Signal. 18, 10781099. PMID:22871241

  9. Genetic deletion of myostatin from the heart prevents skeletal muscle atrophy in heart failure

    PubMed Central

    Heineke, Joerg; Auger-Messier, Mannix; Xu, Jian; Sargent, Michelle; York, Allen; Welle, Stephen; Molkentin, Jeffery D.

    2010-01-01

    Background Cardiac cachexia is characterized by an exaggerated loss of skeletal muscle, weakness, and exercise intolerance, although the etiology of these effects remains unknown. Here we hypothesized that the heart functions as an endocrine organ in promoting systemic cachexia by secreting peptide factors such as myostatin. Myostatin is a cytokine of the transforming growth factor ?(TGF?) superfamily that is known to control muscle wasting. Methods and Results We used a Cre/loxP system to ablate myostatin (Mstn gene) expression in a celltype-specific manner. As expected, elimination of Mstn selectively in skeletal muscle with a myosin light chain 1f (MLC1f)-cre allele induced robust hypertrophy in all skeletal muscle. However, heart-specific deletion of Mstn with a Nkx2.5-cre allele did not alter baseline heart size or secondarily affect skeletal muscle size, but the characteristic wasting and atrophy of skeletal muscle that typifies heart failure was not observed in these heart-specific null mice, indicating that myocardial myostatin expression controls muscle atrophy in heart failure. Indeed, myostatin levels in the plasma were significantly increased in wildtype mice subjected to pressure overload-induced cardiac hypertrophy, but not in Mstn heart-specific deleted mice. Moreover, cardiac-specific overexpression of myostatin, which increased circulating levels of myostatin by 34-fold, caused a reduction in weight of the quadriceps, gastrocnemius, soleus, and even the heart itself. Lastly, to investigate myostatin as a potential therapeutic target for the treatment of muscle wasting in heart failure, we infused a myostatin blocking antibody (JA-16), which promoted greater maintenance of muscle mass in heart failure. Conclusions Myostatin released from cardiomyocytes induces skeletal muscle wasting in heart failure. Targeted inhibition of myostatin in cardiac cachexia might be a therapeutic option in the future. PMID:20065166

  10. A New Approach to Detect Congestive Heart Failure Using Short-Term Heart Rate Variability Measures

    PubMed Central

    Wang, Qian; Zhou, GuangMin; Wang, Ying; Jiang, Qing

    2014-01-01

    Heart rate variability (HRV) analysis has quantified the functioning of the autonomic regulation of the heart and heart's ability to respond. However, majority of studies on HRV report several differences between patients with congestive heart failure (CHF) and healthy subjects, such as time-domain, frequency domain and nonlinear HRV measures. In the paper, we mainly presented a new approach to detect congestive heart failure (CHF) based on combination support vector machine (SVM) and three nonstandard heart rate variability (HRV) measures (e.g. SUM_TD, SUM_FD and SUM_IE). The CHF classification model was presented by using SVM classifier with the combination SUM_TD and SUM_FD. In the analysis performed, we found that the CHF classification algorithm could obtain the best performance with the CHF classification accuracy, sensitivity and specificity of 100%, 100%, 100%, respectively. PMID:24747432

  11. Electrical modalities beyond pacing for the treatment of heart failure.

    PubMed

    Cornelussen, Richard N; Splett, Vincent; Klepfer, Ruth Nicholson; Stegemann, Berthold; Kornet, Lilian; Prinzen, Frits W

    2011-05-01

    In this review, we report on electrical modalities, which do not fit the definition of pacemaker, but increase cardiac performance either by direct application to the heart (e.g., post-extrasystolic potentiation or non-excitatory stimulation) or indirectly through activation of the nervous system (e.g., vagal or sympathetic activation). The physiological background of the possible mechanisms of these electrical modalities and their potential application to treat heart failure are discussed. PMID:21104313

  12. Gene transfer for ischemic heart failure in a preclinical model.

    PubMed

    Ishikawa, Kiyotake; Ladage, Dennis; Tilemann, Lisa; Fish, Kenneth; Kawase, Yoshiaki; Hajjar, Roger J

    2011-01-01

    Various emerging technologies are being developed for patients with heart failure. Well-established preclinical evaluations are necessary to determine their efficacy and safety. Gene therapy using viral vectors is one of the most promising approaches for treating cardiac diseases. Viral delivery of various different genes by changing the carrier gene has immeasurable therapeutic potential. In this video, the full process of an animal model of heart failure creation followed by gene transfer is presented using a swine model. First, myocardial infarction is created by occluding the proximal left anterior descending coronary artery. Heart remodeling results in chronic heart failure. Unique to our model is a fairly large scar which truly reflects patients with severe heart failure who require aggressive therapy for positive outcomes. After myocardial infarct creation and development of scar tissue, an intracoronary injection of virus is demonstrated with simultaneous nitroglycerine infusion. Our injection method provides simple and efficient gene transfer with enhanced gene expression. This combination of a myocardial infarct swine model with intracoronary virus delivery has proven to be a consistent and reproducible methodology, which helps not only to test the effect of individual gene, but also compare the efficacy of many genes as therapeutic candidates. PMID:21633324

  13. Gene Transfer for Ischemic Heart Failure in a Preclinical Model

    PubMed Central

    Ishikawa, Kiyotake; Ladage, Dennis; Tilemann, Lisa; Fish, Kenneth; Kawase, Yoshiaki; Hajjar, Roger J.

    2011-01-01

    Various emerging technologies are being developed for patients with heart failure. Well-established preclinical evaluations are necessary to determine their efficacy and safety. Gene therapy using viral vectors is one of the most promising approaches for treating cardiac diseases. Viral delivery of various different genes by changing the carrier gene has immeasurable therapeutic potential. In this video, the full process of an animal model of heart failure creation followed by gene transfer is presented using a swine model. First, myocardial infarction is created by occluding the proximal left anterior descending coronary artery. Heart remodeling results in chronic heart failure. Unique to our model is a fairly large scar which truly reflects patients with severe heart failure who require aggressive therapy for positive outcomes. After myocardial infarct creation and development of scar tissue, an intracoronary injection of virus is demonstrated with simultaneous nitroglycerine infusion. Our injection method provides simple and efficient gene transfer with enhanced gene expression. This combination of a myocardial infarct swine model with intracoronary virus delivery has proven to be a consistent and reproducible methodology, which helps not only to test the effect of individual gene, but also compare the efficacy of many genes as therapeutic candidates. PMID:21633324

  14. The cardiac enigma: current conundrums in heart failure research

    PubMed Central

    Kapiloff, Michael S.; Emter, Craig A.

    2016-01-01

    The prevalence of heart failure is expected to increase almost 50% in the next 15 years because of aging of the general population, an increased frequency of comorbidities, and an improved survival following cardiac events. Conventional treatments for heart failure have remained largely static over the past 20 years, illustrating the pressing need for the discovery of novel therapeutic agents for this patient population. Given the heterogeneous nature of heart failure, it is important to specifically define the cellular mechanisms in the heart that drive the patient’s symptoms, particularly when considering new treatment strategies. This report highlights the latest research efforts, as well as the possible pitfalls, in cardiac disease translational research and discusses future questions and considerations needed to advance the development of new heart failure therapies. In particular, we discuss cardiac remodeling and the translation of animal work to humans and how advancements in our understanding of these concepts relative to disease are central to new discoveries that can improve cardiovascular health. PMID:26918161

  15. Effects of myosin heavy chain manipulation in experimental heart failure

    PubMed Central

    James, Jeanne; Hor, Kan; Moga, Michael-Alice; Martin, Lisa Ann; Robbins, Jeffrey

    2009-01-01

    The myosin heavy chain (MHC) isoforms, ?- and ?-MHC, are expressed in developmental- and chamber-specific patterns. Healthy human ventricle contains ?2-10% ?-MHC and these levels are reduced even further in the failing ventricle. While down-regulation of ?-MHC in failing myocardium is considered compensatory, we previously demonstrated that persistent transgenic (TG) ?-MHC expression in the cardiomyocytes is cardioprotective in rabbits with tachycardia-induced cardiomyopathy (TIC). We sought to determine if this benefit extends to other types of experimental heart failure and focused on two models relevant to human heart failure: myocardial infarction (MI) and left ventricular pressure overload. TG and nontransgenic rabbits underwent either coronary artery ligation at 8 months or aortic banding at 10 days of age. The effects of ?-MHC expression were assessed at molecular, histological and organ levels. In the MI experiments, we unexpectedly found modest functional advantages to ?-MHC expression. In contrast, despite subtle benefits in TG rabbits subjected to aortic banding, cardiac function was minimally affected. We conclude that the benefits of persistent ?-MHC expression depend upon the mechanism of heart failure. Importantly, in none of the scenarios studied did we find any detrimental effects associated with persistent ?-MHC expression. Thus manipulation of MHC composition may be beneficial in certain types of heart failure and does not appear to compromise heart function in others. Future considerations of myosin isoform manipulation as a therapeutic strategy should consider the underlying etiology of cardiac dysfunction. PMID:19854200

  16. The cardiac enigma: current conundrums in heart failure research.

    PubMed

    Kapiloff, Michael S; Emter, Craig A

    2016-01-01

    The prevalence of heart failure is expected to increase almost 50% in the next 15 years because of aging of the general population, an increased frequency of comorbidities, and an improved survival following cardiac events. Conventional treatments for heart failure have remained largely static over the past 20 years, illustrating the pressing need for the discovery of novel therapeutic agents for this patient population. Given the heterogeneous nature of heart failure, it is important to specifically define the cellular mechanisms in the heart that drive the patient's symptoms, particularly when considering new treatment strategies. This report highlights the latest research efforts, as well as the possible pitfalls, in cardiac disease translational research and discusses future questions and considerations needed to advance the development of new heart failure therapies. In particular, we discuss cardiac remodeling and the translation of animal work to humans and how advancements in our understanding of these concepts relative to disease are central to new discoveries that can improve cardiovascular health. PMID:26918161

  17. Antiarrhythmic effect of converting enzyme inhibitors in congestive heart failure.

    PubMed

    Gürlek, A; Erol, C; Basesme, E

    1994-03-01

    In this study 24-h Holter electrocardiographic recordings were used to measure the effects of an angiotensin converting enzyme inhibitor, enalapril given for 4 weeks, on the frequency of cardiac arrhythmias in 24 patients (14 patients had enalapril, 30 patients had placebo) with congestive heart failure (New York Heart Association Functional Class 3) receiving maintenance therapy with digoxin and furosemide. Although the placebo group had no change in the frequence of arrhythmias, enalapril-treated patients showed significant decrease in the frequency of premature ventricular complexes couplet, bigemine VPS and ventricular tachycardia. Moreover, it was observed that six cases of atrial fibrillation returned to sinus rhythm. During enalapril treatment, some patients experienced increased serum potassium levels, but there was no change in serum digoxin levels. We also observed echocardiographic improvement in left ventricular function as well as clinical symptoms of congestive heart failure. Finally we observed that there was an antiarrhythmic effect of enalapril in congestive heart failure. We thought that the antiarrhythmic effect of enalapril in congestive heart failure was probably due to hemodynamic improvement. PMID:7514156

  18. Management of heart failure with preserved ejection fraction.

    PubMed

    Webb, Jessica; Jackson, Tom; Claridge, Simon; Sammut, Eva; Behar, Jonathan; Carr-White, Gerald

    2015-10-01

    Heart failure affects nearly one million people in the UK. Half of these patients have normal, or near normal, left ventricular ejection fraction and are classified as heart failure with preserved ejection fraction (HFpEF). Newer imaging techniques have confirmed that systolic function in HFpEF patients is not completely normal, with reduced long axis function and extensive but subtle changes on exercise. Patients are likely to be older women with a history of hypertension. Other cardiovascular risk factors, such as diabetes mellitus, atrial fibrillation and coronary artery disease are prevalent in the HFpEF population. Clinical symptoms and signs in HFpEF are often nonspecific although the primary symptoms are breathlessness, fatigue and fluid retention. There is still no single diagnostic test for HFpEF and the cornerstone in the assessment remains a thorough medical history and physical examination. The duration and extent of the symptoms are relevant and it is useful to classify patients according to the NYHA functional assessment. Physical examination should include the patient's BMI and weight, heart rate and rhythm, lying and standing blood pressure and auscultation to rule out valvular disease and pulmonary congestion. Estimating the jugular venous pressure and the presence of peripheral oedema allows assessment of the patient's volume status. Patients with heart failure should be referred to heart failure nurses and have follow-up with local cardiology services as these have both been shown to reduce mortality. PMID:26738248

  19. Leukocyte behavior in atherosclerosis, myocardial infarction, and heart failure

    PubMed Central

    Swirski, Filip K.; Nahrendorf, Matthias

    2013-01-01

    Cardiovascular diseases claim more lives worldwide than any other. Etiologically, the dominant trajectory involves atherosclerosis, a chronic inflammatory process of lipid-rich lesion growth in the vascular wall that can cause life-threatening myocardial infarction (MI). Those who survive MI can develop congestive heart failure, a chronic condition of inadequate pump activity that is frequently fatal. Leukocytes – white blood cells – are important participants at the various stages of cardiovascular disease progression and complication. This review will discuss leukocyte function in atherosclerosis, myocardial infarction, and heart failure. PMID:23307733

  20. Cognitive profiles in heart failure: a cluster analytic approach.

    PubMed

    Miller, Lindsay A; Spitznagel, Mary Beth; Alosco, Michael L; Cohen, Ronald A; Raz, Naftali; Sweet, Lawrence H; Colbert, Lisa; Josephson, Richard; Hughes, Joel; Rosneck, Jim; Gunstad, John

    2012-01-01

    Cognitive impairment is common among individuals with heart failure (HF), but the exact nature of these impairments remains unclear. The current study examined 140 older adults with heart failure and sought to determine whether there are distinct cognitive profiles using a cluster analytic approach. Results indicated three unique profiles comprising individuals who were cognitively intact, memory impaired, and globally impaired. Clusters differed on several important demographic and clinical characteristics. These findings suggest that cognitive impairment in persons with HF is more heterogeneous than commonly believed and has important implications for treatment recommendations. PMID:22375800

  1. Pattern of arrhythmias among Nigerians with congestive heart failure

    PubMed Central

    Ajayi, Olufemi E; Abiodun, Olugbenga O; Akintomide, Anthony O; Adebayo, Rasaaq A; Ogunyemi, Suraj A; Balogun, Michael O; Bamikole, Olaniyi J; Ajibare, Adeola O; Ajayi, Adesuyi A

    2015-01-01

    Background In patients with heart failure, death is often sudden due to life-threatening arrhythmias. This work was carried out to evaluate the pattern of arrhythmias in Nigerians with heart failure. Materials and methods Thirty subjects with congestive heart failure (CHF), 30 subjects with hypertensive heart disease, and 15 normal subjects with no obvious features of heart disease were evaluated with resting and 24-hour electrocardiographic monitoring and transthoracic echocardiography. Data were analyzed with one-way analysis of variance with post hoc Duncans analysis, Fishers exact test, and linear regression analysis using SPSS version 16. Results CHF subjects had more instances of supraventricular tachycardia (P=0.005), ventricular extrasystoles (P<0.001), bigeminy (P<0.001), trigeminy (P<0.001), couplets (P<0.001), triplets (P<0.001), and nonsustained ventricular tachycardia (VT) (P=0.003) than the other two control groups. They also showed a significantly longer VT duration (4.65.6 seconds) compared with the other groups (P<0.001). Linear regression analysis showed a significant direct relationship between VT and the maximum number of ventricular extrasystoles per hour (P=0.001). Conclusion Cardiac arrhythmias are common in subjects with CHF and are more frequent when compared with patients with hypertensive heart disease and normal subjects. PMID:25870514

  2. CARDIOGENIC ACUTE RENAL FAILURE (CARF) FOLLOWING OPEN-HEART SURGERY

    PubMed Central

    Barcenas, Camilo G.; Jones, Peter; Solomon, Stuart; Van Reet, Richard; Cooley, Denton A.

    1979-01-01

    Although previous reports have attributed acute renal failure (ARF) following cardiovascular surgery to acute tubular necrosis (ATN), little emphasis has been placed on renal failure due to congestive heart failure (CARF). Of 100 cases of ARF studied prospectively over an 18-month period, 36 occurred after open-heart surgery. Nineteen of these cases were associated with heart failure. The remaining 17 had ATN as manifested by high urinary sodium, low urine/plasma creatinine, and abnormal urinary sediment. At the onset of CARF, intravascular volume expansion was universally present, and oliguria with pulmonary edema was common. Urinary chemistries were (mean SD): sodium (mEq/L) 8 7, U/P creatinine 72 45, and FENa (%) 0.1 0.1. Therapy consisted of digoxin, furosemide (F), vasopressors (V), and, when indicated, intraaortic balloon counterpulsation. Survivors of CARF responded more frequently to F and required less V. Ultimately, survival depended upon improvement in cardiac performance. All oliguric ATN patients failed to respond to F. Mortality for the CARF group was 52%. In contrast, 82% of the oliguric ATN group expired, whereas overall ATN mortality was 60%. Cardiogenic acute renal failure is a frequent cause of ARF after open-heart surgery in our institution. It is characterized by prerenal urinary chemistries, has a high mortality, and may be reversible. PMID:15216306

  3. Diesel Exhaust Inhalation Increases Cardiac Output, Bradyarrhythmias, and Parasympathetic Tone in Aged Heart FailureProne Rats

    PubMed Central

    Farraj, Aimen K.

    2013-01-01

    Acute air pollutant inhalation is linked to adverse cardiac events and death, and hospitalizations for heart failure. Diesel engine exhaust (DE) is a major air pollutant suspected to exacerbate preexisting cardiac conditions, in part, through autonomic and electrophysiologic disturbance of normal cardiac function. To explore this putative mechanism, we examined cardiophysiologic responses to DE inhalation in a model of aged heart failureprone rats without signs or symptoms of overt heart failure. We hypothesized that acute DE exposure would alter heart rhythm, cardiac electrophysiology, and ventricular performance and dimensions consistent with autonomic imbalance while increasing biochemical markers of toxicity. Spontaneously hypertensive heart failure rats (16 months) were exposed once to whole DE (4h, target PM2.5 concentration: 500 g/m3) or filtered air. DE increased multiple heart rate variability (HRV) parameters during exposure. In the 4h after exposure, DE increased cardiac output, left ventricular volume (end diastolic and systolic), stroke volume, HRV, and atrioventricular block arrhythmias while increasing electrocardiographic measures of ventricular repolarization (i.e., ST and T amplitudes, ST area, T-peak to T-end duration). DE did not affect heart rate relative to air. Changes in HRV positively correlated with postexposure changes in bradyarrhythmia frequency, repolarization, and echocardiographic parameters. At 24h postexposure, DE-exposed rats had increased serum C-reactive protein and pulmonary eosinophils. This study demonstrates that cardiac effects of DE inhalation are likely to occur through changes in autonomic balance associated with modulation of cardiac electrophysiology and mechanical function and may offer insights into the adverse health effects of traffic-related air pollutants. PMID:23047911

  4. A novel distributed model of the heart under normal and congestive heart failure conditions.

    PubMed

    Ravanshadi, Samin; Jahed, Mehran

    2013-04-01

    Conventional models of cardiovascular system frequently lack required detail and focus primarily on the overall relationship between pressure, flow and volume. This study proposes a localized and regional model of the cardiovascular system. It utilizes noninvasive blood flow and pressure seed data and temporal cardiac muscle regional activity to predict the operation of the heart under normal and congestive heart failure conditions. The analysis considers specific regions of the heart, namely, base, mid and apex of left ventricle. The proposed method of parameter estimation for hydraulic electric analogy model is recursive least squares algorithm. Based on simulation results and comparison to clinical data, effect of congestive heart failure in the heart is quantified. Accumulated results for simulated ejection fraction percentage of the apex, mid and base regions of the left ventricle in congestive heart failure condition were 39??6, 36??9 and 38??8, respectively. These results are shown to satisfactorily match those found through clinical measurements. The proposed analytical method can in effect be utilized as a preclinical and predictive tool for high-risk heart patients and candidates for heart transplant, assistive device and total artificial heart. PMID:23637212

  5. Mortality by Heart Failure and Ischemic Heart Disease in Brazil from 1996 to 2011

    PubMed Central

    Gaui, Eduardo Nagib; de Oliveira, Glucia Maria Moraes; Klein, Carlos Henrique

    2014-01-01

    Background Circulatory system diseases are the first cause of death in Brazil. Objective To analyze the evolution of mortality caused by heart failure, by ischemic heart diseases and by ill-defined causes, as well as their possible relations, in Brazil and in the geoeconomic regions of the country (North, Northeast, Center-West, South and Southeast), from 1996 to 2011. Methods Data were obtained from DATASUS and death declaration records with codes I20 and I24 for acute ischemic diseases, I25 for chronic ischemic diseases, and I50 for heart failure, and codes in chapter XIII for ill-defined causes, according to geoeconomic regions of Brazil, from 1996 to 2011. Results Mortality rates due to heart failure declined in Brazil and its regions, except for the North and the Northeast. Mortality rates due to acute ischemic heart diseases increased in the North and Northeast regions, especially from 2005 on; they remained stable in the Center-West region; and decreased in the South and in the Southeast. Mortality due to chronic ischemic heart diseases decreased in Brazil and in the Center-West, South and Southeast regions, and had little variation in the North and in the Northeast. The highest mortality rates due to ill-defined causes occurred in the Northeast until 2005. Conclusions Mortality due to heart failure is decreasing in Brazil and in all of its geoeconomic regions. The temporal evolution of mortality caused by ischemic heart diseases was similar to that of heart failure. The decreasing number of deaths due to ill-defined causes may represent the improvement in the quality of information about mortality in Brazil. The evolution of acute ischemic heart diseases ranged according to regions, being possibly confused with the differential evolution of ill-defined causes. PMID:25004417

  6. Ammonia response to exercise in patients with congestive heart failure.

    PubMed Central

    Ogino, K.; Osaki, S.; Kitamura, H.; Noguchi, N.; Hisatome, I.; Matsumoto, T.; Omodani, H.; Kato, M.; Kinugawa, T.; Miyakoda, H.; Kotake, H.; Mashiba, H.

    1996-01-01

    OBJECTIVE: To assess energy depletion in skeletal muscle in patients with congestive heart failure by measuring blood purine metabolites during exercise and, at the same time, determine the implications of the ammonia response to exercise in these patients. SETTING: Tottori University Hospital, Yonago, Japan. PATIENTS: 49 heart failure patients (New York Heart Association (NYHA) grades I-III) and 16 normal subjects. MAIN OUTCOME MEASURES: Blood lactate, ammonia, and hypoxanthine levels were measured during exercise with expired gas analysis. RESULTS: In normal exercising subjects as well as in each heart failure subgroup, the ammonia threshold was significantly higher than both the lactate threshold [control: 21.8 (SD 5.3) v 17.4 (3.3) ml/kg/min; NYHA class I: 18.9 (3.8) v 15.5 (2.6); class II: 14.8 (2.5) v 12.7 (2.4); class III: 13.5 (2.6) v 11.8 (2.5)] and the ventilatory threshold (P < 0.01). The difference between the ammonia and lactate thresholds was noted in all normal subjects and in all heart failure patients. The ammonia threshold, however, was significantly lower in heart failure patients than in normal subjects and it decreased with increasing NYHA class (P < 0.01). Maximum ammonia levels were lower in the heart failure group and decreased further with higher NYHA classifications [control: 198 (52) mg/dl; NYHA class I: 170 (74); class II: 134 (58); class III: 72 (15); P < 0.01]. There were significant correlations between maximum ammonia values and maximum lactate, oxygen consumption, and hypoxanthine levels (r = 0.74, 0.48, and 0.87, respectively; P < 0.001). CONCLUSIONS: The ammonia threshold may reflect the onset of ATP depletion in exercising skeletal muscles, as opposed to the onset of anaerobic respiration. It seems therefore that energy depletion in skeletal muscles during exercise occurs after attaining the anaerobic threshold. Both aerobic and anaerobic capacities of skeletal muscle are reduced in patients with congestive heart failure. PMID:8705758

  7. Increased walking variability in elderly persons with congestive heart failure

    NASA Technical Reports Server (NTRS)

    Hausdorff, J. M.; Forman, D. E.; Ladin, Z.; Goldberger, A. L.; Rigney, D. R.; Wei, J. Y.

    1994-01-01

    OBJECTIVES: To determine the effects of congestive heart failure on a person's ability to walk at a steady pace while ambulating at a self-determined rate. SETTING: Beth Israel Hospital, Boston, a primary and tertiary teaching hospital, and a social activity center for elderly adults living in the community. PARTICIPANTS: Eleven elderly subjects (aged 70-93 years) with well compensated congestive heart failure (NY Heart Association class I or II), seven elderly subjects (aged 70-79 years) without congestive heart failure, and 10 healthy young adult subjects (aged 20-30 years). MEASUREMENTS: Subjects walked for 8 minutes on level ground at their own selected walking rate. Footswitches were used to measure the time between steps. Step rate (steps/minute) and step rate variability were calculated for the entire walking period, for 30 seconds during the first minute of the walk, for 30 seconds during the last minute of the walk, and for the 30-second period when each subject's step rate variability was minimal. Group means and 5% and 95% confidence intervals were computed. MAIN RESULTS: All measures of walking variability were significantly increased in the elderly subjects with congestive heart failure, intermediate in the elderly controls, and lowest in the young subjects. There was no overlap between the three groups using the minimal 30-second variability (elderly CHF vs elderly controls: P < 0.001, elderly controls vs young: P < 0.001), and no overlap between elderly subjects with and without congestive heart failure when using the overall variability. For all four measures, there was no overlap in any of the confidence intervals, and all group means were significantly different (P < 0.05).

  8. Heart failure: when form fails to follow function.

    PubMed

    Katz, Arnold M; Rolett, Ellis L

    2016-02-01

    Cardiac performance is normally determined by architectural, cellular, and molecular structures that determine the heart's form, and by physiological and biochemical mechanisms that regulate the function of these structures. Impaired adaptation of form to function in failing hearts contributes to two syndromes initially called systolic heart failure (SHF) and diastolic heart failure (DHF). In SHF, characterized by high end-diastolic volume (EDV), the left ventricle (LV) cannot eject a normal stroke volume (SV); in DHF, with normal or low EDV, the LV cannot accept a normal venous return. These syndromes are now generally defined in terms of ejection fraction (EF): SHF became 'heart failure with reduced ejection fraction' (HFrEF) while DHF became 'heart failure with normal or preserved ejection fraction' (HFnEF or HFpEF). However, EF is a chimeric index because it is the ratio between SV - which measures function, and EDV - which measures form. In SHF the LV dilates when sarcomere addition in series increases cardiac myocyte length, whereas sarcomere addition in parallel can cause concentric hypertrophy in DHF by increasing myocyte thickness. Although dilatation in SHF allows the LV to accept a greater venous return, it increases the energy cost of ejection and initiates a vicious cycle that contributes to progressive dilatation. In contrast, concentric hypertrophy in DHF facilitates ejection but impairs filling and can cause heart muscle to deteriorate. Differences in the molecular signals that initiate dilatation and concentric hypertrophy can explain why many drugs that improve prognosis in SHF have little if any benefit in DHF. PMID:26497163

  9. HeartWare left ventricular assist device for the treatment of advanced heart failure.

    PubMed

    Hanke, Jasmin S; Rojas, Sebastian V; Avsar, Murat; Bara, Christoph; Ismail, Issam; Haverich, Axel; Schmitto, Jan D

    2016-01-01

    The importance of mechanical circulatory support in the therapy of advanced heart failure is steadily growing. The rapid developments in the field of mechanical support are characterized by continuous miniaturization and enhanced performance of the assist devices, providing increased pump durability and prolonged patient survival. The HeartWare left ventricular assist device system (HeartWare Inc., Framingham, MA, USA) is a mechanical ventricular assist device with over 8000 implantations worldwide. Compared with other available assist devices it is smaller in size and used in a broad range of patients. The possibility of minimally invasive procedures is one of the major benefits of the device - allowing implants and explants, as well as exchanges of the device with reduced surgical impact. We present here a review of the existing literature on the treatment of advanced heart failure using the HeartWare left ventricular assist device system. PMID:26597386

  10. Novel Strategies for the Treatment of Heart Failure

    PubMed Central

    Kehat, Izhak

    2012-01-01

    Heart failure is a leading cause of morbidity and mortality with a prevalence that is rising throughout the world. Currently the pharmaceutical therapy of heart failure is mainly based on inhibition of the neurohumoral pathways that are activated secondary to the deterioration of cardiac function, and diuretics to alleviate the salt and water overload. With our increasing understanding of the pathophysiology of heart failure, it is now clear that the macroscopic and functional changes in the failing heart result from remodeling at the cellular, interstitial, and molecular levels. Therefore, emerging therapies propose to intervene directly in the remodeling process at the cellular and the molecular levels. Here, several experimental strategies that aim to correct the abnormalities in receptor and post-receptor-function, calcium handling, excitation and contraction coupling, signaling, and changes in the extra-cellular matrix in the failing heart will be discussed. These novel approaches, aiming to reverse the remodeling process at multiple levels, may appear on the clinical arena in the coming years. PMID:23908835

  11. Angiotensin II contributes to arterial compliance in congestive heart failure.

    PubMed

    Lage, Silvia G; Kopel, Liliane; Medeiros, Caio C J; Carvalho, Ricardo T; Creager, Mark A

    2002-10-01

    Arterial compliance is determined by structural factors, such as collagen and elastin, and functional factors, such as vasoactive neurohormones. To determine whether angiotensin II contributes to decreased arterial compliance in patients with heart failure, this study tested the hypothesis that administration of an angiotensin-converting enzyme inhibitor improves arterial compliance. Arterial compliance and stiffness were determined by measuring carotid artery diameter, using high-resolution duplex ultrasonography, and blood pressure in 23 patients with heart failure secondary to idiopathic dilated cardiomyopathy. Measurements were made before and after intravenous administration of enalaprilat (1 mg) or vehicle. Arterial compliance was inversely related to both baseline plasma angiotensin II (r = -0.52; P = 0.015) and angiotensin-converting enzyme concentrations (r = -0.45; P = 0.041). During isobaric conditions, enalaprilat increased carotid artery compliance from 3.0 +/- 0.4 to 5.0 +/- 0.4 x 10(-10) N(-1). m(4) (P = 0.001) and decreased the carotid artery stiffness index from 17.5 +/- 1.8 to 10.1 +/- 0.6 units (P = 0.001), whereas the vehicle had no effect. Thus angiotensin II is associated with reduced carotid arterial compliance in patients with congestive heart failure, and angiotensin-converting enzyme inhibition improves arterial elastic properties. This favorable effect on the pulsatile component of afterload may contribute to the improvement in left ventricular performance that occurs in patients with heart failure treated with angiotensin-converting enzyme inhibitors. PMID:12234793

  12. Teaching Congestive Heart Failure to Doctor of Pharmacy Students.

    ERIC Educational Resources Information Center

    Parker, Robert B.

    1992-01-01

    This paper summarizes a lecture given to pharmacy students that emphasizes the pathophysiologic mechanisms causing congestive heart failure and the effects of drugs on these mechanisms. The approach shows the importance of drug therapy in this disorder and how this knowledge can improve patient care. An appendix provides a case study. (GLR)

  13. [Device therapy of chronic heart failure : Update 2015].

    PubMed

    Israel, C W; Ekosso-Ejangue, L; Sheta, M-K

    2015-12-01

    Cardiac pacemakers, implantable cardioverter defibrillators (ICD) and systems for cardiac resynchronization therapy (CRT) represent an important component of heart failure therapy. Pacemakers only play a role in bradycardia-associated heart failure and require optimal programming to prevent ventricular desynchronization. Primary prophylactic ICD implantation is indicated in patients with a left ventricular ejection fraction of ??35?%, clinical stages NYHA II-III and a life expectancy >?1 year. The CRT is indicated in patients with a left bundle branch block but only in individual cases for other QRS morphologies of heart failure should always include remote monitoring to detect events early and to implement treatment accordingly. New developments include quadripolar left ventricular leads and pacing from multiple sites simultaneously thus enabling better resynchronization. Stimulation for modulation of cardiac contractility and the autonomous nervous system are currently being clinically tested. The optimal utilization of device therapy improves the course of heart failure and prevents cardiac decompensation and fatalities. PMID:26631395

  14. Heart failure: New data do not SUPPORT triple RAAS blockade.

    PubMed

    Danser, A H Jan; van den Meiracker, Anton H

    2015-05-01

    The SUPPORT trial evaluated the effect of adding the angiotensin-receptor blocker olmesartan to a combination of angiotensin-converting-enzyme inhibitors and β-blockers in hypertensive patients with chronic stable heart failure. Unfortunately, this triple renin-angiotensin-aldosterone system blockade was associated with worsening of renal function and increases in cardiac events and mortality. PMID:25802078

  15. Inotropes do not increase mortality in advanced heart failure

    PubMed Central

    Guglin, Maya; Kaufman, Marc

    2014-01-01

    Inotrope use is one of the most controversial topics in the management of heart failure. While the heart failure community utilizes them and recognizes the state of inotrope dependency, retrospective analyses and registry data have overwhelmingly suggested high mortality, which is logically to be expected given the advanced disease states of those requiring their use. Currently, there is a relative paucity of randomized control trials due to the ethical dilemma of creating control groups by withholding inotropes from patients who require them. Nonetheless, results of such trials have been mixed. Many were also performed with agents no longer in use, on patients without an indication for inotropes, or at a time before automatic cardio-defibrillators were recommended for primary prevention. Thus, their results may not be generalizable to current clinical practice. In this review, we discuss current indications for inotrope use, specifically dobutamine and milrinone, depicting their mechanisms of action, delineating their patterns of use in clinical practice, defining the state of inotrope dependency, and ultimately examining the literature to ascertain whether evidence is sufficient to support the current view that these agents increase mortality in patients with heart failure. Our conclusion is that the evidence is insufficient to link inotropes and increased mortality in low output heart failure. PMID:24899821

  16. Systemic sclerosis: a rare cause of heart failure?

    PubMed

    Gonzlez-Cambeiro, Mara Cristina; Abu-Assi, Emad; Abumuaileq, Rami Riziq-Yousef; Raposeiras-Roubn, Sergio; Rigueiro-Veloso, Pedro; Virgs-Lamela, Alejandro; Daz-Castro, Oscar; Gonzlez-Juanatey, Jos Ramn

    2015-10-01

    Systemic sclerosis (SS) is a chronic disease in which there may be multisystem involvement. It is rare (estimated prevalence: 0.5-2/10000) with high morbidity and mortality, and there is as yet no curative treatment. We report the case of a young woman newly diagnosed with SS, in whom decompensated heart failure was the main manifestation. PMID:26421376

  17. Ultrastructural and cellular basis for the development of abnormal myocardial mechanics during the transition from hypertension to heart failure

    PubMed Central

    Shah, Sanjiv J.; Aistrup, Gary L.; Gupta, Deepak K.; O'Toole, Matthew J.; Nahhas, Amanda F.; Schuster, Daniel; Chirayil, Nimi; Bassi, Nikhil; Ramakrishna, Satvik; Beussink, Lauren; Misener, Sol; Kane, Bonnie; Wang, David; Randolph, Blake; Ito, Aiko; Wu, Megan; Akintilo, Lisa; Mongkolrattanothai, Thitipong; Reddy, Mahendra; Kumar, Manvinder; Arora, Rishi; Ng, Jason

    2013-01-01

    Although the development of abnormal myocardial mechanics represents a key step during the transition from hypertension to overt heart failure (HF), the underlying ultrastructural and cellular basis of abnormal myocardial mechanics remains unclear. We therefore investigated how changes in transverse (T)-tubule organization and the resulting altered intracellular Ca2+ cycling in large cell populations underlie the development of abnormal myocardial mechanics in a model of chronic hypertension. Hearts from spontaneously hypertensive rats (SHRs; n = 72) were studied at different ages and stages of hypertensive heart disease and early HF and were compared with age-matched control (Wistar-Kyoto) rats (n = 34). Echocardiography, including tissue Doppler and speckle-tracking analysis, was performed just before euthanization, after which T-tubule organization and Ca2+ transients were studied using confocal microscopy. In SHRs, abnormalities in myocardial mechanics occurred early in response to hypertension, before the development of overt systolic dysfunction and HF. Reduced longitudinal, circumferential, and radial strain as well as reduced tissue Doppler early diastolic tissue velocities occurred in concert with T-tubule disorganization and impaired Ca2+ cycling, all of which preceded the development of cardiac fibrosis. The time to peak of intracellular Ca2+ transients was slowed due to T-tubule disruption, providing a link between declining cell ultrastructure and abnormal myocardial mechanics. In conclusion, subclinical abnormalities in myocardial mechanics occur early in response to hypertension and coincide with the development of T-tubule disorganization and impaired intracellular Ca2+ cycling. These changes occur before the development of significant cardiac fibrosis and precede the development of overt cardiac dysfunction and HF. PMID:24186100

  18. [Therapy of heart failure with beta-blockers?].

    PubMed

    Osterziel, K J; Dietz, R

    1997-01-01

    In heart failure the chronic sympathetic stimulation alters the cardiac beta-adrenergic pathway. This alteration leads to a diminished contractile response to stimulation of the cardiac beta 1 receptor. A blockade of the beta 1 receptor partly restores the physiologic response to sympathetic stimulation at rest and during exercise. Several mechanisms resulting from the competitive blockade of the beta 1 receptor may be important. The major effect of beta-blockers seems to be triggered by a reduction of the heart rate at rest resulting in an increase of the left ventricular ejection fraction on the average by 7-8%. Patients with heart failure who are treated with a beta-blocker experience initially a slight decrease of the left ventricular function. beta-blocker therapy should therefore be initiated only in patients with stable heart failure. The starting dose of the beta-blocker has to be very small, e.g, 5 mg Metoprolol, 1.25 mg Bisoprolol or 3.125 mg Carvedilol. In a stepwise fashion the dose has to be increased to a full beta blocking effect over a period of 4-8 weeks. Despite a careful dose titration only 90% of the patients tolerate this regimen. Patients with high resting heart rates and/or dilated cardiomyopathy will have the greatest benefit. The two main reasons for withdrawal of the beta-blocker are deterioration of heart failure or symptomatic hypotension. Symptomatic improvement and a significant increase of exercise capacity appear gradually and can be measured only after more than 1 month duration of therapy. Three multicenter studies (MDC. CIBIS I, Carvedilol) evaluated the influence of beta-blockers on prognosis of heart failure. The MDC trial demonstrated a slower progression of heart failure with Metoprolol. The MDC and the CIBIS I trial could not show a significant improvement of prognosis. The larger trial with carvedilol was the first study to demonstrate a decreased mortality in patients who initially tolerate the beta-blocker therapy. One major concern in that study is the evaluation and classification of patients in the run-in phase who do not tolerate the beta-blocker. Definite studies (BEST, CIBIS II; COMET; RESOLVED; MERIT) are designed to answer these problems and to evaluate the effect of beta-blockers on mortality. Until the results of these studies are available the main goal of treatment with beta-blockers remains symptomatic improvement. Further, there is good evidence for an additional increase in life expectancy. In order to achieve optimal medical treatment and to avoid side-effects careful clinical evaluation and management of the patients is mandatory during therapy with beta-blockers. PMID:9133118

  19. Statins stimulate atherosclerosis and heart failure: pharmacological mechanisms.

    PubMed

    Okuyama, Harumi; Langsjoen, Peter H; Hamazaki, Tomohito; Ogushi, Yoichi; Hama, Rokuro; Kobayashi, Tetsuyuki; Uchino, Hajime

    2015-03-01

    In contrast to the current belief that cholesterol reduction with statins decreases atherosclerosis, we present a perspective that statins may be causative in coronary artery calcification and can function as mitochondrial toxins that impair muscle function in the heart and blood vessels through the depletion of coenzyme Q10 and 'heme A', and thereby ATP generation. Statins inhibit the synthesis of vitamin K2, the cofactor for matrix Gla-protein activation, which in turn protects arteries from calcification. Statins inhibit the biosynthesis of selenium containing proteins, one of which is glutathione peroxidase serving to suppress peroxidative stress. An impairment of selenoprotein biosynthesis may be a factor in congestive heart failure, reminiscent of the dilated cardiomyopathies seen with selenium deficiency. Thus, the epidemic of heart failure and atherosclerosis that plagues the modern world may paradoxically be aggravated by the pervasive use of statin drugs. We propose that current statin treatment guidelines be critically reevaluated. PMID:25655639

  20. Regenerative cell therapy and pharmacotherapeutic intervention in heart failure

    PubMed Central

    Qian, C.; Schoemaker, R.G.; van Gilst, W.H.; Yu, B.; Roks, A.J.M.

    2008-01-01

    Regenerative medicine represents a promising perspective on therapeutic angiogenesis in patients with cardiovascular disease, including heart failure. However, previous or ongoing clinical trials show ambiguous outcomes with respect to the benefit of regenerative therapy by means of bone marrow stem cell infusion in myocardial infarction patients. Therefore, it is necessary to set up a rational therapeutic strategy in the treatment of congestive heart failure. Chemokines, cytokines and growth factors, as well as pharmaceutical agents, may have an impact on endothelial progenitor cell (EPC) physiology and thus can provide targets for pharmacological intervention. Indeed, EPCs and stem cell niches both in bone marrow and myocardial tissue can be treated as an integral target for recruitment of EPCs from the bone marrow to the cardiac ischaemic niche. In this article, we individually place the signalling factors in their specified context, and explain their roles in the various phases of neovascularisation (see Part 1). (Neth Heart J 2008;16:337-43.) PMID:18958257

  1. The kidney in heart failure: friend or foe?

    PubMed

    Kshatriya, Shilpa; Kozman, Hani; Siddiqui, Danish; Bhatta, Luna; Liu, Kan; Salah, Ali; Ford, Timothy; Michiel, Robert; Carhart, Robert; Villarreal, Daniel

    2012-09-01

    Heart failure constitutes a significant source of morbidity and mortality in the United States and its incidence and prevalence continue to grow, increasing its burden on the health care system. Renal dysfunction in patients with heart failure is common and has been associated with adverse clinical outcomes. This complex interaction is characterized by a pathophysiological disequilibrium between the heart and the kidney, in which cardiac malfunction promotes renal impairment, which in turn feeds back for further deterioration of cardiovascular function. Multiple neurohumoral and hemodynamic mechanisms are involved in this cardiorenal dyshomeostasis, including the deficiency of and/or resistance to compensatory natriuretic peptides, leading to sodium retention, volume overload and organ remodeling. Management of patients with cardiorenal dysfunction can be challenging and should be individualized. Emerging therapies must address the impairment of both organs to secure better clinical outcomes. To this end, a multidisciplinary approach is warranted to achieve optimal results. PMID:22317900

  2. Renal failure induces telomere shortening in the rat heart

    PubMed Central

    Wong, L.S.; Windt, W.A.; Roks, A.J.; van Dokkum, R.P.; Schoemaker, R.G.; de Zeeuw, D.; Henning, R.H.

    2009-01-01

    Background Renal failure aggravates pathological cardiac remodelling induced by myocardial infarction (MI). Cardiac remodelling is associated with telomere shortening, a marker for biological ageing. We investigated whether mild and severe renal failure shorten cardiac telomeres and excessively shorten telomeres after MI. Methods Rats were subjected to sham, unilateral (UNX) or 5/6th nephrectomy (5/6NX) to induce none, mild or severe renal failure. MI was induced by left coronary artery ligation. Renal function parameters and blood pressure were measured. DNA was isolated from non-infarcted cardiac tissue. Telomere length was assessed by quantitative polymerase chain reaction (PCR). Results Proteinuria was unchanged in UNX and MI compared with control, but strongly increased in 5/6NX, UNX+MI and 5/6NX+MI. Serum creatinine levels were increased fourfold in 5/6NX and tenfold in 5/6NX+MI. 5/6NX and groups with both renal failure and MI showed an approximate 20% reduction of telomere length, similar to the MI group. No excess telomere shortening was observed in hearts from rats with renal ablation after MI. Conclusion Severe renal failure, but not mild renal failure, leads to shortening of cardiac telomeres to a similar extent as found after MI. Renal failure did not induce excessive telomere shortening after MI. (Neth Heart J 2009;17:190-4.) PMID:19484154

  3. Heart failure and carotid body chemoreception.

    PubMed

    Schultz, Harold D; Marcus, Noah J

    2012-01-01

    There is substantial evidence to implicate a role of the carotid body (CB) chemoreflex in sympathetic and breathing dysregulation in several cardio-respiratory diseases, drawing renewed interest in its potential implications for clinical treatment and management. Evidence from both chronic heat failure (CHF) patients and animal models indicates that the CB chemoreflex is enhanced in CHF and contributes to the tonic elevation in sympathetic nerve activity (SNA) and periodic breathing associated with the disease. Although this maladaptive change likely derives from altered function at all levels of the reflex arc, a change in afferent function of the CB is likely to be a main driving force. This review will focus on recent advances in our understanding of the physiological mechanisms that alter CB function in CHF and their potential translational impact on treatment of CHF. PMID:23080187

  4. [Diastolic heart failure treated by diet].

    PubMed

    Heilmeyer, Peter; von Bibra, Helene

    2016-01-01

    History and admission findings | An obese patient with type 2 diabetes (on 90 IU insulin daily) and exertional dyspnoea (NYHA II-III) for 3 weeks presented in a rehabilitation clinic hoping to reduce his weight. Clinical and laboratory findings excluded any inflammatory or systemic disease apart from diabetes mellitus. Blood pressure and serum lipid levels were normal. Investigations | An unremarkable ECG stress test and echocardiogram excluded ischemic and hypertensive heart disease and primary cardiomyopathy. Pulsed tissue Doppler revealed diastolic cardiac dysfunction. Unremarkable were also chest X-ray, pulmonary function testing and 24-hour ECG. Treatment and Course | The findings supported the diagnosis of HFpEF and diabetic/insulin resistance cardiomyopathy. Insulin resistance was treated for three weeks by low-carbohydrate nutrition and moderate exercise. At discharge, weight was reduced by 2 kg, exercise capacity and diastolic function were normalized, as were insulin resistance and postprandial glucose levels, whilst antidiabetic therapy was reduced to low-carbohydrate nutrition. Conclusion | HFpEF due to insulin resistance cardiomyopathy is often not recognized, especially in obese individuals, and may be further aggravated by the traditional recommendation of low-fat nutrition. Due to the high reversibility of metabolically dysregulated cardiovascular mechanisms, a causal, i.e. metabolic therapeutic strategy that normalizes insulin resistance by low-carbohydrate nutrition is a promising option. PMID:26800073

  5. Ventilation heterogeneity is increased in patients with chronic heart failure

    PubMed Central

    Kee, Kirk; Stuart-Andrews, Christopher; Nilsen, Kris; Wrobel, Jeremy P; Thompson, Bruce R; Naughton, Matthew T

    2015-01-01

    In the healthy lung, ventilation is distributed heterogeneously due to factors such as anatomical asymmetry and gravity. This ventilation heterogeneity increases pathologically in conditions such as asthma, chronic obstructive lung disease, and cystic fibrosis. In chronic heart failure, lung biopsy demonstrates evidence of peripheral lung fibrosis and small airways narrowing and distortion. We hypothesized that this would lead to increased ventilation heterogeneity. Furthermore, we proposed that rostral fluid shifts when seated patients lie supine would further increase ventilation heterogeneity. We recruited 30 ambulatory chronic heart failure patients (5710years, 83% male, left ventricular ejection fraction 3112%) as well as 10 healthy controls (5113years, 90% male). Heart failure patients were clinically euvolemic. Subjects underwent measurement of ventilation heterogeneity using the multiple-breath nitrogen washout technique in the seated position, followed by repeat measurements after 5 and 45min in the supine position. Ventilation heterogeneity was calculated using the lung clearance index (LCI), Sacin and Scond which represent overall, acinar, and small conducting airway function, respectively. Lung clearance index (9.61.2 vs. 8.61.4 lung turnovers, P=0.034) and Scond (0.0290.014 vs. 0.0060.016/L, P=0.007) were higher in the heart failure patients. There was no difference in Sacin (0.1970.171 vs. 0.1250.081/L, P=0.214). Measures of ventilation heterogeneity did not change in the supine position. This study confirms the presence of peripheral airway pathology in patients with chronic heart failure. This leads to subtle but detectable functional abnormalities which do not change after 45min in the supine position. PMID:26493954

  6. CXCR4 gene transfer prevents pressure overload induced heart failure

    PubMed Central

    LaRocca, Thomas J.; Jeong, Dongtak; Kohlbrenner, Erik; Lee, Ahyoung; Chen, JiQiu; Hajjar, Roger J.; Tarzami, Sima T.

    2012-01-01

    Stem cell and gene therapies are being pursued as strategies for repairing damaged cardiac tissue following myocardial infarction in an attempt to prevent heart failure. The chemokine receptor-4 (CXCR4) and its ligand, CXCL12, play a critical role in stem cell recruitment post-acute myocardial infarction. Whereas progenitor cell migration via the CXCL12/CXCR4 axis is well characterized, little is known about the molecular mechanisms of CXCR4 mediated modulation of cardiac hypertrophy and failure. We used gene therapy to test the effects of CXCR4 gene delivery on adverse ventricular remodeling due to pressure overload. We assessed the effect of cardiac overexpression of CXCR4 during trans-aortic constriction (TAC) using a cardiotropic adeno-associated viral vector (AAV9) carrying the CXCR4 gene. Cardiac overexpression of CXCR4 in mice with pressure overload prevented ventricular remodeling, preserved capillary density and maintained function as determined by echocardiography and in vivo hemodynamics. In isolated adult rat cardiac myocytes, CXCL12 treatment prevented isoproterenol induced hypertrophy and interrupted the calcineurin/NFAT pathway. Finally, a complex involving the L-type calcium channel, ?2-adenoreceptor, and CXCR4 (Cav1.2/?2AR/CXCR4) was identified in healthy cardiac myocytes and was shown to dissociate as a consequence of heart failure. CXCR4 administered to the heart via gene transfer prevents pressure overload induced heart failure. The identification of CXCR4 participation in a Cav1.2-?2AR regulatory complex provides further insight into the mechanism by which CXCR4 modulates calcium homeostasis and chronic pressure overload responses in the cardiac myocyte. Together these results suggest AAV9.CXCR4 gene therapy is a potential therapeutic approach for congestive heart failure. PMID:22668785

  7. Self-care in heart failure patients 1

    PubMed Central

    da Conceio, Ana Paula; dos Santos, Mariana Alvina; dos Santos, Bernardo; da Cruz, Din de Almeida Lopes Monteiro

    2015-01-01

    Abstract Objective: to describe self-care behavior and its associated factors in a sample of heart failure Brazilian patients. Method: descriptive cross-sectional study with non-probabilistic sample of 116 ambulatory patients undergoing heart failure treatment. Self-care was evaluated using the Self-Care of Heart Failure Index, (scores ?70 points=appropriate self-care). Association tests were applied, considering a descriptive level of 0.05. Results: the mean age of participants was 57.7 (SD =11.3) years; 54.3% were male; the mean schooling was 5.5 (SD = 4.0) years; and 74.1% had functional class II-III. The mean scores on the subscales of the Self-Care of Heart Failure Index indicated inappropriate self-care (self-care maintenance: 53.2 (SD =14.3), selfcare management: 50.0 (SD = 20.3) and self-care confidence: 52.6 (SD=22.7)) and it was found low frequencies of participants with appropriate self-care (self-care maintenance, 6.9%), self-care management (14.7%) and self-care confidence (19%). Higher scores of the Self-Care of Heart Failure Index were associated with: reduced left ventricular ejection fraction (p=0.001), longer time of experience with the disease (p=0.05) and joint monitoring by physician and nurse (p=0.007). Conclusion: investments are needed to improve the self-care behavior and the nursing can play a relevant role in this improvement. PMID:26444158

  8. Artificial muscle for end-stage heart failure.

    PubMed

    Tozzi, Piergiorgio; Michalis, Alexandre; Hayoz, Daniel; Locca, Didier; von Segesser, Ludwig K

    2012-01-01

    We describe a device made of artificial muscle for the treatment of end-stage heart failure as an alternative to current heart assist devices. The key component is a matrix of nitinol wires and aramidic fibers called Biometal muscle (BM). When heated electrically, it produces a motorless, smooth, and lifelike motion. The BM is connected to a carbon fiber scaffold, tightening the heart and providing simultaneous assistance to the left and right ventricles. A pacemaker-like microprocessor drives the contraction of the BM. We tested the device in a dedicated bench model of diseased heart. It generated a systolic pressure of 75 mm Hg and ejected a maximum of 330 ml/min, with an ejection fraction of 12%. The device required a power supply of 6 V, 250 mA. This could be the beginning of an era in which BMs integrate or replace the mechanical function of natural muscles. PMID:22370680

  9. Troglitazone improves cardiac function in patients with congestive heart failure.

    PubMed

    Ogino, Kazuhide; Furuse, Yoshiyuki; Uchida, Kazuhiko; Shimoyama, Masaki; Kinugawa, Toru; Osaki, Shuichi; Kato, Masahiko; Endo, Akihiro; Igawa, Osamu; Hisatome, Ichiro; Ikawa, Shiro; Shigemasa, Chiaki

    2002-05-01

    Troglitazone increased cardiac output and stroke volume, as a result of decreased peripheral resistance, in diabetic patients with normal cardiac function. The cardiovascular effects of troglitazone in patients with heart failure are unknown. The aim of the study was to evaluate the cardiovascular effects of troglitazone in patients with heart failure. Blood pressure and echocardiographic findings were evaluated before and 1, 2, 3 and 4 hours after a single dose of troglitazone (400 mg) or placebo, in eight type II diabetic patients with congestive heart failure. The plasma catecholamines and coefficient of variance of RR intervals (CVRR) were also measured. Neither heart rate nor blood pressure changed after the administration of troglitazone. Left ventricular (LV) end-diastolic dimension did not change either, however, the LV end-systolic dimension significantly decreased compared with its baseline value and with that of the placebo group. On the other hand, the % fractional shortening and the E/A ratio increased significantly after troglitazone. The LV end-diastolic volume did not change, whereas the LV end-systolic volume significantly decreased. The stroke volume and the LV ejection fraction significantly increased compared with its baseline value and with that of the placebo group. The peripheral vascular resistance did not change after the administration of troglitazone, whereas plasma catecholamines significantly decreased, and CVRR remained unchanged in both groups. These hemodynamic changes suggest that a single oral dose of troglitazone induced inotropy without activation of the sympathetic nervous system. PMID:12374899

  10. Chronic vagal stimulation in patients with congestive heart failure.

    PubMed

    De Ferrari, Gaetano M; Sanzo, Antonio; Schwartz, Peter J

    2009-01-01

    Increased sympathetic and reduced vagal activity predict increased mortality in patients with congestive heart failure (CHF). Experimentally, vagal stimulation (VS) is protective both during acute myocardial ischemia and in chronic heart failure. In man, VS is used in refractory epilepsy but has never been used in cardiovascular diseases. Thus, there is a strong rationale to investigate the effects of chronic VS in patients with CHF. We assesses the feasibility and safety of chronic VS with CardioFit (BioControl Medical), a VS implantable system delivering pulses synchronous with heart beats to the right cervical vagus nerve in a preliminary pilot study in eight advanced CHF patients with favorable results, and subsequently in a larger multicenter study. Overall, 32 patients have been successfully implanted (mostly in NYHA Class III; mean age 56 years, ischemic etiology in 69%; prior implantable cardioverter-defibrillator (ICD) in 63%; concomitant beta blocker and angiotensin converting enzyme inhibitor (ACE-I) or angiotensin receptor blocker (ARB) in 100%). Preliminary results confirm feasibility of the study, an acceptable side effect profile and promising preliminary efficacy data. Several mechanisms may contribute to the beneficial effect observed in patients with heart failure. Should these results be confirmed in larger controlled studies, chronic vagal stimulation could be a further treatment option for CHF patients, possibly integrated with defibrillator and resynchronization therapies. PMID:19964772

  11. Cardiorenal Syndrome in Acute Heart Failure: Revisiting Paradigms.

    PubMed

    Nez, Julio; Miana, Gema; Santas, Enrique; Bertomeu-Gonzlez, Vicente

    2015-05-01

    Cardiorenal syndrome has been defined as the simultaneous dysfunction of both the heart and the kidney. Worsening renal function that occurs in patients with acute heart failure has been classified as cardiorenal syndrome type 1. In this setting, worsening renal function is a common finding and is due to complex, multifactorial, and not fully understood processes involving hemodynamic (renal arterial hypoperfusion and renal venous congestion) and nonhemodynamic factors. Traditionally, worsening renal function has been associated with worse outcomes, but recent findings have revealed mixed and heterogeneous results, perhaps suggesting that the same phenotype represents a diversity of pathophysiological and clinical situations. Interpreting the magnitude and chronology of renal changes together with baseline renal function, fluid overload status, and clinical response to therapy might help clinicians to unravel the clinical meaning of renal function changes that occur during an episode of heart failure decompensation. In this article, we critically review the contemporary evidence on the pathophysiology and clinical aspects of worsening renal function in acute heart failure. PMID:25758162

  12. Hawthorn Extract Randomized Blinded Chronic Heart Failure (HERB CHF) Trial

    PubMed Central

    Zick, Suzanna M.; Vautaw, Bonnie Motyka; Gillespie, Brenda; Aaronson, Keith D.

    2009-01-01

    Aims Hawthorn's efficacy when added to contemporary evidence-based heart failure therapy is unknown. We aimed to determine whether hawthorn increases submaximal exercise capacity when added to standard medical therapy. Methods and results We performed a randomized, double-blind, placebo-controlled trial in 120 ambulatory patients aged ?18 years with New York Heart Association (NYHA) class II-III chronic heart failure. All patients received conventional medical therapy, as tolerated, and were randomized to either hawthorn 450 mg twice daily or placebo for 6 months. The primary outcome was change in 6 min walk distance at 6 months. Secondary outcomes included quality of life (QOL) measures, peak oxygen consumption, and anaerobic threshold during maximal treadmill exercise testing, NYHA classification, left ventricular ejection fraction (LVEF), neurohormones, and measures of oxidative stress and inflammation. There were no significant differences between groups in the change in 6 min walk distance (P = 0.61), or on measures of QOL, functional capacity, neurohormones, oxidative stress, or inflammation. A modest difference in LVEF favoured hawthorn (P = 0.04). There were significantly more adverse events reported in the hawthorn group (P = 0.02), although most were non-cardiac. Conclusion Hawthorn provides no symptomatic or functional benefit when given with standard medical therapy to patients with heart failure. This trial is registered in ClinicalTrials.gov ID: NCT00343902. PMID:19789403

  13. Heart Rate at Hospital Discharge in Patients With Heart Failure Is Associated With Mortality and Rehospitalization

    PubMed Central

    Laskey, Warren K.; Alomari, Ihab; Cox, Margueritte; Schulte, Phillip J.; Zhao, Xin; Hernandez, Adrian F.; Heidenreich, Paul A.; Eapen, Zubin J.; Yancy, Clyde; Bhatt, Deepak L.; Fonarow, Gregg C.

    2015-01-01

    Background Whether heart rate upon discharge following hospitalization for heart failure is associated with long?term adverse outcomes and whether this association differs between patients with sinus rhythm (SR) and atrial fibrillation (AF) have not been well studied. Methods and Results We conducted a retrospective cohort study from clinical registry data linked to Medicare claims for 46 217 patients participating in Get With The GuidelinesHeart Failure. Cox proportional?hazards models were used to estimate the association between discharge heart rate and all?cause mortality, all?cause readmission, and the composite outcome of mortality/readmission through 1 year. For SR and AF patients with heart rate ?75, the association between heart rate and mortality (expressed as hazard ratio [HR] per 10 beats?per?minute increment) was significant at 0 to 30 days (SR: HR 1.30, 95% CI 1.22 to 1.39; AF: HR 1.23, 95% CI 1.16 to 1.29) and 31 to 365 days (SR: HR 1.15, 95% CI 1.12 to 1.20; AF: HR 1.05, 95% CI 1.01 to 1.08). Similar associations between heart rate and all?cause readmission and the composite outcome were obtained for SR and AF patients from 0 to 30 days but only in the composite outcome for SR patients over the longer term. The HR from 0 to 30 days exceeded that from 31 to 365 days for both SR and AF patients. At heart rates <75, an association was significant for mortality only for both SR and AF patients. Conclusions Among older patients hospitalized with heart failure, higher discharge heart rate was associated with increased risks of death and rehospitalization, with higher risk in the first 30 days and for SR compared with AF. PMID:25904590

  14. Melatonin protects against ischemic heart failure in rats.

    PubMed

    ?ehirli, Ahmet zer; Koyun, Derya; Tetik, ?ermin; zsavc?, Derya; Yi?iner, mer; etinel, ?ule; Tok, Olgu Enis; Kaya, Zehra; Akkiprik, Mustafa; K?l?, Ertugrul; ?ener, Gksel

    2013-09-01

    Ischemic injury, which occurs as a result of sympathetic hyperactivity, plays an important role in heart failure. Melatonin is thought to have antiatherogenic, antioxidant, and vasodilatory effects. In this study, we investigated whether melatonin protects against ischemic heart failure (HF). In Wistar albino rats, HF was induced by left anterior descending (LAD) coronary artery ligation and rats were treated with either vehicle or melatonin (10mg/kg) for 4weeks. At the end of this period, echocardiographic measurements were recorded and the rats were decapitated to obtain plasma and cardiac tissue samples. Lactate dehydrogenase, creatine kinase, aspartate aminotransferase, alanine aminotransferase, and lysosomal enzymes (?-D-glucuronidase, ?-galactosidase, ?-D-N-acetyl-glucosaminidase, acid phosphatase, and cathepsin-D) were studied in plasma samples, while malondialdehyde and glutathione levels and Na+, K+-ATPase, caspase-3 and myeloperoxidase activities were determined in the cardiac samples. Sarco/endoplasmic reticulum calcium ATPase (SERCA) and caveolin-3 levels in cardiac tissues were evaluated using Western blot analyses. Furthermore, caveolin-3 levels were also determined by histological analyses. In the vehicle-treated HF group, cardiotoxicity resulted in decreased cardiac Na+, K+-ATPase and SERCA activities, GSH contents and caveolin-3 levels, while plasma LDH, CK, and lysosomal enzyme activities and cardiac MDA and Myeloperoxidase (MPO) activities were found to be increased. On the other hand, melatonin treatment reversed all the functional and biochemical changes. The present results demonstrate that Mel ameliorates ischemic heart failure in rats. These observations highlight that melatonin is a promising supplement for improving defense mechanisms in the heart against oxidative stress caused by heart failure. PMID:23551402

  15. ST2 and patient prognosis in chronic heart failure.

    PubMed

    Bayes-Genis, Antoni; Zhang, Yuhui; Ky, Bonnie

    2015-04-01

    Biomarkers of cardiovascular diseases are indispensable tools for diagnosis and prognosis, and the use of several biomarkers is now considered the standard of care.New markers continue to be developed, but few prove to be substantially better thanestablished markers. Suppression of tumorigenicity 2 (ST2) is a marker of cardiomyocyte stress and fibrosis that provides incremental value to natriuretic peptides for risk stratification of patients with a wide spectrum of cardiovascular diseases. On the basis of all available data, the 2013 American College of Cardiology and American Heart Association guidelines now recommend measurement of ST2 for additive risk stratification in patients with acute or chronic ambulatory heart failure (HF). This report provides an up-to-date overview of the clinical studies that led to the endorsement of ST2 as a cardiovascular prognostic marker in chronic HF. The presented data suggest that the addition of ST2 to a model that includes established mortality risk factors, including natriuretic peptides, substantially improves the risk stratification for death and HF hospitalization in patients with HF. ST2's prognostic value remains strong even in the subset of patients with renal insufficiency and is superior to other remodeling-fibrosis biomarkers currently being evaluated. In conclusion, these results have been repeatedly validated; thus, ST2 could be rapidly incorporated into clinical practice for risk prediction. Indeed, the body of evidence supporting the use of ST2 in chronic HF stratification continues to grow, with consistent data from cohorts around the world in single-center (Barcelona, Brussels, and San Diego cohorts) and multicenter (Penn Heart Failure Study [PHFS] and Muerte Subita en Insuficiencia Cardiac [MUSIC]) studies and in post hoc studies from clinical trials (Prospective Randomized Amlodipine Survival Evaluation 2 [PRAISE-2], Heart Failure: A Controlled Trial Investigating Outcomes of Exercise Training [HF-ACTION], and Controlled Rosuvastatin Multinational Trial in Heart Failure [CORONA]). PMID:25665758

  16. Comparison of partners-heart failure algorithm vs care alert in remote heart failure management

    PubMed Central

    Calo’, Leonardo; Martino, Annamaria; Tota, Claudia; Fagagnini, Alessandro; Iulianella, Renzo; Rebecchi, Marco; Sciarra, Luigi; Giunta, Giuseppe; Romano, Maria Grazia; Colaceci, Roberto; Ciccaglioni, Antonio; Ammirati, Fabrizio; de Ruvo, Ermenegildo

    2015-01-01

    AIM: To compare the utility of the partners-heart failure (HF) algorithm with the care alert strategy for remote monitoring, in guiding clinical actions oriented to treat impending HF. METHODS: Consecutive cardiac resynchronization-defibrillator recipients were followed with biweekly automatic transmissions. After every transmission, patients received a phone contact in order to check their health status, eventually followed by clinical actions, classified as “no-action”, “non-active” and “active”. Active clinical actions were oriented to treat impending HF. The sensitivity, specificity, positive and negative predictive values and diagnostic accuracy of the partners-HF algorithm vs care alert in determining active clinical actions oriented to treat pre-HF status and to prevent an acute decompensation, were also calculated. RESULTS: The study population included 70 patients with moderate to advanced systolic HF and QRS duration longer than 120 ms. During a mean follow-up of 8 ± 2 mo, 665 transmissions were collected. No deaths or HF hospitalizations occurred. The sensitivity and specificity of the partners-HF algorithm for active clinical actions oriented to treat impending HF were 96.9% (95%CI: 0.96-0.98) and 92.5% (95%CI: 0.90-0.94) respectively. The positive and negative predictive values were 84.6% (95%CI: 0.82-0.87) and 98.6% (95%CI: 0.98-0.99) respectively. The partners-HF algorithm had an accuracy of 93.8% (95%CI: 0.92-0.96) in determining active clinical actions. With regard to active clinical actions, care alert had a sensitivity and specificity of 11.05% (95%CI: 0.09-0.13) and 93.6% respectively (95%CI: 0.92-0.95). The positive predictive value was 42.3% (95%CI: 0.38-0.46); the negative predictive value was 71.1% (95%CI: 0.68-0.74). Care alert had an accuracy of 68.9% (95%CI: 0.65-0.72) in determining active clinical actions. CONCLUSION: The partners-HF algorithm proved higher accuracy and sensitivity than care alert in determining active clinical actions oriented to treat impending HF. Future studies in larger populations should evaluate partners-HF ability to improve HF-related clinical outcomes. PMID:26730298

  17. Bio-Artificial Heart as Ultimate Treatment of End-Stage Heart Failure

    PubMed Central

    Smit, Francis E.; Dohmen, Pascal M.

    2014-01-01

    End-stage heart failure is a major health problem, but implementation of guidelines and optimizing medical therapy for this devastating disease should decrease mortality. If optimal conservative therapy is no longer sufficient, a mechanical support system may be required as final destination therapy or as bridge-to-transplant. Since the first heart transplantation in 1967, this therapy has become the criterion standard for end-stage heart failure, but is limited due to organ shortage. Tissue engineering could help overcome this limitation and provide regeneration, remodeling, and growth potential. This so-called bio-artificial heart would be available, created by a decellularized extracellular matrix and seeded with in vitro proliferated autologous cardiovascular cells. Results of the first experimental studies have been promising, but numerous challenges must be met before this procedure will be available. PMID:25321347

  18. Quality of Life After Bypass Surgery in Patients with Chest Pain and Heart Failure

    MedlinePLUS

    ... Bypass Surgery in Patients With Chest Pain and Heart Failure The full report is titled “Quality-of-Life ... in patients who have coronary artery disease plus heart failure, which can cause additional symptoms, such as shortness ...

  19. Drug Does Not Improve Set of Cardiovascular Outcomes for Diastolic Heart Failure

    MedlinePLUS

    ... not improve set of cardiovascular outcomes for diastolic heart failure NIH-supported study finds drug does appear to reduce hospitalizations for diastolic heart failure. A drug that blocks the action of a ...

  20. Risks and benefits of weight loss in heart failure.

    PubMed

    Lavie, Carl J; Alpert, Martin A; Ventura, Hector O

    2015-01-01

    Obesity adversely affects many cardiovascular disease (CVD) risk factors and increases the risk of most CVD, including heart failure (HF). HF is markedly increased in the setting of obesity. However, obese patients with HF have a better prognosis than lean patients with HF, which has been termed the obesity paradox. Therefore, the role of weight loss, which generally improves ventricular structure, systolic and diastolic ventricular function, and New York Heart Association functional class in HF, remains controversial. This article discusses the pros and cons of weight loss and differentiates purposeful (healthy) from nonpurposeful (unhealthy) weight loss. PMID:25432481

  1. Novel molecular mechanisms and regeneration therapy for heart failure.

    PubMed

    Oka, Toru; Morita, Hiroyuki; Komuro, Issei

    2016-03-01

    Heart failure (HF) is one of the leading causes of mortality in the world. Various molecular mechanisms have been proposed for HF, but its precise mechanisms are still largely unknown. In this review, summarizing the "President's Distinguished Lecture Award" of XX World Congress of International Society for Heart Research 2010 in Kyoto, Japan, we introduce recent our studies on HF, including 1) p53-induced suppression of Hif-1-induced angiogenesis as a novel mechanism of HF, 2) angiogenesis as a potential therapeutic strategy for HF, and 3) IGFBP-4 as a novel factor for cardiomyogenesis by inhibiting canonical Wnt signaling. PMID:26829118

  2. The role of coronary artery disease in heart failure.

    PubMed

    Lala, Anuradha; Desai, Akshay S

    2014-04-01

    Enhanced survival following acute myocardial infarction and the declining prevalence of hypertension and valvular heart disease as contributors to incident heart failure (HF) have fueled the emergence of coronary artery disease (CAD) as the primary risk factor for HF development. Despite the acknowledged role of CAD in the development of HF, the role of coronary revascularization in reducing HF-associated morbidity and mortality remains controversial. The authors review key features of the epidemiology and pathophysiology of CAD in patients with HF as well as the emerging data from recent clinical trials that inform the modern approach to management. PMID:24656111

  3. Heart failure in elderly patients: distinctive features and unresolved issues

    PubMed Central

    Lazzarini, Valentina; Mentz, Robert J.; Fiuzat, Mona; Metra, Marco; O'Connor, Christopher M.

    2013-01-01

    The prevalence of heart failure (HF) increases with age. While clinical trials suggest that contemporary evidence-based HF therapies have reduced morbidity and mortality, these trials largely excluded the elderly. Questions remain regarding the clinical characteristics of elderly HF patients and the impact of contemporary therapies on their outcomes. This review presents the epidemiology of HF in the elderly and summarizes the data on the pathophysiology of the ageing heart. The clinical characteristics, treatment patterns, and outcomes of elderly HF patients are explored. Finally, the main gaps regarding HF therapies in the elderly and the opportunities for future trials are highlighted. PMID:23429975

  4. Pimobendan and its use in treating canine congestive heart failure.

    PubMed

    Bowles, Danielle; Fry, Darren

    2011-11-01

    Pimobendan, a calcium sensitizer and phosphodiesterase III inhibitor, has positive inotropic and vasodilatory properties. Its use in patients with naturally occurring congestive heart failure (CHF) has been studied in a number of blinded, randomized, multicenter clinical trials. It has been shown to improve quality of life, reduce heart insufficiency scores, and increase median survival times for patients with CHF due to dilated cardiomyopathy and myxomatous valvular disease. Although most studies have reported positive findings, some potential adverse effects have also been described. Studies are under way to further evaluate the effects of this novel positive inotrope and vasodilator in canine cardiac disease. PMID:22101450

  5. Effects of Personal Exposure to Ambient Fine Particulate Matter on Acute Change in Nocturnal Heart Rate Variability in Subjects Without Overt Heart Disease.

    PubMed

    Lee, Mi-Sun; Eum, Ki-Do; Rodrigues, Ema G; Magari, Shannon R; Fang, Shona C; Modest, Geoffrey A; Christiani, David C

    2016-01-01

    The immediate effect within minutes to hours of personal exposure to ambient fine particulate matter (PM2.5) on cardiac autonomic function is limited, particularly at night. Our study aimed to assess the lagged association between personal exposure to PM2.5 and nocturnal heart rate variability. Repeated measures panel study among 21 community adults recruited from a local health clinic during the period of March 1, 2004, to August 31, 2004, in Boston, Massachusetts, in the United States. Ambulatory electrocardiogram and continuous monitoring of personal exposure to PM2.5 and were measured for up to 2 consecutive days. We calculated 5-minute time-specific average PM2.5 exposure for each participant. Mixed-effects models were fit for 5-minute SD of normal-to-normal intervals (SDNN) and 5-minute heart rate in relation to 5-minute PM2.5 exposure lagged in 5-minute intervals up to 4hours. We found an 8.4% decrease in nocturnal SDNN (95% confidence interval [CI]-11.3% to-5.5%) and a 1.9% increase in nighttime heart rate (95% CI 1.1% to 2.7%) for an interquartile range increase in PM2.5 (13.6?g/m(3)), after adjusting for confounders. Significant decreases in nocturnal SDNN associated with PM2.5 exposure occurred within 2.5hours. The largest decrease in nocturnal SDNN of-12.8% (95% CI-16.4 to-9.1%) that was associated with PM2.5 exposure wasfound with a lag of 25minutes. Rapid changes in nocturnal heart rate variability associated with personal PM2.5 exposure occurred within the previous 2.5hours, with the largest effects at25minutes, suggesting immediate cardiac autonomic effects of fine particulate exposure. PMID:26552502

  6. The landscape of DNA repeat elements in human heart failure

    PubMed Central

    2012-01-01

    Background The epigenomes of healthy and diseased human hearts were recently examined by genome-wide DNA methylation profiling. Repetitive elements, heavily methylated in post-natal tissue, have variable methylation profiles in cancer but methylation of repetitive elements in the heart has never been examined. Results We analyzed repetitive elements from all repeat families in human myocardial samples, and found that satellite repeat elements were significantly hypomethylated in end-stage cardiomyopathic hearts relative to healthy normal controls. Satellite repeat elements are almost always centromeric or juxtacentromeric, and their overexpression correlates with disease aggressiveness in cancer. Similarly, we found that hypomethylation of satellite repeat elements correlated with up to 27-fold upregulation of the corresponding transcripts in end-stage cardiomyopathic hearts. No other repeat family exhibited differential methylation between healthy and cardiomyopathic hearts, with the exception of the Alu element SINE1/7SL, for which a modestly consistent trend of increased methylation was observed. Conclusions Satellite repeat element transcripts, a form of non-coding RNA, have putative functions in maintaining genomic stability and chromosomal integrity. Further studies will be needed to establish the functional significance of these non-coding RNAs in the context of heart failure. PMID:23034148

  7. Lifestyle modification with diet and exercise in obese patients with heart failure - A pilot study

    Technology Transfer Automated Retrieval System (TEKTRAN)

    There is a paucity of data regarding intentional weight loss in obese heart failure patients. This study sought to ascertain the safety and effectiveness of a lifestyle modification program in patients with systolic heart failure and metabolic syndrome. Patients (n=20) with systolic heart failure (e...

  8. Pathophysiology and clinical evaluation of acute heart failure.

    PubMed

    Mentz, Robert J; O'Connor, Christopher M

    2016-01-01

    Acute heart failure (AHF) is a complex syndrome characterized by worsening heart failure (HF) symptoms that requires escalation of therapy. Intrinsic cardiac abnormalities and comorbid conditions, including lung and renal disease, and sleep-disordered breathing, can contribute to the development of AHF. In this Review, we summarize and discuss the literature on the clinical evaluation and underlying pathophysiology of AHF. Important features of AHF evaluation include identification of precipitating factors to the disease, and assessment of circulatory-renal limitations associated with use of HF medications, prior HF hospitalizations, congestion and perfusion profiles, and end-organ dysfunction. The pathophysiological contributions of endothelial dysfunction, neurohormonal activation, venous congestion, and myocardial injury to the development of AHF are also discussed. These potential causative mechanisms provide a framework for clinicians to evaluate and manage patients with AHF and highlight possible future targets for therapies designed to improve clinical outcomes. PMID:26370473

  9. Heart Failure with Preserved Ejection Fraction: Persistent Diagnosis, Therapeutic Enigma

    PubMed Central

    Bhuiyan, Taslima

    2011-01-01

    Heart failure with preserved ejection fraction (HFPEF) is increasing in prevalence with the aging of the population, and morbidity and mortality rates are comparable to that of heart failure with reduced ejection fraction (HFREF). The diagnosis can be difficult to make, especially in older adults, stemming from the presence of multiple comorbid illnesses with confounding symptoms. New diagnostic tools have resulted in guidelines proposed to define and diagnose HFPEF. Recent literature focusing on the pathophysiology underlying this disease suggests multiple mechanisms are involved in the generation of the phenotype, such as abnormal relaxation and ventricular-vascular coupling, chronotropic incompetence, volume overload, and redistribution and /or endothelial dysfunction. Currently, no clinically proven treatments are shown to decrease morbidity and mortality in this population; however, there may be a novel multidisciplinary and multistage treatment strategy that can be studied to address this complex disease which incorporates pharmacologic and non-pharmacologic therapeutics. PMID:22081782

  10. Update on heart failure with preserved ejection fraction

    PubMed Central

    Hummel, Scott L.; Kitzman, Dalane W.

    2013-01-01

    Heart failure with preserved ejection fraction (HFPEF) is the most common form of heart failure (HF) in older adults, and is increasing in prevalence as the population ages. Morbidity and long-term mortality in HFPEF are substantial and can be similar to HF with reduced ejection fraction (HFREF), yet HFPEF therapy remains empirical and treatment guidelines are based primarily on expert consensus. Neurohormonal blockade has revolutionized the management of HFREF, but trials in HFPEF based on this strategy have been disappointing to date. However, many recent studies have increased knowledge about HFPEF. The concept of HFPEF has evolved from a cardio-centric model to a syndrome that may involve multiple cardiovascular and non-cardiovascular mechanisms. Emerging data highlight the importance of non-pharmacological management strategies and assessment of non-cardiovascular comorbidities. Animal models, epidemiological cohorts, and small human studies suggest that oxidative stress and inflammation contribute to HFPEF, potentially leading to development of new therapeutic targets. PMID:24860638

  11. Novelties in the early management of acute heart failure syndromes.

    PubMed

    Salem, Reda; Sibellas, Franck; Socrates, Thenral; Arenja, Nisha; Yilmaz, Mehmet Birhan; Mueller, Christian; Mebazaa, Alexandre

    2010-01-01

    The recent European Society of Cardiology (ESC) guidelines delineate the diagnosis and management of distinct categories of acute heart failure syndromes. However, physicians dealing with these patients may need guidance in choosing therapeutic alternatives as soon as the dyspneic patient arrives at the emergency department, until distinct categories of the ESC guidelines are identified. Hence, this manuscript summarizes practical recommendations for the very early management of patients with acute heart failure syndromes. The recommendations are based on a clinical classification system considering the initial systolic blood pressure and other symptoms. Early initiation of diagnostic and goal-directed treatment strategies are key factors in improving patient outcomes. Early and frequent reassessment is also imperative so that adjustments to the initial therapeutic approach can be made, as clinically indicated. PMID:20407961

  12. Targeting Cardiomyocyte Ca2+ Homeostasis in Heart Failure

    PubMed Central

    Re, smund T.; Frisk, Michael; Louch, William E.

    2015-01-01

    Improved treatments for heart failure patients will require the development of novel therapeutic strategies that target basal disease mechanisms. Disrupted cardiomyocyte Ca2+ homeostasis is recognized as a major contributor to the heart failure phenotype, as it plays a key role in systolic and diastolic dysfunction, arrhythmogenesis, and hypertrophy and apoptosis signaling. In this review, we outline existing knowledge of the involvement of Ca2+ homeostasis in these deficits, and identify four promising targets for therapeutic intervention: the sarcoplasmic reticulum Ca2+ ATPase, the Na+-Ca2+ exchanger, the ryanodine receptor, and t-tubule structure. We discuss experimental data indicating the applicability of these targets that has led to recent and ongoing clinical trials, and suggest future therapeutic approaches. PMID:25483944

  13. [Mitochondrial dynamics: a potential new therapeutic target for heart failure].

    PubMed

    Kuzmicic, Jovan; Del Campo, Andrea; Lpez-Crisosto, Camila; Morales, Pablo E; Pennanen, Christian; Bravo-Sagua, Roberto; Hechenleitner, Jonathan; Zepeda, Ramiro; Castro, Pablo F; Verdejo, Hugo E; Parra, Valentina; Chiong, Mario; Lavandero, Sergio

    2011-10-01

    Mitochondria are dynamic organelles able to vary their morphology between elongated interconnected mitochondrial networks and fragmented disconnected arrays, through events of mitochondrial fusion and fission, respectively. These events allow the transmission of signaling messengers and exchange of metabolites within the cell. They have also been implicated in a variety of biological processes including embryonic development, metabolism, apoptosis, and autophagy. Although the majority of these studies have been confined to noncardiac cells, emerging evidence suggests that changes in mitochondrial morphology could participate in cardiac development, the response to ischemia-reperfusion injury, heart failure, and diabetes mellitus. In this article, we review how the mitochondrial dynamics are altered in different cardiac pathologies, with special emphasis on heart failure, and how this knowledge may provide new therapeutic targets for treating cardiovascular diseases. PMID:21820793

  14. Systems Biology Applied to Heart Failure With Normal Ejection Fraction

    PubMed Central

    Mesquita, Evandro Tinoco; Jorge, Antonio Jose Lagoeiro; de Souza, Celso Vale; Cassino, Joo Paulo Pedroza

    2014-01-01

    Heart failure with normal ejection fraction (HFNEF) is currently the most prevalent clinical phenotype of heart failure. However, the treatments available have shown no reduction in mortality so far. Advances in the omics sciences and techniques of high data processing used in molecular biology have enabled the development of an integrating approach to HFNEF based on systems biology. This study aimed at presenting a systems-biology-based HFNEF model using the bottom-up and top-down approaches. A literature search was conducted for studies published between 1991 and 2013 regarding HFNEF pathophysiology, its biomarkers and systems biology. A conceptual model was developed using bottom-up and top-down approaches of systems biology. The use of systems-biology approaches for HFNEF, a complex clinical syndrome, can be useful to better understand its pathophysiology and to discover new therapeutic targets. PMID:24918915

  15. Vasopressin receptor antagonists, heart failure, and polycystic kidney disease.

    PubMed

    Torres, Vicente E

    2015-01-01

    The synthesis of nonpeptide orally bioavailable vasopressin antagonists devoid of agonistic activity (vaptans) has made possible the selective blockade of vasopressin receptor subtypes for therapeutic purposes. Vaptans acting on the vasopressin V2 receptors (aquaretics) have attracted attention as a possible therapy for heart failure and polycystic kidney disease. Despite a solid rationale and encouraging preclinical testing, aquaretics have not improved clinical outcomes in randomized clinical trials for heart failure. Additional clinical trials with select population targets, more flexible dosing schedules, and possibly a different drug type or combination (balanced V1a/V2 receptor antagonism) may be warranted. Aquaretics are promising for the treatment of autosomal dominant polycystic kidney disease and have been approved in Japan for this indication. More studies are needed to better define their long-term safety and efficacy and optimize their utilization. PMID:25493947

  16. The risk of heart failure and cardiometabolic complications in obesity may be masked by an apparent healthy status of normal blood glucose.

    PubMed

    Tiwari, Shuchita; Mishra, Manish; Jadhav, Ashok; Gerger, Courtney; Lee, Paul; Weber, Lynn; Ndisang, Joseph Fomusi

    2013-01-01

    Although many obese individuals are normoglycemic and asymptomatic of cardiometabolic complications, this apparent healthy state may be a misnomer. Since heart failure is a major cause of mortality in obesity, we investigated the effects of heme-oxygenase (HO) on heart failure and cardiometabolic complications in obese normoglycemic Zucker-fatty rats (ZFs). Treatment with the HO-inducer, hemin, reduced markers of heart failure, such as osteopontin and osteoprotegerin, abated left-ventricular (LV) hypertrophy/fibrosis, extracellular matrix/profibrotic proteins including collagen IV, fibronectin, TGF-?1, and reduced cardiac lesions. Furthermore, hemin suppressed inflammation by abating macrophage chemoattractant protein-1, macrophage-inflammatory protein-1 alpha, TNF-?, IL-6, and IL-1? but enhanced adiponectin, atrial-natriuretic peptide (ANP), HO activity, insulin sensitivity, and glucose metabolism. Correspondingly, hemin improved several hemodynamic/echocardiographic parameters including LV-diastolic wall thickness, LV-systolic wall thickness, mean-arterial pressure, arterial-systolic pressure, arterial-diastolic pressure, LV-developed pressure, +dP/dt, and cardiac output. Contrarily, the HO-inhibitor, stannous mesoporphyrin nullified the hemin effect, exacerbating inflammatory/oxidative insults and aggravated insulin resistance (HOMA-index). We conclude that perturbations in insulin signaling and cardiac function may be forerunners to overt hyperglycemia and heart failure in obesity. Importantly, hemin improves cardiac function by suppressing markers of heart failure, LV hypertrophy, cardiac lesions, extracellular matrix/profibrotic proteins, and inflammatory/oxidative mediators, while concomitantly enhancing the HO-adiponectin-ANP axis. PMID:24454978

  17. The Risk of Heart Failure and Cardiometabolic Complications in Obesity May Be Masked by an Apparent Healthy Status of Normal Blood Glucose

    PubMed Central

    Tiwari, Shuchita; Mishra, Manish; Jadhav, Ashok; Gerger, Courtney; Lee, Paul; Weber, Lynn

    2013-01-01

    Although many obese individuals are normoglycemic and asymptomatic of cardiometabolic complications, this apparent healthy state may be a misnomer. Since heart failure is a major cause of mortality in obesity, we investigated the effects of heme-oxygenase (HO) on heart failure and cardiometabolic complications in obese normoglycemic Zucker-fatty rats (ZFs). Treatment with the HO-inducer, hemin, reduced markers of heart failure, such as osteopontin and osteoprotegerin, abated left-ventricular (LV) hypertrophy/fibrosis, extracellular matrix/profibrotic proteins including collagen IV, fibronectin, TGF-?1, and reduced cardiac lesions. Furthermore, hemin suppressed inflammation by abating macrophage chemoattractant protein-1, macrophage-inflammatory protein-1 alpha, TNF-?, IL-6, and IL-1? but enhanced adiponectin, atrial-natriuretic peptide (ANP), HO activity, insulin sensitivity, and glucose metabolism. Correspondingly, hemin improved several hemodynamic/echocardiographic parameters including LV-diastolic wall thickness, LV-systolic wall thickness, mean-arterial pressure, arterial-systolic pressure, arterial-diastolic pressure, LV-developed pressure, +dP/dt, and cardiac output. Contrarily, the HO-inhibitor, stannous mesoporphyrin nullified the hemin effect, exacerbating inflammatory/oxidative insults and aggravated insulin resistance (HOMA-index). We conclude that perturbations in insulin signaling and cardiac function may be forerunners to overt hyperglycemia and heart failure in obesity. Importantly, hemin improves cardiac function by suppressing markers of heart failure, LV hypertrophy, cardiac lesions, extracellular matrix/profibrotic proteins, and inflammatory/oxidative mediators, while concomitantly enhancing the HO-adiponectin-ANP axis. PMID:24454978

  18. Cellular cardiomyoplasty for a patient with heart failure

    SciTech Connect

    Zhang Fumin; Chen Yijiang; Yang Zhijian; Gao Xiang; Ma Wenzhu; Li Chuanfu; Kao, Race L

    2003-03-01

    Background: A 73-year-old man with a history of myocardial infarction and hypertension for 5 years suffered heart failure (NYHA III-IV). Methods: 2D echo indicated hypokinesia at septal, left ventricular anterior wall and apical regions. Coronary angiograms demonstrated 60% stenosis in distal left main and 99% stenosis in proximal and distal left anterior descending coronary arteries (LAD). Both proximal artery and middle left circumflex coronary artery (LC) had 90% stenosis, and diffuse stenosis of right coronary artery (RC) was found. Myocardial perfusion imaging using {sup 99m}Tc-MIBI indicated defective perfusion of left ventricular apex, anterior wall and septal region and severe reduced perfusion of posterior inferior wall. Myocardial metabolic activities ({sup 18}F-deoxyglucose) also showed comparable reductions. After exposing the heart, LAD, LC, and RC were all completely occluded and bypass procedure could not be completed. Autologous satellite cells were implanted without any complication and the patient had an uneventful recovery. Results: During the first 2 months, he remained in heart failure, and by the third month, he gradually improved and reached NYHA II. At fifth month after the procedure, significant increased ejection fraction (37.1-48.6%) and wall movement with modest reduction of left ventricular systolic diameter (48-45 mm) were observed. Imaging with {sup 18}F-deoxyglucose showed dramatic improvement in myocardial metabolic activity with similar improvement in myocardial perfusion ({sup 99m}Tc-MIBI). Conclusion: This is the first successful case of cellular cardiomyoplasty without any conjunctional procedure for patient with severe coronary heart disease and heart failure.

  19. Heart failure with preserved ejection fraction: uncertainties and dilemmas.

    PubMed

    Ferrari, Roberto; Bhm, Michael; Cleland, John G F; Paulus, Walter J S; Pieske, Burkert; Rapezzi, Claudio; Tavazzi, Luigi

    2015-07-01

    Many uncertainties surround the syndrome of heart failure with preserved ejection fraction (HFpEF), which was the topic reviewed in an Expert Meeting at the University of Ferrara. This concluded that the absence of clear diagnostic clinical criteria was the major barrier to progress. There was general agreement that symptoms or signs of heart failure, normal LVEF despite an elevated plasma concentration of natriuretic peptides, and signs of abnormal LV relaxation, LV filling, LV hypertrophy, or left atrial enlargement, or diastolic dysfunction supported the diagnosis. However, HFpEF, like all heart failure syndromes, is heterogeneous in aetiology and pathophysiology, rather than being a single disease. HFpEF may account for about half of all patients with heart failure. The classical risk factors for developing HFpEF include age and co-morbidities, notably hypertension, atrial fibrillation, and the metabolic syndrome. When complicated by increasing congestion requiring hospital admission, the prognosis is poor; 30% or more of patients will die within 1 year (nearly two-thirds die from cardiovascular causes). Patients with chronic stable symptoms have a much better prognosis. Despite many clinical trials, there is no solid evidence that any treatment alters the natural history of HFpEF. Several treatments have shown promising early results and are now being tested in substantial randomized clinical trials. Further basic research is required to better characterize the disease and accelerate progress. Our review highlights the many difficulties encountered in performing randomized clinical trials in HFpEF, often due to difficulties in characterizing HFpEF itself. PMID:26079097

  20. Novel device-based interventional strategies for advanced heart failure.

    PubMed

    Toth, Gabor G; Vanderheyden, Marc; Bartunek, Jozef

    2016-01-01

    While heart failure is one of the leading causes of mortality and morbidity, our tools to provide ultimate treatment solutions are still limited. Recent developments in new devices are designed to fill this therapeutic gap. The scope of this review is to focus on two particular targets, namely (1) left ventricular geometric restoration and (2) atrial depressurization. (1) Reduction of the wall stress by shrinking the ventricular cavity has been traditionally attempted surgically. Recently, the Parachute device (CardioKinetix Inc., Menlo Park, CA, USA) has been introduced to restore ventricular geometry and cardiac mechanics. The intervention aims to partition distal dysfunctional segments that are non-contributory to the ventricular mechanics and forward cardiac output. (2) Diastolic heart failure is characterized by abnormal relaxation and chamber stiffness. The main therapeutic goal achieved should be the reduction of afterload and diastolic pressure load. Recently, new catheter-based approaches were proposed to reduce left atrial pressure and ventricular decompression: the InterAtrial Shunt Device (IASD™) (Corvia Medical Inc., Tewksbury, MA, USA) and the V-Wave Shunt (V-Wave Ltd, Or Akiva, Israel). Both are designed to create a controlled atrial septal defect in symptomatic patients with heart failure. While the assist devices are aimed at end-stage heart failure, emerging device-based percutaneous or minimal invasive techniques comprise a wide spectrum of innovative concepts that target ventricular remodeling, cardiac contractility or neuro-humoral modulation. The clinical adoption is in the early stages of the initial feasibility and safety studies, and clinical evidence needs to be gathered in appropriately designed clinical trials. PMID:26966444

  1. Macro- and micronutrients in African-Americans with heart failure.

    PubMed

    Bhattacharya, Syamal K; Ahokas, Robert A; Carbone, Laura D; Newman, Kevin P; Gerling, Ivan C; Sun, Yao; Weber, Karl T

    2006-03-01

    An emerging body of evidence suggests secondary hyperparathyroidism (SHPT) may be an important covariant of congestive heart failure (CHF), especially in African-Americans (AA) where hypovitaminosis D is prevalent given that melanin, a natural sunscreen, mandates prolonged exposure of skin to sunlight and where a housebound lifestyle imposed by symptomatic CHF limits outdoor activities and hence sunlight exposure. In addition to the role of hypovitaminosis D in contributing to SHPT is the increased urinary and fecal losses of macronutrients Ca(2+) and Mg(2+) associated with the aldosteronism of CHF and their heightened urinary losses with furosemide treatment of CHF. Thus, a precarious Ca(2+) balance seen with reduced serum 25(OH)D is further compromised when AA develop CHF with circulating RAAS activation and are then treated with a loop diuretic. SHPT accounts for a paradoxical Ca(2+) overloading of diverse tissues and the induction of oxidative stress at these sites which spills over to the systemic circulation. In addition to SHPT, hypozincemia and hyposelenemia have been found in AA with compensated and decompensated heart failure and where an insufficiency of these micronutrients may have its origins in inadequate dietary intake, altered rates of absorption or excretion and/or tissue redistribution, and treatment with an ACE inhibitor or AT(1) receptor antagonist. Zn and Se deficiencies, which compromise the activity of several endogenous antioxidant defenses, could prove contributory to the severity of heart failure and its progressive nature. These findings call into question the need for nutriceutical treatment of heart failure and which is complementary to today's pharmaceuticals, especially in AA. PMID:16819577

  2. Novel device-based interventional strategies for advanced heart failure

    PubMed Central

    Vanderheyden, Marc; Bartunek, Jozef

    2016-01-01

    While heart failure is one of the leading causes of mortality and morbidity, our tools to provide ultimate treatment solutions are still limited. Recent developments in new devices are designed to fill this therapeutic gap. The scope of this review is to focus on two particular targets, namely (1) left ventricular geometric restoration and (2) atrial depressurization. (1) Reduction of the wall stress by shrinking the ventricular cavity has been traditionally attempted surgically. Recently, the Parachute device (CardioKinetix Inc., Menlo Park, CA, USA) has been introduced to restore ventricular geometry and cardiac mechanics. The intervention aims to partition distal dysfunctional segments that are non-contributory to the ventricular mechanics and forward cardiac output. (2) Diastolic heart failure is characterized by abnormal relaxation and chamber stiffness. The main therapeutic goal achieved should be the reduction of afterload and diastolic pressure load. Recently, new catheter-based approaches were proposed to reduce left atrial pressure and ventricular decompression: the InterAtrial Shunt Device (IASD™) (Corvia Medical Inc., Tewksbury, MA, USA) and the V-Wave Shunt (V-Wave Ltd, Or Akiva, Israel). Both are designed to create a controlled atrial septal defect in symptomatic patients with heart failure. While the assist devices are aimed at end-stage heart failure, emerging device-based percutaneous or minimal invasive techniques comprise a wide spectrum of innovative concepts that target ventricular remodeling, cardiac contractility or neuro-humoral modulation. The clinical adoption is in the early stages of the initial feasibility and safety studies, and clinical evidence needs to be gathered in appropriately designed clinical trials. PMID:26966444

  3. Homoarginine, heart failure, and sudden cardiac death in haemodialysis patients

    PubMed Central

    Drechsler, Christiane; Meinitzer, Andreas; Pilz, Stefan; Krane, Vera; Tomaschitz, Andreas; Ritz, Eberhard; Mrz, Winfried; Wanner, Christoph

    2011-01-01

    Aims Sudden cardiac death (SCD) is a major contributor to the excess mortality of patients on maintenance dialysis. Homoarginine deficiency may lead to decreased nitric oxide availability and endothelial dysfunction. Based on this rationale we assessed whether homoarginine deficiency is a risk factor for SCD in dialysis patients. Methods and results This study examined the association of homoarginine with cardiovascular outcomes in 1255 diabetic haemodialysis patients from the German diabetes and dialysis study. During a median of 4 years of follow-up, hazard ratios (HR) (95% CI) for reaching the following pre-specified, adjudicated endpoints were determined: SCD, myocardial infarction, stroke, death due to heart failure, and combined cardiovascular events. There was a strong association of low homoarginine concentrations with the presence of congestive heart failure and left ventricular hypertrophy as well as increased levels of brain natriuretic peptide. Per unit decrease in homoarginine, the risk of SCD increased three-fold (HR 3.1, 95% CI 2.04.9), attenuating slightly in multivariate models (HR 2.4; 95% CI 1.53.9). Patients in the lowest homoarginine quintile experienced a more than two-fold increased risk of SCD, and more than three-fold increased risk of heart failure death than patients in the highest quintile, which accounted for the high incidence of combined cardiovascular events. Low homoarginine showed a trend towards increased risk of stroke, however, myocardial infarction was not meaningfully affected. Conclusion Low homoarginine is a strong risk factor for SCD and death due to heart failure in haemodialysis patients. Further studies are needed to elucidate the underlying mechanisms, offering the potential to develop new interventional strategies. PMID:21791541

  4. UT-A urea transporter protein in heart: increased abundance during uremia, hypertension, and heart failure.

    PubMed

    Duchesne, R; Klein, J D; Velotta, J B; Doran, J J; Rouillard, P; Roberts, B R; McDonough, A A; Sands, J M

    2001-07-20

    Urea transporters have been cloned from kidney medulla (UT-A) and erythrocytes (UT-B). We determined whether UT-A proteins could be detected in heart and whether their abundance was altered by uremia or hypertension or in human heart failure. In normal rat heart, bands were detected at 56, 51, and 39 kDa. In uremic rats, the abundance of the 56-kDa protein increased 1.9-fold compared with pair-fed, sham-operated rats, whereas the 51- and 39-kDa proteins were unchanged. We also detected UT-A2 mRNA in hearts from control and uremic rats. Because uremia is accompanied by hypertension, the effects of hypertension per se were studied in uninephrectomized deoxycorticosterone acetate salt-treated rats, where the abundance of the 56-kDa protein increased 2-fold versus controls, and in angiotensin II-infused rats, where the abundance of the 56 kDa protein increased 1.8-fold versus controls. The 51- and 39-kDa proteins were unchanged in both hypertensive models. In human left ventricle myocardium, UT-A proteins were detected at 97, 56, and 51 kDa. In failing left ventricle (taken at transplant, New York Heart Association class IV), the abundance of the 56-kDa protein increased 1.4-fold, and the 51-kDa protein increased 4.3-fold versus nonfailing left ventricle (donor hearts). We conclude that (1) multiple UT-A proteins are detected in rat and human heart; (2) the 56-kDa protein is upregulated in rat heart in uremia or models of hypertension; and (3) the rat results can be extended to human heart, where 56- and 51-kDa proteins are increased during heart failure. PMID:11463720

  5. Patient Selection for Advanced Heart Failure Therapy Referral

    PubMed Central

    Fanaroff, Alexander C.; DeVore, Adam D.; Mentz, Robert J.; Daneshmand, Mani A.; Patel, Chetan B.

    2014-01-01

    Despite advances in medical therapy for chronic heart failure (HF), advanced HF carries a dismal prognosis. Options such as transplantation and durable mechanical circulatory support have greatly improved outcomes for these patients, but their introduction has introduced signifcant complexity to patient management. Although much of this management occurs at specialized heart transplant centers, it is the responsibility of the primary cardiologist of the patient with advanced HF to refer patients at the appropriate time and to help them navigate the difficult decisions related to the pursuit of advanced therapies. We present a unique pathway that incorporates guidelines, recent data, and expert opinion to help general cardiologists determine which patients should be referred for transplantation or durable mechanical circulatory support, and when they should be referred. Decision making on referral to the heart transplant center is also summarized. PMID:24526143

  6. The Adrenergic Nervous System in Heart Failure: Pathophysiology and Therapy

    PubMed Central

    Lymperopoulos, Anastasios; Rengo, Giuseppe; Koch, Walter J.

    2013-01-01

    Heart failure (HF), the leading cause of death in the western world, develops when a cardiac injury or insult impairs the ability of the heart to pump blood and maintain tissue perfusion. It is characterized by a complex interplay of several neurohormonal mechanisms that get activated in the syndrome in order to try and sustain cardiac output in the face of decompensating function. Perhaps the most prominent among these neurohormonal mechanisms is the adrenergic (or sympathetic) nervous system (ANS), whose activity and outflow are enormously elevated in HF. Acutely, and if the heart works properly, this activation of the ANS will promptly restore cardiac function. However, if the cardiac insult persists over time, chances are the ANS will not be able to maintain cardiac function, the heart will progress into a state of chronic decompensated HF, and the hyperactive ANS will continue to “push” the heart to work at a level much higher than the cardiac muscle can handle. From that point on, ANS hyperactivity becomes a major problem in HF, conferring significant toxicity to the failing heart and markedly increasing its morbidity and mortality. The present review discusses the role of the ANS in cardiac physiology and in HF pathophysiology, the mechanisms of regulation of ANS activity and how they go awry in chronic HF, methods of measuring ANS activity in HF, the molecular alterations in heart physiology that occur in HF along with their pharmacological and therapeutic implications, and, finally, drugs and other therapeutic modalities used in HF treatment that target or affect the ANS and its effects on the failing heart. PMID:23989716

  7. Beta-blocker titration failure is independent of severity of heart failure.

    PubMed

    Anthonio, R L; van Veldhuisen, D J; Breekland, A; Crijns, H J; van Gilst, W H

    2000-02-15

    In the present study, predictors of complicated initiation of beta blockade in patients with idiopathic dilated cardiomyopathy was studied. We found that generally accepted measures of severity of heart failure are not predictable, whereas low systolic blood pressure (< or =120 mm Hg) was the strongest predictor for problematic (up)titration. PMID:10728963

  8. Advanced Therapies For End-Stage Heart Failure

    PubMed Central

    Katz, Jason N; Waters, Sarah B; Hollis, Ian B; Chang, Patricia P

    2015-01-01

    Management of the advanced heart failure patient can be complex. Therapies include cardiac transplantation and mechanical circulatory support, as well inotropic agents for the short-term. Despite a growing armamentarium of resources, the clinician must carefully weigh the risks and benefits of each therapy to develop an optimal treatment strategy. While cardiac transplantation remains the only true “cure” for end-stage disease, this resource is limited and the demand continues to far outpace the supply. For patients who are transplant-ineligible or likely to succumb to their illness prior to transplant, ventricular assist device therapy has now become a viable option for improving morbidity and mortality. Particularly for the non-operative pa-tient, intravenous inotropes can be utilized for symptom control. Regardless of the treatments considered, care of the heart failure patient requires thoughtful dialogue, multidisciplinary collaboration, and individualized care. While survival is important, most patients covet quality of life above all outcomes. An often overlooked component is the patient’s control over the dying process. It is vital that clinicians make goals-of-care discussions a priority when seeing patients with advanced heart failure. The use of palliative care consultation is well-validated and facilitates these difficult conversations to ensure that all patient needs are ultimately met. PMID:24251460

  9. Iron Deficiency in Heart Failure: A Practical Guide

    PubMed Central

    Ebner, Nicole; von Haehling, Stephan

    2013-01-01

    Iron is an element necessary for cells due to its capacity of transporting oxygen and electrons. One of the important co-morbidities in heart failure is iron deficiency. Iron has relevant biological functions, for example, the formation of haemoglobin, myoglobin and numerous enzymatic groups. The prevalence of iron deficiency increases with the severity of heart failure. For a long time, the influence of iron deficiency was underestimated especially in terms of worsening of cardiovascular diseases and of developing anaemia. In recent years, studies with intravenous iron agents in patients with iron deficiency and cardiovascular diseases indicated new insights in the improvement of therapy. Experimental studies support the understanding of iron metabolism. Many physicians remain doubtful of the use of intravenous iron due to reports of side effects. The aim of this review is to describe iron metabolism in humans, to highlight the influence of iron deficiency on the course and symptoms of heart failure, discuss diagnostic tools of iron deficiency and provide guidance on the use of intravenous iron. PMID:24064572

  10. Biomarkers in heart failure with preserved ejection fraction.

    PubMed

    Meijers, W C; van der Velde, A R; de Boer, R A

    2016-04-01

    Biomarkers are widely used and studied in heart failure. Most studies have described the utility and performance of biomarkers in sub-studies of randomised clinical trials, where the vast majority of the patients suffered from heart failure with reduced ejection fraction (HFrEF), and not with preserved ejection fraction (HFpEF). As a result, there is a scarcity of data describing the levels, dynamics, clinical and biochemical correlates, and biology of biomarkers in patients suffering from HFpEF, whereas HFpEF is in fact a very frequent clinical entity. This article discusses the value of different biomarkers in HFpEF. We describe various aspects of natriuretic peptide measurements in HFpEF patients, with a focus on diagnosis, prognosis and the risk prediction of developing heart failure. Further, we will discuss several emerging biomarkers such as galectin-3 and suppression of tumorigenicity 2, and recently discovered ones such as growth differentiation factor-15 and syndecan-1. PMID:26942916

  11. [Prescribing beta blockers in elderly patients with heart failure].

    PubMed

    Galinier, Michel; Emeriau, Jean-Paul

    2008-06-01

    Beta blockers remain underused in elderly patients with heart failure. Age is not a contraindication to beta blockers. The SENIORS study confirmed that beta blockers are both efficacious and well tolerated in elderly people with heart failure, regardless of their ejection fraction. Because adverse effects may be both more frequent and more serious in the elderly, prescription protocols must be strictly applied. Patients in stable NYHA stages II or III may begin beta blocker treatment, at least 1 month after any decompensation. The initial dose must be as low as possible (1.25 mg/d for bisoprolol and nebivolol). Doses must be increased very progressively and stages longer than 15 days may be necessary. The objective is to reach the target dose (10mg/d for bisoprolol and nebivolol), given the dose-response effect that exists for beta blockers in elderly people with heart failure. In the case of low blood pressure, antihypertensive treatments must be reduced or stopped (for example, nitrate derivatives or calcium channel blockers). A reduction in the dosage of any diuretic dosage and finally of the beta blocker may follow, if necessary. Should bradycardia occur, any anti-bradycardia treatments (such as digoxin or amiodarone) must be reduced or stopped before the beta blocker dosage is reduced. PMID:18450415

  12. Heart failure and chronic kidney disease: should we use spironolactone?

    PubMed

    Agrawal, Sahil; Agrawal, Nikhil; Garg, Jalaj; Mohandas, Rajesh; Gupta, Tanush; Segal, Mark

    2015-08-01

    Half of all deaths in patients with chronic kidney disease (CKD) arise from cardiovascular causes. Congestive heart failure (CHF) is specifically more frequent with CKD. Cardiovascular therapies with proven benefit are often withheld from patients with renal disease for fear of adverse events. The renin-angiotensin-aldosterone system (RAAS) has been implicated as an important maladaptive neurohormonal pathway in heart failure. Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers have been shown to suppress it ineffectively. Current guidelines support the use of spironolactone for more comprehensive suppression of the RAAS in heart failure patients. Most supporting trials have however excluded patients with renal dysfunction resulting in a dearth of data to support use of spironolactone in CKD patients with CHF. Several small studies that prospectively interrogated the benefits of augmented RAAS blockade with spironolactone in CKD patients have shown improvement in predictors of cardiovascular mortality. More recently, improved mortality outcomes were demonstrated with the use of spironolactone in hemodialysis patients. Although reduction in glomerular filtration rate and hyperkalemia are potential adverse effects with its use, the available evidence suggests that it is uncommon and serious consequences can be avoided with close monitoring. Studies investigating the optimal spironolactone dosage in such a setting recommend starting with a low dose and careful uptitration. This review attempts to provide a comprehensive insight into the issues associated with the use of spironolactone in the setting of concomitant CHF and CKD. PMID:26086152

  13. Telomere attrition and Chk2 activation in human heart failure

    PubMed Central

    Oh, Hidemasa; Wang, Sam C.; Prahash, Arun; Sano, Motoaki; Moravec, Christine S.; Taffet, George E.; Michael, Lloyd H.; Youker, Keith A.; Entman, Mark L.; Schneider, Michael D.

    2003-01-01

    The postmitotic phenotype in adult cardiac muscle exhibits similarities to replicative senescence more generally and constitutes a barrier to effective restorative growth in heart disease. Telomere dysfunction is implicated in senescence and apoptotic signaling but its potential role in heart disorders is unknown. Here, we report that cardiac apoptosis in human heart failure is associated specifically with defective expression of the telomere repeat- binding factor TRF2, telomere shortening, and activation of the DNA damage checkpoint kinase, Chk2. In cultured cardiomyocytes, interference with either TRF2 function or expression triggered telomere erosion and apoptosis, indicating that cell death can occur via this pathway even in postmitotic, noncycling cells; conversely, exogenous TRF2 conferred protection from oxidative stress. In vivo, mechanical stress was sufficient to down-regulate TRF2, shorten telomeres, and activate Chk2 in mouse myocardium, and transgenic expression of telomerase reverse transcriptase conferred protection from all three responses. Together, these data suggest that apoptosis in chronic heart failure is mediated in part by telomere dysfunction and suggest an essential role for TRF2 even in postmitotic cells. PMID:12702777

  14. Nitrendipine binding in congestive heart failure due to myocardial infarction

    SciTech Connect

    Dixon, I.M.; Lee, S.L.; Dhalla, N.S. )

    1990-03-01

    Depressed cardiac pump function is the hallmark of congestive heart failure, and it is suspected that decreased influx of Ca2+ into the cardiac cell is responsible for depressed contractile function. Since Ca2+ channels in the sarcolemmal membrane are considered to be an important route for the entry of Ca2+, we examined the status of Ca2+ receptors/channels in failing rat hearts after myocardial infarction of the left ventricular free wall. For this purpose, the left coronary artery was ligated and hearts were examined 4, 8, and 16 weeks later; sham-operated animals served as controls. Hemodynamic assessment revealed decreased total mechanical energy (left ventricular systolic pressure x heart rate), increased left ventricular diastolic pressure, and decreased positive and negative dP/dt in experimental animals at 4, 8, and 16 weeks. Although accumulation of ascites in the abdominal cavity was evident at 4 weeks, other clinical signs of congestive heart failure in experimental rats were evident from the presence of lung congestion and cardiac dilatation at 8 and 16 weeks after induction of myocardial infarction. The density of Ca2+ receptors/channels in crude membranes, as assessed by (3H)nitrendipine binding assay, was found to be decreased in the uninfarcted experimental left ventricle at 8 and 16 weeks; however, no change in the affinity of nitrendipine was evident. A similar depression in the specific binding of another dihydropyridine compound, (3H)PN200-110, was also evident in failing hearts. Brain and skeletal muscle crude membrane preparations, unlike those of the right ventricle and liver, revealed a decrease in Ca2+ receptors/channels density in experimental animals at 16 weeks.

  15. Liguzinediol improved the heart function and inhibited myocardial cell apoptosis in rats with heart failure

    PubMed Central

    Li, Yu; Song, Ping; Zhu, Qing; Yin, Qiu-yi; Ji, Jia-wen; Li, Wei; Bian, Hui-min

    2014-01-01

    Aim: Liguzinediol is a novel derivative of ligustrazine isolated from the traditional Chinese medicine Chuanxiong (Ligusticum wallichii Franch), and produces significant positive inotropic effect in isolated rat hearts. In this study we investigated the effects of liguzinediol on a rat model of heart failure. Methods: To induce heart failure, male SD rats were injected with doxorubicin (DOX, 2 mg/kg, ip) once a week for 4 weeks. Then the rats were administered with liguzinediol (5, 10, 20 mgkg?1d?1, po) for 2 weeks. Hemodynamic examination was conducted to evaluate heart function. Myocardial cell apoptosis was examined morphologically. The expression of related genes and proteins were analyzed using immunohistochemical staining and Western blot assays, respectively. Results: Oral administration of liguzinediol dose-dependently improved the heart function in DOX-treated rats. Electron microscopy revealed that liguzinediol (10 mgkg?1d?1) markedly attenuated DOX-induced injury of cardiomyocytes, and decreased the number of apoptotic bodies in cardiomyocytes. Furthermore, liguzinediol significantly decreased Bax protein level, and increased Bcl-2 protein level in cardiomyocytes of DOX-treated rats, led to an increase in the ratio of Bcl-2/Bax. Moreover, liguzinediol significantly decreased the expression of both cleaved caspase-3 and NF-?B in cardiomyocytes of DOX-treated rats. Administration of digitalis (0.0225 mgkg?1d?1) also markedly improved the heart function and the morphology of cardiomyocytes in DOX-treated rats. Conclusion: Liguzinediol improves the heart function and inhibits myocardial cell apoptosis in the rat model of heart failure, which is associated with regulating Bcl-2, Bax, caspase-3 and NF-?B expression. PMID:25220638

  16. Simulation of Dilated Heart Failure with Continuous Flow Circulatory Support

    PubMed Central

    Wang, Yajuan; Loghmanpour, Natasha; Vandenberghe, Stijn; Ferreira, Antonio; Keller, Bradley; Gorcsan, John; Antaki, James

    2014-01-01

    Lumped parameter models have been employed for decades to simulate important hemodynamic couplings between a left ventricular assist device (LVAD) and the native circulation. However, these studies seldom consider the pathological descending limb of the Frank-Starling response of the overloaded ventricle. This study introduces a dilated heart failure model featuring a unimodal end systolic pressure-volume relationship (ESPVR) to address this critical shortcoming. The resulting hemodynamic response to mechanical circulatory support are illustrated through numerical simulations of a rotodynamic, continuous flow ventricular assist device (cfVAD) coupled to systemic and pulmonary circulations with baroreflex control. The model further incorporated septal interaction to capture the influence of left ventricular (LV) unloading on right ventricular function. Four heart failure conditions were simulated (LV and bi-ventricular failure with/without pulmonary hypertension) in addition to normal baseline. Several metrics of LV function, including cardiac output and stroke work, exhibited a unimodal response whereby initial unloading improved function, and further unloading depleted preload reserve thereby reducing ventricular output. The concept of extremal loading was introduced to reflect the loading condition in which the intrinsic LV stroke work is maximized. Simulation of bi-ventricular failure with pulmonary hypertension revealed inadequacy of LV support alone. These simulations motivate the implementation of an extremum tracking feedback controller to potentially optimize ventricular recovery. PMID:24465511

  17. Individualized biomonitoring in heart failure--Biomon-HF "Keep an eye on heart failure--especially at night".

    PubMed

    Vollmer, Thomas; Schauerte, Patrick; Zink, Matthias; Glöggler, Sigrid; Schiefer, Johannes; Schiek, Michael; Johnen, Udo; Leonhardt, Steffen

    2014-04-01

    In the project "Individualized Biomonitoring in Heart Failure (Biomon-HF)," innovative sensors and algorithms for measuring vital signs, i.e., during the nocturnal sleep period, have been developed and successfully tested in five clinical feasibility studies involving 115 patients. The Biomon-HF sensor concepts are an important step toward future patient-customized telemonitoring and sensor-guided therapy management in chronic heart failure, including early detection of upcoming HF exacerbation and comorbidities at home. The resulting preventable disease complications and emergencies and reduction of consequences of disease are very important advantages for the patients, causing relief for medical staff and, thus, offer an enormous potential for improvements and cost savings in healthcare systems. PMID:24535297

  18. Ventilation heterogeneity is increased in patients with chronic heart failure.

    PubMed

    Kee, Kirk; Stuart-Andrews, Christopher; Nilsen, Kris; Wrobel, Jeremy P; Thompson, Bruce R; Naughton, Matthew T

    2015-10-01

    In the healthy lung, ventilation is distributed heterogeneously due to factors such as anatomical asymmetry and gravity. This ventilation heterogeneity increases pathologically in conditions such as asthma, chronic obstructive lung disease, and cystic fibrosis. In chronic heart failure, lung biopsy demonstrates evidence of peripheral lung fibrosis and small airways narrowing and distortion. We hypothesized that this would lead to increased ventilation heterogeneity. Furthermore, we proposed that rostral fluid shifts when seated patients lie supine would further increase ventilation heterogeneity. We recruited 30 ambulatory chronic heart failure patients (57 ± 10 years, 83% male, left ventricular ejection fraction 31 ± 12%) as well as 10 healthy controls (51 ± 13 years, 90% male). Heart failure patients were clinically euvolemic. Subjects underwent measurement of ventilation heterogeneity using the multiple-breath nitrogen washout technique in the seated position, followed by repeat measurements after 5 and 45 min in the supine position. Ventilation heterogeneity was calculated using the lung clearance index (LCI), Sacin and Scond which represent overall, acinar, and small conducting airway function, respectively. Lung clearance index (9.6 ± 1.2 vs. 8.6 ± 1.4 lung turnovers, P = 0.034) and Scond (0.029 ± 0.014 vs. 0.006 ± 0.016/L, P = 0.007) were higher in the heart failure patients. There was no difference in Sacin (0.197 ± 0.171 vs. 0.125 ± 0.081/L, P = 0.214). Measures of ventilation heterogeneity did not change in the supine position. This study confirms the presence of peripheral airway pathology in patients with chronic heart failure. This leads to subtle but detectable functional abnormalities which do not change after 45 min in the supine position. PMID:26493954

  19. Medical treatment of end-stage heart failure.

    PubMed

    Binetti, G; Senni, M; Colombo, F; Tasca, G; Mamprin, F; Caporale, R; Ferrazzi, P; Gamba, A; Glauber, M; Troise, G; Fiocchi, R

    1996-11-01

    Congestive heart failure is a lethal condition that affects an increasing number of patients. In recent years a great amount of data have accumulated on the pathophysiology and medical and surgical therapy of this condition. In spite of the advances in its management and the great number of patients affected, common errors are still made by internists and cardiologists in the use of drugs and therapeutic strategies. Digitalis has only recently been shown to affect hemodynamics, exercise capacity, and clinical symptoms, but the effects on survival still have to be demonstrated. Loop diuretics, eventually combined with thiazides and antialdosterone drugs in patients with clinical signs and symptoms of fluid retention, are the mainstays of therapy of congestive heart failure. In order to make diuretic therapy efficacious, moderate salt and water intake restriction is mandatory. Angiotensin-converting enzyme (ACE) inhibitors are now considered unavoidable drugs in the management of heart failure, and an attempt to reach the doses that have been shown to be efficacious for survival in the large trials has to be made in every patient with this condition. Other vasodilators, such as hydralazine and nitrates, which show a less pronounced effect on survival but more effective hemodynamic actions than ACE inhibitors, may be used to control mitral insufficiency or to improve hemodynamics in very sick patients. Hemodynamic instability refractory to increasing doses of vasodilators and diuretics is a severe condition that requires hospital admission to administer drugs parenterally. These patients are usually treated with the combination of catecholamines and phosphodiesterase inhibitors associated with intravenous diuretics until clinical stability is again achieved and oral therapy is resumed and restructured. The use of aggressive pharmacological therapy and phosphodiesterase inhibitors has reduced the need for assisted circulatory support in these patients. Beta-blockers have shown promising results when administered to patients with heart failure, although a definitive demonstration of their effects on survival is still lacking. Other additional measures that need to be considered in patients with end-stage congestive heart failure are the use of antiarrhythmic drugs and anticoagulation. PMID:9115955

  20. The fibrosis-cell death axis in heart failure.

    PubMed

    Piek, A; de Boer, R A; Silljé, H H W

    2016-03-01

    Cardiac stress can induce morphological, structural and functional changes of the heart, referred to as cardiac remodeling. Myocardial infarction or sustained overload as a result of pathological causes such as hypertension or valve insufficiency may result in progressive remodeling and finally lead to heart failure (HF). Whereas pathological and physiological (exercise, pregnancy) overload both stimulate cardiomyocyte growth (hypertrophy), only pathological remodeling is characterized by increased deposition of extracellular matrix proteins, termed fibrosis, and loss of cardiomyocytes by necrosis, apoptosis and/or phagocytosis. HF is strongly associated with age, and cardiomyocyte loss and fibrosis are typical signs of the aging heart. Fibrosis results in stiffening of the heart, conductivity problems and reduced oxygen diffusion, and is associated with diminished ventricular function and arrhythmias. As a consequence, the workload of cardiomyocytes in the fibrotic heart is further augmented, whereas the physiological environment is becoming less favorable. This causes additional cardiomyocyte death and replacement of lost cardiomyocytes by fibrotic material, generating a vicious cycle of further decline of cardiac function. Breaking this fibrosis-cell death axis could halt further pathological and age-related cardiac regression and potentially reverse remodeling. In this review, we will describe the interaction between cardiac fibrosis, cardiomyocyte hypertrophy and cell death, and discuss potential strategies for tackling progressive cardiac remodeling and HF. PMID:26883434

  1. Mechanical Unloading Promotes Myocardial Energy Recovery in Human Heart Failure

    PubMed Central

    Gupte, Anisha A.; Hamilton, Dale J.; Cordero-Reyes, Andrea M.; Youker, Keith A.; Yin, Zheng; Estep, Jerry D.; Stevens, Robert D.; Wenner, Brett; Ilkayeva, Olga; Loebe, Matthias; Peterson, Leif E.; Lyon, Christopher J.; Wong, Stephen T.C.; Newgard, Christopher B.; Torre-Amione, Guillermo; Taegtmeyer, Heinrich; Hsueh, Willa A.

    2015-01-01

    Background Impaired bioenergetics is a prominent feature of the failing heart, but the underlying metabolic perturbations are poorly understood. Methods and Results We compared metabolomic, gene transcript, and protein data from six paired failing human left ventricular (LV) tissue samples obtained during left ventricular assist device (LVAD) insertion (heart failure (HF) samples) and at heart transplant (post-LVAD samples). Non-failing left ventricular (NFLV) wall samples procured from explanted hearts of patients with right HF served as novel comparison samples. Metabolomic analyses uncovered a distinct pattern in HF tissue: 2.6 fold increased pyruvate concentrations coupled with reduced Krebs cycle intermediates and short-chain acylcarnitines, suggesting a global reduction in substrate oxidation. These findings were associated with decreased transcript levels for enzymes that catalyze fatty acid oxidation and pyruvate metabolism and for key transcriptional regulators of mitochondrial metabolism and biogenesis, peroxisome proliferator-activated receptor gamma co-activator1? (PGC1A, 1.3 fold) and estrogen-related receptor ? (ERRA, 1.2 fold) and ? (ERRG, 2.2 fold). Thus, parallel decreases in key transcription factors and their target metabolic enzyme genes can explain the decreases in associated metabolic intermediates. Mechanical support with LVAD improved all of these metabolic and transcriptional defects. Conclusions These observations underscore an important pathophysiologic role for severely defective metabolism in HF, while the reversibility of these defects by LVAD suggests metabolic resilience of the human heart. PMID:24825877

  2. Neurohumoral activation in heart failure: the role of adrenergic receptors.

    PubMed

    Brum, Patricia C; Rolim, Natale P L; Bacurau, Aline V N; Medeiros, Alessandra

    2006-09-01

    Heart failure (HF) is a common endpoint for many forms of cardiovascular disease and a significant cause of morbidity and mortality. The development of end-stage HF often involves an initial insult to the myocardium that reduces cardiac output and leads to a compensatory increase in sympathetic nervous system activity. Acutely, the sympathetic hyperactivity through the activation of beta-adrenergic receptors increases heart rate and cardiac contractility, which compensate for decreased cardiac output. However, chronic exposure of the heart to elevated levels of catecholamines released from sympathetic nerve terminals and the adrenal gland may lead to further pathologic changes in the heart, resulting in continued elevation of sympathetic tone and a progressive deterioration in cardiac function. On a molecular level, altered beta-adrenergic receptor signaling plays a pivotal role in the genesis and progression of HF. beta-adrenergic receptor number and function are decreased, and downstream mechanisms are altered. In this review we will present an overview of the normal beta-adrenergic receptor pathway in the heart and the consequences of sustained adrenergic activation in HF. The myopathic potential of individual components of the adrenergic signaling will be discussed through the results of research performed in genetic modified animals. Finally, we will discuss the potential clinical impact of beta-adrenergic receptor gene polymorphisms for better understanding the progression of HF. PMID:16936938

  3. Right ventricular long noncoding RNA expression in human heart failure

    PubMed Central

    Guo, Yan; Su, Yan Ru; Clark, Travis; Brittain, Evan; Absi, Tarek; Maltais, Simon; Hemnes, Anna

    2015-01-01

    Abstract The expression of long noncoding RNAs (lncRNAs) in human heart failure (HF) has not been widely studied. Using RNA sequencing (RNA-Seq), we compared lncRNA expression in 22 explanted human HF hearts with lncRNA expression in 5 unused donor human hearts. We used Cufflinks to identify isoforms and DESeq to identify differentially expressed genes. We identified the noncoding RNAs by cross-reference to Ensembl release 73 (Genome Reference Consortium human genome build 37) and explored possible functional roles using a variety of online tools. In HF hearts, RNA-Seq identified 84,793 total messenger RNA coding and noncoding different transcripts, including 13,019 protein-coding genes, 2,085 total lncRNA genes, and 1,064 pseudogenes. By Ensembl noncoding RNA categories, there were 48 lncRNAs, 27 pseudogenes, and 30 antisense RNAs for a total of 105 differentially expressed lncRNAs in HF hearts. Compared with donor hearts, HF hearts exhibited differential expression of 7.7% of protein-coding genes, 3.7% of lncRNAs (including pseudogenes), and 2.5% of pseudogenes. There were not consistent correlations between antisense lncRNAs and parent genes and between pseudogenes and parent genes, implying differential regulation of expression. Exploratory in silico functional analyses using online tools suggested a variety of possible lncRNA regulatory roles. By providing a comprehensive profile of right ventricular polyadenylated messenger RNA transcriptome in HF, RNA-Seq provides an inventory of differentially expressed lncRNAs, including antisense transcripts and pseudogenes, for future mechanistic study. PMID:25992278

  4. Effect of a community heart failure clinic on uptake of ? blockers by patients with obstructive airways disease and heart failure

    PubMed Central

    Shelton, R J; Rigby, A S; Cleland, J G F; Clark, A L

    2006-01-01

    Objective To determine the pattern of ? blocker prescribing over one year in a heart failure clinic with a structured approach towards initiation and dose titration and to give a real life perspective on ? blocker use, compliance, and target dose achievement. Methods Data were retrospectively analysed on 513 consecutive patients regularly attending a community heart failure clinic over a year. Systolic dysfunction was determined from two dimensional echocardiography (left ventricular ejection fraction ??40%) and lung function was assessed by spirometry. All patients were considered for ? blocker initiation and dose up titration. Results Within one year 157 patients died. 143 patients started ? blockers resulting in 315 (88%) patients taking ? blockers at one year; 38% were taking the target dose. 124 had evidence of airways obstruction at baseline, 100 (81%) of whom were taking ? blockers at one year. Forced expiratory volume in one second (1.1 v 1.5?l, p?heart failure and obstructive airways disease can safely tolerate low dose initiation and gradual up titration of ? blockers. PMID:15951394

  5. Ambulatory heart rate range predicts mode-specific mortality and hospitalisation in chronic heart failure

    PubMed Central

    Cubbon, Richard M; Ruff, Naomi; Groves, David; Eleuteri, Antonio; Denby, Christine; Kearney, Lorraine; Ali, Noman; Walker, Andrew M N; Jamil, Haqeel; Gierula, John; Gale, Chris P; Batin, Phillip D; Nolan, James; Shah, Ajay M; Fox, Keith A A; Sapsford, Robert J; Witte, Klaus K; Kearney, Mark T

    2016-01-01

    Objective We aimed to define the prognostic value of the heart rate range during a 24 h period in patients with chronic heart failure (CHF). Methods Prospective observational cohort study of 791 patients with CHF associated with left ventricular systolic dysfunction. Mode-specific mortality and hospitalisation were linked with ambulatory heart rate range (AHRR; calculated as maximum minus minimum heart rate using 24 h Holter monitor data, including paced and non-sinus complexes) in univariate and multivariate analyses. Findings were then corroborated in a validation cohort of 408 patients with CHF with preserved or reduced left ventricular ejection fraction. Results After a mean 4.1 years of follow-up, increasing AHRR was associated with reduced risk of all-cause, sudden, non-cardiovascular and progressive heart failure death in univariate analyses. After accounting for characteristics that differed between groups above and below median AHRR using multivariate analysis, AHRR remained strongly associated with all-cause mortality (HR 0.991/bpm increase in AHRR (95% CI 0.999 to 0.982); p=0.046). AHRR was not associated with the risk of any non-elective hospitalisation, but was associated with heart-failure-related hospitalisation. AHRR was modestly associated with the SD of normal-to-normal beats (R2=0.2; p<0.001) and with peak exercise-test heart rate (R2=0.33; p<0.001). Analysis of the validation cohort revealed AHRR to be associated with all-cause and mode-specific death as described in the derivation cohort. Conclusions AHRR is a novel and readily available prognosticator in patients with CHF, which may reflect autonomic tone and exercise capacity. PMID:26674986

  6. Influence of heart failure on nucleolar organization and protein expression in human hearts

    SciTech Connect

    Rosello-Lleti, Esther; Rivera, Miguel; Cortes, Raquel; Azorin, Inmaculada; Sirera, Rafael; Martinez-Dolz, Luis; Hove, Leif; Cinca, Juan; Lago, Francisca; Gonzalez-Juanatey, Jose R.; Salvador, Antonio; Portoles, Manuel

    2012-02-10

    Highlights: Black-Right-Pointing-Pointer Heart failure alters nucleolar morphology and organization. Black-Right-Pointing-Pointer Nucleolin expression is significant increased in ischemic and dilated cardiomyopathy. Black-Right-Pointing-Pointer Ventricular function of heart failure patients was related with nucleolin levels. -- Abstract: We investigate for the first time the influence of heart failure (HF) on nucleolar organization and proteins in patients with ischemic (ICM) or dilated cardiomyopathy (DCM). A total of 71 human hearts from ICM (n = 38) and DCM (n = 27) patients, undergoing heart transplantation and control donors (n = 6), were analysed by western-blotting, RT-PCR and cell biology methods. When we compared protein levels according to HF etiology, nucleolin was increased in both ICM (117%, p < 0.05) and DCM (141%, p < 0.01). Moreover, mRNA expression were also upregulated in ICM (1.46-fold, p < 0.05) and DCM (1.70-fold, p < 0.05. Immunofluorescence studies showed that the highest intensity of nucleolin was into nucleolus (p < 0.0001), and it was increased in pathological hearts (p < 0.0001). Ultrastructure analysis by electron microscopy showed an increase in the nucleus and nucleolus size in ICM (17%, p < 0.05 and 131%, p < 0.001) and DCM (56%, p < 0.01 and 69%, p < 0.01). Nucleolar organization was influenced by HF irrespective of etiology, increasing fibrillar centers (p < 0.001), perinucleolar chromatin (p < 0.01) and dense fibrillar components (p < 0.01). Finally, left ventricular function parameters were related with nucleolin levels in ischemic hearts (p < 0.0001). The present study demonstrates that HF influences on morphology and organization of nucleolar components, revealing changes in the expression and in the levels of nucleolin protein.

  7. Differential clinical characteristics and prognosis of intraventricular conduction defects in patients with chronic heart failure

    PubMed Central

    Cinca, Juan; Mendez, Ana; Puig, Teresa; Ferrero, Andreu; Roig, Eulalia; Vazquez, Rafael; Gonzalez-Juanatey, Jose R.; Alonso-Pulpon, Luis; Delgado, Juan; Brugada, Josep; Pascual-Figal, Domingo; Brugada, J.; Batlle, M.; Berruezo, A.; Hevia, S.; Mont, L.; Prez-Villa, F.; Cinca, J.; Roig, E.; Bays de Luna, A.; Borrs, X.; Carreras, F.; Ferrero, A.; Guerra, J.M.; Hove-Madsen, L.; Jorge, E.; Martnez, R.; Padr, J.; Puig, T.; Ribas, N.; Violas, X.; Alvarez-Garcia, J.; Gonzlez-Juanatey, J.R.; Bandn, M.; Eiras, S.; Fernndez-Hernndez, L.; Garca-Acua, J.; Gmez-Otero, I.; Grigorian-Shamagian, L.; Lago, F.; Manzn, P.; Moure, M.; Otero-Ravia, F.; Otero-Santiago, F.; Rodino Janeiro, B.K.; Rubio, J.; Salgado, A.; Seoane, A.; Varela, A.; Lear, P.V.; Fernndez-Cruz, A.; Alvarez de Arcaya Vicente, A.; Avila, M.; Bordiu, E.; Calle, L.; Fernndez-Pinilla, C.; Gmez-Garre, D.; Gonzlez-Rubio, L.; Marco, J.; Martell, N.; Muoz-Pacheco, P.; Ortega, A.; Patio, R.; Pedrajas, J.; Reinares, L.; Prez-Villacastn, J.; Bover, R.; Cobos, M.; Garca-Quintanilla, J.; Moreno, J.; Prez-Castellano, N.; Prez-Serrano, M.; Vila, I.; Delgado, J.F.; Arribas, F.; Escribano, P.; Flox, A.; Jimnez Lpez-Guarch, C.; Paradina, M.; Ruiz-Cano, J.; Senz de la Calzada, C.; Salguero, R.; Snchez-Snchez, V.; Tello de Meneses, R.; Vicente-Hernndez, M.; Alonso-Pulpn, L.; Fernndez -Lozano, I.; Garca-Pava, P.; Garca-Touchard, A.; Gmez-Bueno, M.; Mrquez, J.; Segovia, J.; Silva, L.; Vzquez-Mosquera, M.; Valds, M.; Garca-Alberola, A.; Garrido, I.; Pascual-Figal, D. A.; Pastor-Prez, F.J.; Snchez-Ms, J.; Tornel, P.; Rivera, M.; Almenar, L.; Corts, R.; Martnez-Dolz, L.; Montero, J.; Portols, M.; Rosell-Lleti, E.; Salvador, A.; Vila, V.; Vzquez, R.; Cubero, J.; Fernndez-Palacn, A.; Garca-Medina, D.; Garca-Rey, S.; Laguna, E.; Leal del Ojo, J.; Miano, F.; Pastor-Torres, L.; Pavn, R.; Prez-Navarro, A.; Villagmez, D.; Vzquez, R.; Arana, R.; Bartolom, D.; Cabeza, P.; Calle-Prez, G.; Camacho, F.; Cano, L.; Carrillo, A.; Daz-Retamino, E.; Escolar, V.; Fernndez-Rivero, R.; Gamaza, S.; Girldes, A.; Hernndez-Vicente, N.; Lagares, M.; Lpez-Bentez, J.; Marante, M.; Otero, E.; Pedregal, J.; Sancho-Jaldn, M.; Sevillano, R.; Zayas, R.; Verd, J.M.; Aguilar, S.; Aizpura, M.; Alguacil, F.; Casacuberta, J.; Cerain, J.; Domingo, M.; Garca-Lareo, M.; Herrero-Melechn, J.; Lpez-Pareja, N.; Mena, A.; Prez-Orcero, A.; Rodrguez- Cristbal, J.; Rozas, M.; Sorribes, J.; Torn, P.; Worner, F.; Barta, L.; Bravo, C.; Cabau, J.; Casanova, J.; Daga, B.; De la Puerta, I.; Hernndez-Martn, I.; Piol, E.; Pueo, E.; Torres, G.; Troncoso, A.; Viles, D.; Bardaj, A.; Merc, J.; Sanz-Girgas, E.; Valdovinos, P.; Aramburu, O.; Arias, J.; Garca-Gonzlez, C.; Alonso, M.; Bischofberger, C.; Domnguez-De Pablos, G.; Jimnez-Cervantes, D.; Urea, I.; Grau-Seplveda, A.; Fiol, C.; Pericas, P.; Villalonga, M.; Orosa, P.; Agero, J.; Planas-Aym, F.; Grau-Amoros, J.; Planas-Comes, F.; San Vicente, L.

    2013-01-01

    Aims Intraventricular conduction defects (IVCDs) can impair prognosis of heart failure (HF), but their specific impact is not well established. This study aimed to analyse the clinical profile and outcomes of HF patients with LBBB, right bundle branch block (RBBB), left anterior fascicular block (LAFB), and no IVCDs. Methods and results Clinical variables and outcomes after a median follow-up of 21 months were analysed in 1762 patients with chronic HF and LBBB (n = 532), RBBB (n = 134), LAFB (n = 154), and no IVCDs (n = 942). LBBB was associated with more marked LV dilation, depressed LVEF, and mitral valve regurgitation. Patients with RBBB presented overt signs of congestive HF and depressed right ventricular motion. The LAFB group presented intermediate clinical characteristics, and patients with no IVCDs were more often women with less enlarged left ventricles and less depressed LVEF. Death occurred in 332 patients (interannual mortality = 10.8%): cardiovascular in 257, extravascular in 61, and of unknown origin in 14 patients. Cardiac death occurred in 230 (pump failure in 171 and sudden death in 59). An adjusted Cox model showed higher risk of cardiac death and pump failure death in the LBBB and RBBB than in the LAFB and the no IVCD groups. Conclusion LBBB and RBBB are associated with different clinical profiles and both are independent predictors of increased risk of cardiac death in patients with HF. A more favourable prognosis was observed in patients with LAFB and in those free of IVCDs. Further research in HF patients with RBBB is warranted. PMID:23512097

  8. Rationale and benefits of trimetazidine by acting on cardiac metabolism in heart failure.

    PubMed

    Lopatin, Yuri M; Rosano, Giuseppe M C; Fragasso, Gabriele; Lopaschuk, Gary D; Seferovic, Petar M; Gowdak, Luis Henrique W; Vinereanu, Dragos; Hamid, Magdy Abdel; Jourdain, Patrick; Ponikowski, Piotr

    2016-01-15

    Heart failure is a systemic and multiorgan syndrome with metabolic failure as a fundamental mechanism. As a consequence of its impaired metabolism, other processes are activated in the failing heart, further exacerbating the progression of heart failure. Recent evidence suggests that modulating cardiac energy metabolism by reducing fatty acid oxidation and/or increasing glucose oxidation represents a promising approach to the treatment of patients with heart failure. Clinical trials have demonstrated that the adjunct of trimetazidine to the conventional medical therapy improves symptoms, cardiac function and prognosis in patients with heart failure without exerting negative hemodynamic effects. This review focuses on the rationale and clinical benefits of trimetazidine by acting on cardiac metabolism in heart failure, and aims to draw attention to the readiness of this agent to be included in all the major guidelines dealing with heart failure. PMID:26618252

  9. Monoamine oxidases (MAO) in the pathogenesis of heart failure and ischemia/reperfusion injury

    PubMed Central

    Kaludercic, Nina; Carpi, Andrea; Menab, Roberta; Lisa, Fabio Di; Paolocci, Nazareno

    2010-01-01

    Recent evidence highlights monoamine oxidases (MAO) as another prominent source of oxidative stress. MAO are a class of enzymes located in the outer mitochondrial membrane, deputed to the oxidative breakdown of key neurotransmitters such as norepinephrine, epinephrine and dopamine, and in the process generate H2O2. All these monoamines are endowed with potent modulatory effects on myocardial function. Thus, when the heart is subjected to chronic neuro-hormonal and/or peripheral hemodynamic stress, the abundance of circulating/tissue monoamines can make MAO-derived H2O2 production particularly prominent. This is the case of acute cardiac damage due to ischemia/reperfusion injury or, on a more chronic stand, of the transition from compensated hypertrophy to overt ventricular dilation/pump failure. Here, we will first briefly discuss mitochondrial status and contribution to acute and chronic cardiac disorders. We will illustrate possible mechanisms by which MAO activity affects cardiac biology and function, along with a discussion as to their role as a prominent source of reactive oxygen species. Finally, we will speculate on why MAO inhibition might have therapeutic value for treating cardiac affections of ischemic and non-ischemic origin. PMID:20869994

  10. Dietary Sodium Modulation of Aldosterone Activation and Renal Function During the Progression of Experimental Heart Failure Miller: Dietary Sodium and Early Heart Failure

    PubMed Central

    Miller, Wayne L.; Borgeson, Daniel D.; Grantham, J. Aaron; Luchner, Andreas; Redfield, Margaret M.; Burnett, John C.

    2015-01-01

    Aims Aldosterone activation is central to the sodium-fluid retention that marks the progression of heart failure (HF). The actions of dietary sodium restriction, a mainstay in HF management, on cardiorenal and neuroendocrine adaptations during the progression of HF are poorly understood. The study aim was to assess the role of dietary sodium during the progression of experimental HF. Methods and Results Experimental HF was produced in a canine model by rapid right ventricular pacing which evolves from early mild HF to overt, severe HF. Dogs were fed one of three diets: 1) high sodium [250 mEq (5.8 grams) per day, n=6]; 2) standard sodium [58 mEq (1.3 grams) per day, n=6]; and 3) sodium restriction [11 mEq (0.25 grams) per day, n=6]. During the 38 day study hemodynamics, renal function, renin activity (PRA), and aldosterone were measured. Changes in hemodynamics at 38 days were similar in all three groups, as were changes in renal function. Aldosterone activation was demonstrated in all three groups, however, dietary sodium restriction, in contrast to high sodium, resulted in early (10 days) activation of PRA and aldosterone. High sodium demonstrated significant suppression of aldosterone activation over the course of HF progression. Conclusions Excessive dietary sodium restriction particularly in early stage HF results in early aldosterone activation, while normal and excess sodium intake are associated with delayed or suppressed activation. These findings warrant evaluation in humans to determine if dietary sodium manipulation, particularly during early stage HF, may have a significant impact on neuroendocrine disease progression. PMID:25823360

  11. Glycoproteins identified from heart failure and treatment models

    PubMed Central

    Yang, Shuang; Chen, Lijun; Sun, Shisheng; Shah, Punit; Yang, Weiming; Zhang, Bai; Zhang, Zhen; Chan, Daniel W.; Kass, David A.; van Eyk, Jennifer E.; Zhang, Hui

    2015-01-01

    Conduction abnormalities can lead to dyssynchronous contraction, which significantly worsens morbidity and mortality of heart failure. Cardiac resynchronization therapy (CRT) can reverse ventricular remodeling and improve cardiac function. Although the underlying molecular changes are unknown, the use of a canine model of dyssynchrony heart failure (DHF) and CRT has shown that there are global changes across the cardiac proteome. This study determines changes in serum glycoprotein concentration from DHF and CRT compared to normal. We hypothesize that CRT invokes protective or advantageous pathways that can be reflected in the circulating proteome. A two prong discovery approaches were carried out on pooled normal, DHF and CRT samples composed of individual canine serum to determine the overall protein concentration and the N-linked glycosites of circulating glycoproteins. The level of the glycoproteins was altered in DHF and CRT compared to control sera, with 63 glycopeptides substantially increased in DHF and/or CRT. Among the 32 elevated glycosite-containing peptides in DHF, 13 glycopeptides were reverted to normal level after CRT therapy. We further verify the changes of glycopeptides using label-free LC-MS from individual canine serum. Circulating glycoproteins such as alpha-fetoprotein, alpha-2-macroglobulin, galectin-3-binding protein, collectin-10 show association to failing heart and CRT treatment model. PMID:25141849

  12. Reversal of Mitochondrial Transhydrogenase Causes Oxidative Stress in Heart Failure.

    PubMed

    Nickel, Alexander G; von Hardenberg, Albrecht; Hohl, Mathias; Löffler, Joachim R; Kohlhaas, Michael; Becker, Janne; Reil, Jan-Christian; Kazakov, Andrey; Bonnekoh, Julia; Stadelmaier, Moritz; Puhl, Sarah-Lena; Wagner, Michael; Bogeski, Ivan; Cortassa, Sonia; Kappl, Reinhard; Pasieka, Bastian; Lafontaine, Michael; Lancaster, C Roy D; Blacker, Thomas S; Hall, Andrew R; Duchen, Michael R; Kästner, Lars; Lipp, Peter; Zeller, Tanja; Müller, Christian; Knopp, Andreas; Laufs, Ulrich; Böhm, Michael; Hoth, Markus; Maack, Christoph

    2015-09-01

    Mitochondrial reactive oxygen species (ROS) play a central role in most aging-related diseases. ROS are produced at the respiratory chain that demands NADH for electron transport and are eliminated by enzymes that require NADPH. The nicotinamide nucleotide transhydrogenase (Nnt) is considered a key antioxidative enzyme based on its ability to regenerate NADPH from NADH. Here, we show that pathological metabolic demand reverses the direction of the Nnt, consuming NADPH to support NADH and ATP production, but at the cost of NADPH-linked antioxidative capacity. In heart, reverse-mode Nnt is the dominant source for ROS during pressure overload. Due to a mutation of the Nnt gene, the inbred mouse strain C57BL/6J is protected from oxidative stress, heart failure, and death, making its use in cardiovascular research problematic. Targeting Nnt-mediated ROS with the tetrapeptide SS-31 rescued mortality in pressure overload-induced heart failure and could therefore have therapeutic potential in patients with this syndrome. PMID:26256392

  13. Air Travel Considerations for the Patients With Heart Failure

    PubMed Central

    Izadi, Morteza; Alemzadeh-Ansari, Mohammad Javad; Kazemisaleh, Davood; Moshkani-Farahani, Maryam

    2014-01-01

    Context: Prevalence of patients with heart failure (HF) is increasing in worldwide, and also the number of people with HF traveling long distances is increasing. These patients are more prone to experience problems contributed air travel and needs more attention during flight. However, observational studies about problems of HF patients during flight and appropriated considerations for them are limited. Evidence Acquisition: We evaluated the conditions that may be encountered in a HF patient and provide the recommendations to prevent the exacerbation of cardiac failure during air travel. For this review article, a comprehensive search was undertaken for the studies that evaluated the complications and considerations of HF patients during flight. Data bases searched were: MEDLINE, EMBASE, Science Direct, and Google Scholar. Results: HF patients are more prone to experience respiratory distress, anxiety, stress, cardiac decompensation, and venous thromboembolism (VTE) during air travel. Although stable HF patients can tolerate air travel, but those with acute heart failure syndrome should not fly until complete improvement is achieved. Conclusions: Thus, identifying the HF patients before the flight and providing them proper education about the events that may occur during flight is necessary. PMID:25068047

  14. Dystrophic heart failure blocked by membrane sealant poloxamer

    NASA Astrophysics Data System (ADS)

    Yasuda, Soichiro; Townsend, Dewayne; Michele, Daniel E.; Favre, Elizabeth G.; Day, Sharlene M.; Metzger, Joseph M.

    2005-08-01

    Dystrophin deficiency causes Duchenne muscular dystrophy (DMD) in humans, an inherited and progressive disease of striated muscle deterioration that frequently involves pronounced cardiomyopathy. Heart failure is the second leading cause of fatalities in DMD. Progress towards defining the molecular basis of disease in DMD has mostly come from studies on skeletal muscle, with comparatively little attention directed to cardiac muscle. The pathophysiological mechanisms involved in cardiac myocytes may differ significantly from skeletal myofibres; this is underscored by the presence of significant cardiac disease in patients with truncated or reduced levels of dystrophin but without skeletal muscle disease. Here we show that intact, isolated dystrophin-deficient cardiac myocytes have reduced compliance and increased susceptibility to stretch-mediated calcium overload, leading to cell contracture and death, and that application of the membrane sealant poloxamer 188 corrects these defects in vitro. In vivo administration of poloxamer 188 to dystrophic mice instantly improved ventricular geometry and blocked the development of acute cardiac failure during a dobutamine-mediated stress protocol. Once issues relating to optimal dosing and long-term effects of poloxamer 188 in humans have been resolved, chemical-based membrane sealants could represent a new therapeutic approach for preventing or reversing the progression of cardiomyopathy and heart failure in muscular dystrophy.

  15. Mechanisms of carotid body chemoreflex dysfunction during heart failure

    PubMed Central

    Schultz, Harold D.; Marcus, Noah J.; Del Rio, Rodrigo

    2015-01-01

    Recent advances have drawn interest in the potential for carotid body (CB) ablation or desensitization as an effective strategy for clinical treatment and management of cardio-respiratory diseases including hypertension, heart failure, diabetes mellitus, metabolic syndrome, and renal failure. These disease states have in common sympathetic overactivity, which plays an important role in the development and progression of the disease and is often associated with breathing dysregulation, which in turn likely mediates or aggravates the autonomic imbalance. Evidence from both chronic heart failure (CHF) patients and animal models indicates that the CB chemoreflex is enhanced in CHF and contributes to the tonic elevation in sympathetic activity and the development of periodic breathing associated with the disease. Although this maladaptive change likely derives from altered function at all levels of the reflex arc, a tonic increase in afferent activity from CB glomus cells is likely to be a main driving force. This report will focus on our understanding of mechanisms that alter CB function in CHF and their potential translational impact on treatment of CHF. PMID:25398713

  16. Emerging hemodynamic signatures of the right heart (Third International Right Heart Failure Summit, part 2)

    PubMed Central

    2014-01-01

    Abstract Despite the importance of preserved right ventricular structure and function with respect to outcome across the spectrum of lung, cardiac, and pulmonary vascular diseases, only recently have organized efforts developed to consider the pulmonary vascularright ventricular apparatus as a specific unit within the larger context of cardiopulmonary pathophysiology. The Third International Right Heart Failure Summit (Boston, MA) was a multidisciplinary event dedicated to promoting a dialogue about the scientific and clinical basis of right heart disease. The current review provides a synopsis of key discussions presented during the section of the summit titled Emerging Hemodynamic Signatures of the Right Heart. Specifically, topics emphasized in this element of the symposium included (1) the effects of pulmonary vascular dysfunction at rest or provoked by exercise on the right ventricular pressure-volume relationship, (2) the role of pressure-volume loop analysis as a method to characterize right ventricular inefficiency and predict right heart failure, and (3) the importance of a systems biology approach to identifying novel factors that contribute to pathophenotypes associated with pulmonary arterial hypertension and/or right ventricular dysfunction. Collectively, these concepts frame a forward-thinking paradigm shift in the approach to right heart disease by emphasizing factors that regulate the transition from adaptive to maladaptive right ventricularpulmonary vascular (patho)physiology. PMID:25610606

  17. Oxidative Stress and Heart Failure in Altered Thyroid States

    PubMed Central

    Mishra, Pallavi; Samanta, Luna

    2012-01-01

    Increased or reduced action of thyroid hormone on certain molecular pathways in the heart and vasculature causes relevant cardiovascular derangements. It is well established that hyperthyroidism induces a hyperdynamic cardiovascular state, which is associated with a faster heart rate, enhanced left ventricular systolic and diastolic function whereas hypothyroidism is characterized by the opposite changes. Hyperthyroidism and hypothyroidism represent opposite clinical conditions, albeit not mirror images. Recent experimental and clinical studies have suggested the involvement of ROS tissue damage under altered thyroid status. Altered-thyroid state-linked changes in heart modify their susceptibility to oxidants and the extent of the oxidative damage they suffer following oxidative challenge. Chronic increase in the cellular levels of ROS can lead to a catastrophic cycle of DNA damage, mitochondrial dysfunction, further ROS generation and cellular injury. Thus, these cellular events might play an important role in the development and progression of myocardial remodeling and heart failure in altered thyroid states (hypo- and hyper-thyroidism). The present review aims at elucidating the various signaling pathways mediated via ROS and their modulation under altered thyroid state and the possibility of antioxidant therapy. PMID:22649319

  18. A Patient with Heart Failure and Worsening Kidney Function

    PubMed Central

    2014-01-01

    There is high prevalence of CKD, defined by reduced GFR, in patients with heart failure. Reduced kidney function is associated with increased morbidity and mortality in this patient population. The cardiorenal syndrome (CRS) involves a bidirectional relationship between the heart and kidneys whereby dysfunction in either may exacerbate the function of the other, but this syndrome has been difficult to precisely define because it has many complex physiologic, biochemical, and hormonal abnormalities. The pathophysiology of CRS is not completely understood, but potential mechanisms include reduced kidney perfusion due to decreased forward flow, increased right ventricular and venous pressure, and neurohormonal adaptations. Treatment options include inotropic medications; diuretics; ultrafiltration; and medications, such as β-blockers, inhibitors of the renin-angiotensin-aldosterone system, and more novel treatments that focus on unique aspects of the pathophysiology. Recent observational studies suggest that treatments that result in a decrease in venous pressure and lead to hemoconcentration may be associated with improved outcomes. Patients with CRS that is not responsive to medical interventions should be considered for ventricular assist devices, heart transplantation, or combined heart and kidney transplantation. PMID:24763864

  19. Heart Failure: Advanced Development in Genetics and Epigenetics

    PubMed Central

    Yang, Jian; Xu, Wei-wei; Hu, Shen-jiang

    2015-01-01

    Heart failure (HF) is a complex pathophysiological syndrome that arises from a primary defect in the ability of the heart to take in and/or eject sufficient blood. Genetic mutations associated with familial dilated cardiomyopathy, hypertrophic cardiomyopathy, and arrhythmogenic right ventricular cardiomyopathy can contribute to the various pathologies of HF. Therefore, genetic screening could be an approach for guiding individualized therapies and surveillance. In addition, epigenetic regulation occurs via key mechanisms, including ATP-dependent chromatin remodeling, DNA methylation, histone modification, and RNA-based mechanisms. MicroRNA is also a hot spot in HF research. This review gives an overview of genetic mutations associated with cardiomyopathy and the roles of some epigenetic mechanisms in HF. PMID:25949994

  20. Treatment of chronic heart failure with pirbuterol: acute haemodynamic responses.

    PubMed Central

    Dawson, J R; Canepa-Anson, R; Kuan, P; Whitaker, N H; Carnie, J; Warnes, C; Reuben, S R; Poole-Wilson, P A; Sutton, G C

    1981-01-01

    Fifty-nine patients with severe chronic heart failure were given pirbuterol, a beta agonist with vasodilator and positive inotropic properties. The acute haemodynamic responses to both single (20 patients) and incremental doses (39 patients) were measured. Pirbuterol increased cardiac index and reduced left ventricular filling pressure and systemic vascular resistance with only small changes in heart rate and blood pressure. Maximal effects were observed at an average of 170 minutes after a single oral dose of pirbuterol. In the incremental dose studies the plasma pirbuterol concentration was found to increase with increasing doses and was related to the magnitude of the haemodynamic response. Pirbuterol was well tolerated, and no drug-related side effects were recorded. Oral pirbuterol clearly improved pump performance in these patients, the haemodynamic changes being consistent with vasodilatation as the dominant mechanism rather than a direct inotropic effect. PMID:6112039

  1. Remodeling of Calcium Handling in Human Heart Failure

    PubMed Central

    Lou, Qing; Janardhan, Ajit; Efimov, Igor R.

    2013-01-01

    Heart failure (HF) is an increasing public health problem accelerated by a rapidly aging global population. Despite considerable progress in managing the disease, the development of new therapies for effective treatment of HF remains a challenge. To identify targets for early diagnosis and therapeutic intervention, it is essential to understand the molecular and cellular basis of calcium handling and the signaling pathways governing the functional remodeling associated with HF in humans. Calcium (Ca2+) cycling is an essential mediator of cardiac contractile function, and remodeling of calcium handling is thought to be one of the major factors contributing to the mechanical and electrical dysfunction observed in HF. Active research in this field aims to bridge the gap between basic research and effective clinical treatments of HF. This chapter reviews the most relevant studies of calcium remodeling in failing human hearts and discusses their connections to current and emerging clinical therapies for HF patients. PMID:22453987

  2. Multimarker testing with ST2 in chronic heart failure.

    PubMed

    Bayes-Genis, Antoni; Richards, A Mark; Maisel, Alan S; Mueller, Christian; Ky, Bonnie

    2015-04-01

    Despite important progress in recent decades, mortality remains high for patients with chronic heart failure. Risk stratification may be refined by the use of biomarkers for different pathophysiological processes that established mortality risk factors do not directly reflect. Biomarkers that are currently available can provide information about at least 7 pathobiological processes operative in HF, help to identify the specific processes involved in individual patients, and aid in constructing management plans. However, the additional prognostic information gained by any biomarker over a clinical risk model plus other biomarkers needs to be determined with adequate statistical tools. A major problem in selecting a biomarker profile is the proportional increase in economic burden; thus, the addition of any biomarker to a profile should be justified by adequate discrimination, calibration, reclassification, and likelihood analyses. Three studies that implemented such rigorous analyses have assessed a multimarker panel in chronic heart failure that incorporated the biomarker ST2: the Penn HF Study, the Barcelona Study, and the ProBNP Outpatient Tailored Chronic Heart Failure (PROTECT) biomarker substudy. In all 3 studies, a multimarker panel appeared to provide significant information over conventional risk stratification. The latter 2 reports proposed that ST2 might be superior to natriuretic peptides. The Barcelona Bio-HF calculator (www.bcnbiohfcalculator.cat) is a novel risk calculator that considers clinical variables, treatment, and biomarkers (i.e., N terminal pro-brain natriuretic peptide [NT-proBNP], ST2, and high sensitivity troponin T [hsTnT]). The optimal panel of markers, the change in these markers over time, and how these changes might help guide therapeutic interventions remain to be defined. PMID:25697916

  3. Liver Enzymes and Uric acid in Acute Heart Failure

    PubMed Central

    Vakilian, Farveh; Rafighdoost, Abbas Ali; Rafighdoost, Amir Hossein; Amin, Ahmad; Salehi, Maryam

    2015-01-01

    Background: Acute heart failure (AHF) is defined as the new onset or recurrence of gradual or rapidly worsening signs and symptoms of heart failure, requiring urgent or emergent therapy. Objectives: This study attempts to assess the association of liver function tests (LFT) and uric acid level with in hospital outcome and echocardiography parameters, in patients with acute decompensated heart failure. Patients and Methods: A total of 100 patients (aged 16 - 90 years, 60% men) admitted with AHF were enrolled. LFTs and uric acid levels were assessed on first day and before discharge, and patients were followed for 3 months. Results: In-hospital outcomes were considered. Mean Left Ventricular Ejection Fraction (LVEF) was 35% (20 - 45%). Mean Uric acid level was 8.4 mg/dL, significantly higher than chronic HF and normal groups (P < 0.02). Elevated liver enzymes were seen in 52% patients, mostly (87%) in transaminases. Liver enzymes were decreased in 85% patients before discharge. LFT and uric acid levels were inversely and significantly correlated with LVEF on echocardiography (P = 0.02), but not with diastolic parameters. Although there was no significant correlation between uric acid level and in-hospital mortality, risk of intubation and rehospitalization in 3 months, enzyme levels increased in these groups. Increased aspartate transaminase (AST level) was associated with inotrope infusion in AHF patients (42 vs. 82 mg/dL, P = 0.03). Conclusions: Abnormal transaminases and uric acid levels are seen in AHF patients. Increased AST levels may be a predictor of the need for inotrope during hospital course in these patients. PMID:26528447

  4. Charting a Roadmap for Heart Failure Biomarker Studies

    PubMed Central

    Ahmad, Tariq; Fiuzat, Mona; Pencina, Michael J.; Geller, Nancy L.; Zannad, Faiez; Cleland, John G. F.; Snider, James V.; Blankenberg, Stephan; Adams, Kirkwood F.; Redberg, Rita F.; Kim, Jae B.; Mascette, Alice; Mentz, Robert J.; O'Connor, Christopher M.; Felker, G. Michael; Januzzi, James L.

    2014-01-01

    Heart failure is a syndrome with a pathophysiological basis that can be traced to dysfunction in several interconnected molecular pathways. Identification of biomarkers of heart failure that allow measurement of the disease on a molecular level has resulted in enthusiasm for their use in prognostication and selection of appropriate therapies. However, despite considerable amounts of information available on numerous biomarkers, inconsistent research methodologies and lack of clinical correlations have made bench-to-bedside translations rare and left the literature with countless publications of varied quality. There is a need for a systematic and collaborative approach aimed at definitively studying the clinical benefits of novel biomarkers. In this review, on the basis of input from academia, industry, and governmental agencies, we propose a systematized approach based on adherence to specific quality measures for studies looking to augment current prediction model or use biomarkers to tailor therapeutics. We suggest that study quality, rather than results, should determine publication and propose a system for grading biomarker studies. We outline the need for collaboration between clinical investigators and statisticians to introduce more advanced statistical methodologies into the field of biomarkers that would allow for data from a large number of variables to be distilled into clinically actionable information. Lastly, we propose the creation of a heart failure biomarker consortium that would allow for a comprehensive list of biomarkers to be concomitantly analyzed in a pooled sample of randomized clinical trials and hypotheses to be generated for testing in biomarker-guided trials. Such a consortium could collaborate in sharing samples to identify biomarkers, undertake meta- analyses on completed trials, and spearhead clinical trials to test the clinical utility of new biomarkers. PMID:24929535

  5. Correlates of Quality of Life in Rural Heart Failure Patients

    PubMed Central

    Nesbitt, Thomas; Doctorvaladan, Sahar; Southard, Jeffrey A.; Singh, Satinder; Fekete, Anne; Marie, Kate; Moser, Debra K.; Pelter, Michelle M.; Robinson, Susan; Wilson, Machelle D.; Cooper, Lawton; Dracup, Kathleen

    2014-01-01

    Background There is abundant research indicating poor physical, psychological and social functioning of patients with chronic heart failure (HF), a reality that can lead to poor health related quality of life (HRQoL). Little is known about the experience of rural HF patients. Methods and Results This study was part of a randomized clinical trial titled Rural Education to Improve Outcomes in Heart Failure (REMOTE-HF) designed to test an education and counseling intervention to improve self-care in patients with HF. We evaluated 612 rural patients. Multiple validated questionnaires were administered to assess patient perceptions of health and health literacy. Baseline factors were collected and compared to baseline QoL measures only. Patients’ HRQoL was assessed using the Minnesota Living with Heart Failure (MLWHF) scale. The data were analyzed using a general linear model to test the association of various patient characteristics with quality of life in rural patients with HF. Patients were 65.8 (+12.9) years of age. The majority were male (58.7%), married (56.4%) and had completed a high school education (80.9%). Factors associated with reduced quality of life amongst this population include: geographic location, younger age, male gender, higher NYHA class, worse HF knowledge, poorer perceived control and symptoms of depression or anxiety. The data provided no evidence of an association between left ventricular ejection fraction and quality of life. Conclusions This study of rural HF patients confirms previously identified factors associated with perceptions of quality of life. However, further study is warranted with an urban control group. PMID:25146960

  6. Augmented Phosphorylation of Cardiac Troponin I in Hypertensive Heart Failure*

    PubMed Central

    Dong, Xintong; Sumandea, C. Amelia; Chen, Yi-Chen; Garcia-Cazarin, Mary L.; Zhang, Jiang; Balke, C. William; Sumandea, Marius P.; Ge, Ying

    2012-01-01

    An altered cardiac myofilament response to activating Ca2+ is a hallmark of human heart failure. Phosphorylation of cardiac troponin I (cTnI) is critical in modulating contractility and Ca2+ sensitivity of cardiac muscle. cTnI can be phosphorylated by protein kinase A (PKA) at Ser22/23 and protein kinase C (PKC) at Ser22/23, Ser42/44, and Thr143. Whereas the functional significance of Ser22/23 phosphorylation is well understood, the role of other cTnI phosphorylation sites in the regulation of cardiac contractility remains a topic of intense debate, in part, due to the lack of evidence of in vivo phosphorylation. In this study, we utilized top-down high resolution mass spectrometry (MS) combined with immunoaffinity chromatography to determine quantitatively the cTnI phosphorylation changes in spontaneously hypertensive rat (SHR) model of hypertensive heart disease and failure. Our data indicate that cTnI is hyperphosphorylated in the failing SHR myocardium compared with age-matched normotensive Wistar-Kyoto rats. The top-down electron capture dissociation MS unambiguously localized augmented phosphorylation sites to Ser22/23 and Ser42/44 in SHR. Enhanced Ser22/23 phosphorylation was verified by immunoblotting with phospho-specific antibodies. Immunoblot analysis also revealed up-regulation of PKC-? and -?, decreased PKC?, but no changes in PKA or PKC-? levels in the SHR myocardium. This provides direct evidence of in vivo phosphorylation of cTnI-Ser42/44 (PKC-specific) sites in an animal model of hypertensive heart failure, supporting the hypothesis that PKC phosphorylation of cTnI may be maladaptive and potentially associated with cardiac dysfunction. PMID:22052912

  7. Inflammation as a therapeutic target in heart failure? A scientific statement from the Translational Research Committee of the Heart Failure Association of the European Society of Cardiology

    PubMed Central

    Heymans, Stephane; Hirsch, Emilio; Anker, Stefan D.; Aukrust, Pal; Balligand, Jean-Luc; Cohen-Tervaert, Jan W.; Drexler, Helmut; Filippatos, Gerasimos; Felix, Stephan B.; Gullestad, Lars; Hilfiker-Kleiner, Denise; Janssens, Stefan; Latini, Roberto; Neubauer, Gitte; Paulus, Walter J.; Pieske, Burkert; Ponikowski, Piotr; Schroen, Blanche; Schultheiss, Heinz-Peter; Tschpe, Carsten; Van Bilsen, Marc; Zannad, Faiez; McMurray, John; Shah, Ajay M.

    2009-01-01

    The increasing prevalence of heart failure poses enormous challenges for health care systems worldwide. Despite effective medical interventions that target neurohumoral activation, mortality and morbidity remain substantial. Evidence for inflammatory activation as an important pathway in disease progression in chronic heart failure has emerged in the last two decades. However, clinical trials of anti-inflammatory therapies (such as anti-tumor necrosis factor-? approaches) have to date failed to show benefit in heart failure patients. The Heart Failure Association of the European Society of Cardiology recently organized an expert workshop to address the issue of inflammation in heart failure from a basic science, translational and clinical perspective, and to assess whether specific inflammatory pathways may yet serve as novel therapeutic targets for this condition. This consensus document represents the outcome of the workshop and defines key research questions that still need to be addressed as well as considering the requirements for future clinical trials in this area. PMID:19168509

  8. Critical care for paediatric patients with heart failure.

    PubMed

    Costello, John M; Mazwi, Mjaye L; McBride, Mary E; Gambetta, Katherine E; Eltayeb, Osama; Epting, Conrad L

    2015-08-01

    This review offers a critical-care perspective on the pathophysiology, monitoring, and management of acute heart failure syndromes in children. An in-depth understanding of the cardiovascular physiological disturbances in this population of patients is essential to correctly interpret clinical signs, symptoms and monitoring data, and to implement appropriate therapies. In this regard, the myocardial force-velocity relationship, the Frank-Starling mechanism, and pressure-volume loops are discussed. A variety of monitoring modalities are used to provide insight into the haemodynamic state, clinical trajectory, and response to treatment. Critical-care treatment of acute heart failure is based on the fundamental principles of optimising the delivery of oxygen and minimising metabolic demands. The former may be achieved by optimising systemic arterial oxygen content and the variables that determine cardiac output: heart rate and rhythm, preload, afterload, and contractility. Metabolic demands may be decreased by a number of ways including positive pressure ventilation, temperature control, and sedation. Mechanical circulatory support should be considered for refractory cases. In the near future, monitoring modalities may be improved by the capture and analysis of complex clinical data such as pressure waveforms and heart rate variability. Using predictive modelling and streaming analytics, these data may then be used to develop automated, real-time clinical decision support tools. Given the barriers to conducting multi-centre trials in this population of patients, the thoughtful analysis of data from multi-centre clinical registries and administrative databases will also likely have an impact on clinical practice. PMID:26377713

  9. Tai Chi Exercise in Patients With Chronic Heart Failure

    PubMed Central

    Yeh, Gloria Y.; McCarthy, Ellen P.; Wayne, Peter M.; Stevenson, Lynne W.; Wood, Malissa J.; Forman, Daniel; Davis, Roger B.; Phillips, Russell S.

    2012-01-01

    Background Preliminary evidence suggests that meditative exercise may have benefits for patients with chronic systolic heart failure (HF); this has not been rigorously tested in a large clinical sample. We sought to investigate whether tai chi, as an adjunct to standard care, improves functional capacity and quality of life in patients with HF. Methods A single-blind, multisite, parallel-group, randomized controlled trial evaluated 100 outpatients with systolic HF (New York Heart Association class I-III, left ventricular ejection fraction ?40%) who were recruited between May 1, 2005, and September 30, 2008. A group-based 12-week tai chi exercise program (n=50) or time-matched education (n=50, control group) was conducted. Outcome measures included exercise capacity (6-minute walk test and peak oxygen uptake) and disease-specific quality of life (Minnesota Living With Heart Failure Questionnaire). Results Mean (SD) age of patients was 67(11) years; baseline values were left ventricular ejection fraction, 29% (8%) and peak oxygen uptake, 13.5 mL/kg/min; the median New York Heart Association class of HF was class II. At completion of the study, there were no significant differences in change in 6-minute walk distance and peak oxygen uptake (median change [first quartile, third quartile], 35 [?2, 51] vs 2 [?7, 54] meters, P=.95; and 1.1 [?1.1, 1.5] vs ?0.5 [?1.2, 1.8] mL/kg/min, P=.81) when comparing tai chi and control groups; however, patients in the tai chi group had greater improvements in quality of life (Minnesota Living With Heart Failure Questionnaire, ?19 [?23, ?3] vs 1 [?16, 3], P=.02). Improvements with tai chi were also seen in exercise self-efficacy (Cardiac Exercise Self-efficacy Instrument, 0.1 [0.1, 0.6] vs ?0.3 [?0.5, 0.2], P<.001) and mood (Profile of Mood States total mood disturbance, ?6 [?17, 1] vs ?1 [?13, 10], P=.01). Conclusion Tai chi exercise may improve quality of life, mood, and exercise self-efficacy in patients with HF. Trial Registration clinicaltrials.gov Identifier: NCT00110227 PMID:21518942

  10. Mineralocorticoid receptor antagonists as diuretics: Can congestive heart failure learn from liver failure?

    PubMed

    Masoumi, Amirali; Ortiz, Fernando; Radhakrishnan, Jai; Schrier, Robert W; Colombo, Paolo C

    2015-05-01

    Despite significant improvements in diagnosis, understanding the pathophysiology and management of the patients with acute decompensated heart failure (ADHF), diuretic resistance, yet to be clearly defined, is a major hurdle. Secondary hyperaldosteronism is a pivotal factor in pathogenesis of sodium retention, refractory congestion in heart failure (HF) as well as diuretic resistance. In patients with decompensated cirrhosis who suffer from ascites, similar pathophysiological complications have been recognized. Administration of natriuretic doses of mineralocorticoid receptor antagonists (MRAs) has been well established in management of cirrhotic patients. However, this strategy in patients with ADHF has not been well studied. This article will discuss the potential use of natriuretic doses of MRAs to overcome the secondary hyperaldosteronism as an alternative diuretic regimen in patients with HF. PMID:25447845

  11. Cheyne-Stokes respiration in patients with heart failure: prevalence, causes, consequences and treatments.

    PubMed

    Brack, Thomas; Randerath, Winfried; Bloch, Konrad E

    2012-01-01

    Cheyne-Stokes respiration (CSR) is characterized by a pattern of cyclic oscillations of tidal volume and respiratory rate with periods of hyperpnea alternating with hypopnea or apnea in patients with heart failure. CSR harms the failing heart through intermittent hypoxia brought about by apnea and hypopnea and recurrent sympathetic surges. CSR impairs the quality of life and increases cardiac mortality in patients with heart failure. Thus, CSR should actively be pursued in patients with severe heart failure. When CSR persists despite optimal therapy of heart failure, noninvasive adaptive servoventilation is currently the most promising treatment. PMID:22025128

  12. [Chronic heart failure and its consequences on the partner relationship].

    PubMed

    Sztajzel, Juan

    2015-12-01

    There are presently few data on chronic heart failure (CHF) and its consequences on the partner relationship. The aim of our study was to assess how patients with severe CHF and their female partners were affected in their relationship. First, there was a need to address the issue of sexuality with the doctor because of fear of the occurrence of a cardiac event or an implantable cardioverter defibrillator shock. Second, there was often a significant decrease in libido and erectile dysfunction associated with general depressive symptoms. Finally, the female partners in several couples developed an overprotective behavior leading to resentment and frustration in patients towards them. PMID:26790235

  13. Heart failure with preserved ejection fraction - unwinding the diagnosis mystique

    PubMed Central

    Asrar ul Haq, Muhammad; Mutha, Vivek; Rudd, Nima; Hare, David L; Wong, Chiew

    2014-01-01

    A precise diagnosis of diastolic dysfunction is often difficult and requires invasive techniques to determine left ventricular volume, relaxation, and compliance properties. At this current point of time there is no single non-invasive index available to adequately reflect diastolic function, perhaps because of the numerous factors that can alter diastolic function. In most clinical settings, diastolic function is estimated using Doppler echocardiography. Cardiac magnetic resonance imaging (CMRI) is yet another emerging modality for diastolic function analysis. Here we present a comprehensive review of the various parameters used to assess diastolic function as part of diagnosis of clinical syndrome “Heart failure with preserved ejection fraction (HFPEF)”. PMID:25360388

  14. Biomarkers in paediatric heart failure: is there value?

    PubMed

    Lin, Kimberly Y

    2015-12-01

    A biomarker is any measurable, surrogate characteristic, which reflects either the presence or the absence of a disease state. This can be a blood test, an imaging characteristic, an exercise parameter, and even a genetic profile. Serum biomarkers are particularly attractive in that their cost to the patient is relatively low in terms of money, time, risk, and ease of obtaining a sample. The potential benefits of a good biomarker are manifold. This manuscript will review serum biomarkers of proposed utility in paediatric heart failure, especially with respect to their ability to aid clinical decision making, diagnosis, and prognosis. PMID:26675592

  15. Germany's Disease Management Program: Improving Outcomes in Congestive Heart Failure

    PubMed Central

    Kottmair, Stefan; Frye, Christian; Ziegenhagen, Dieter J.

    2005-01-01

    Hospital admissions among patients with congestive heart failure (CHF) are a major contributor to health care costs. A comprehensive disease management program for CHF was developed for private and statutory health insurance companies in order to improve health outcomes and reduce rehospitalization rates and costs. The program comprises care calls, written training material, telemetric monitoring, and health reports. Currently, 909 members from six insurance companies are enrolled. Routine evaluation, based on medical data warehouse software, demonstrates benefits in terms of improved health outcomes and processes of care. Economical evaluation of claims data indicates significant cost savings in a pre/post study design. PMID:17288080

  16. Pimobendan in heart failure therapy--a silver bullet?

    PubMed

    Gordon, Sonya G; Miller, Matthew W; Saunders, Ashley B

    2006-01-01

    Pimobendan is a novel agent with properties that are highly desirable in the clinical management of congestive heart failure (CHF) secondary to both dilated cardiomyopathy (DCM) and chronic degenerative valvular disease in dogs. Review of available data suggests that pimobendan is safe, well tolerated, and leads to enhanced quality of life in dogs with CHF secondary to DCM or chronic valvular disease when used in combination with furosemide or other conventional therapies (e.g., angiotensin-converting enzyme inhibitors, digoxin). Pimobendan leads to a reduction in mortality from CHF associated with DCM, and ongoing studies are evaluating its effects on mortality associated with chronic valvular disease. PMID:16527909

  17. Ultrafiltration in Decompensated Heart Failure with Cardiorenal Syndrome

    PubMed Central

    Bart, Bradley A.; Goldsmith, Steven R.; Lee, Kerry L.; Givertz, Michael M.; OConnor, Christopher M.; Bull, David A.; Redfield, Margaret M.; Deswal, Anita; Rouleau, Jean L.; LeWinter, Martin M.; Ofili, Elizabeth O.; Stevenson, Lynne W.; Semigran, Marc J.; Felker, G. Michael; Chen, Horng H.; Hernandez, Adrian F.; Anstrom, Kevin J.; McNulty, Steven E.; Velazquez, Eric J.; Ibarra, Jenny C.; Mascette, Alice M.; Braunwald, Eugene

    2013-01-01

    BACKGROUND Ultrafiltration is an alternative strategy to diuretic therapy for the treatment of patients with acute decompensated heart failure. Little is known about the efficacy and safety of ultrafiltration in patients with acute decompensated heart failure complicated by persistent congestion and worsened renal function. METHODS We randomly assigned a total of 188 patients with acute decompensated heart failure, worsened renal function, and persistent congestion to a strategy of stepped pharmacologic therapy (94 patients) or ultrafiltration (94 patients). The primary end point was the bivariate change from baseline in the serum creatinine level and body weight, as assessed 96 hours after random assignment. Patients were followed for 60 days. RESULTS Ultrafiltration was inferior to pharmacologic therapy with respect to the bivariate end point of the change in the serum creatinine level and body weight 96 hours after enrollment (P=0.003), owing primarily to an increase in the creatinine level in the ultrafiltration group. At 96 hours, the mean change in the creatinine level was ?0.040.53 mg per deciliter (?3.546.9 ?mol per liter) in the pharmacologic-therapy group, as compared with +0.230.70 mg per deciliter (20.361.9 ?mol per liter) in the ultrafiltration group (P=0.003). There was no significant difference in weight loss 96 hours after enrollment between patients in the pharmacologic-therapy group and those in the ultrafiltration group (a loss of 5.55.1 kg [12.111.3 lb] and 5.73.9 kg [12.68.5 lb], respectively; P=0.58). A higher percentage of patients in the ultrafiltration group than in the pharmacologic-therapy group had a serious adverse event (72% vs. 57%, P=0.03). CONCLUSIONS In a randomized trial involving patients hospitalized for acute decompensated heart failure, worsened renal function, and persistent congestion, the use of a stepped pharmacologic-therapy algorithm was superior to a strategy of ultrafiltration for the preservation of renal function at 96 hours, with a similar amount of weight loss with the two approaches. Ultrafiltration was associated with a higher rate of adverse events. PMID:23131078

  18. [Ventilatory disorders in patients with chronic heart failure].

    PubMed

    Grzywa-Celi?ska, Anna; Dyczko, Monika; R?kas-Wjcik, Agata; Szmygin-Milanowska, Katarzyna; Witczak, Agnieszka; Ostrowski, Stanis?aw; Barud, Wojciech; Mosiewicz, Jerzy

    2015-10-01

    Chronic heart failure (CHF) is a condition in which both structure and functional capacity of cardiac muscle are impaired, resulting in ineffective peripheral tissue perfusion. Affecting numerous organs and systems, it is currently considered to be a systemic illness. Among significant, however until now, hardly recognized consequences of CHF there are ventilatory disorders. Their presence may be explained by proximity of heart and lungs inside rib cage or by close functional cooperation between these two organs. Ventilatory disorders clinically manifest as exacerbations of the underlying disease, i.e. intense dyspnea--primarily exertional in nature, over time, present even at rest. On the basis of functional pulmonary tests, ventilatory disorders may be classified into three categories: restrictive, obstructive and most commonly--mixed. The restrictive model is represented in bodypletysmography as reduction in the total lung capacity to values less than 5th percentile of the predicted values for normals, while Tiffeneau index remains intact. Such condition may probably result from the chronic inflammatory process affecting lung tissue, for which the reaction of macrophage cells to both pulmonary stasis, as well as increased volume of interstitial and alveolar fluid remains the underlying cause. The increased formation of connective tissue fibers engenders thickening of alveolar-capillary membrane, occurrence of disturbed oxygen diffusion and emergence of hypoxemic respiratory failure. Ventilatory disorders of obstructive nature are characterised by reduction of Tiffeneau index--the calculated ratio between forced expiratory volume in 1. second and forced vital capacity--to values below 5th percentile of the predicted range. The research results indicate for the presence of bronchiolar narrowing--dominant in small-diameter bronchi and bronchioles, with larger structures being unaffected--clearly depicted in spirometry as reduced levels of forced expiratory flow after exhaling 50% and 75% of forced vital capacity. Due to a considerable epidemiological problem, as well as significance of the clinical symptoms manifesting ventilatory disorders in course of chronic heart failure, there should be put emphasis on cardiac injury prevention in individuals from risk groups and the proper treatment of patients already suffering from chronic heart failure. PMID:26608495

  19. Improving Congestive Heart Failure Care with a Clinical Decision Unit.

    PubMed

    Carpenter, Jo Ellen; Short, Nancy; Williams, Tracy E; Yandell, Ben; Bowers, Margaret T

    2015-01-01

    Evidence supporting the development of Clinical Decision Units (CDUs) to impact congestive heart failure readmission rates comes from several categories of the literature. In this study, a pre-post design with comparison group was used to evaluate the impact of the CDU. Early changes in clinical and financial outcome indicators are encouraging. Nurse leaders seek ways to improve clinical outcomes while managing the current financially challenging environment. Implementation of a CDU provides many opportunities for nurse leaders to positively impact clinical care and financial performance within their institutions. PMID:26625578

  20. The Prevention of Hospital Readmissions in Heart Failure.

    PubMed

    Ziaeian, Boback; Fonarow, Gregg C

    2016-01-01

    Heart failure (HF) is a growing healthcare burden and one of the leading causes of hospitalizations and readmission. Preventing readmissions for HF patients is an increasing priority for clinicians, researchers, and various stakeholders. The following review will discuss the interventions found to reduce readmissions for patients and improve hospital performance on the 30-day readmission process measure. While evidence-based therapies for HF management have proliferated, the consistent implementation of these therapies and development of new strategies to more effectively prevent readmissions remain areas for continued improvement. PMID:26432556

  1. Stem cell therapy: promising treatment in heart failure?

    PubMed

    Loughran, John H; Chugh, Atul R; Ismail, Imtiaz; Bolli, Roberto

    2013-03-01

    Cardiac repair through the use of regenerative medicine has been a considerable research focus over the last decade. Several stem cell types have been investigated over this timeframe as potential candidates to target post-infarction heart failure. The progression of investigation through the rigors of clinical trial design has provided some answers as to the potential clinical utility of this therapy; although there are many questions that remain. This review will concentrate on the clinical trial results of stem cell therapy for cardiac repair since the turn of the century and discuss some of the points that need clarification before this form of therapy can be considered for widespread applicability. PMID:23354783

  2. Cellular basis of triggered arrhythmias in heart failure.

    PubMed

    Pogwizd, Steven M; Bers, Donald M

    2004-02-01

    Ventricular tachycardia in nonischemic heart failure (HF) initiates by a nonreentrant mechanism that appears to be due to triggered activity primarily from delayed afterdepolarizations that arise from altered cellular Ca handling and ionic currents. In HF, factors that conspire to enhance triggered arrhythmias include upregulated Na/Ca exchange, preserved beta-adrenergic responsiveness, and decreased I(K1). Overall, the further delineation of key factors that underlie triggered arrhythmias in HF will provide the basis for new therapeutic strategies directed toward novel targets that can reduce the high incidence of sudden death in patients with HF. PMID:15030791

  3. Prognosis: does exercise training reduce adverse events in heart failure?

    PubMed

    Myers, Jonathan; Brawner, Clinton A; Haykowsky, Mark J F; Taylor, Rod S

    2015-01-01

    Patients with heart failure (HF) were once discouraged from participating in exercise programs because of concerns regarding safety and the potential for harm to an already damaged myocardium. However, studies over the last 3 decades have provided extensive insights into both the health outcome benefits of exercise and the mechanisms underlying these benefits. Studies on the outcome benefits of exercise training, including mortality and hospitalization, have been convincing. This article reviews the physiologic benefits of exercise training in HF, studies on exercise training in women, results and implications of the HF-ACTION trial, and recent meta-analyses using the Cochrane data base. PMID:25432474

  4. Exercise physiology in heart failure and preserved ejection fraction.

    PubMed

    Haykowsky, Mark J; Kitzman, Dalane W

    2014-07-01

    Recent advances in the pathophysiology of exercise intolerance in patients with heart failure with preserved ejection fraction (HFPEF) suggest that noncardiac peripheral factors contribute to the reduced peak V(o2) (peak exercise oxygen uptake) and to its improvement after endurance exercise training. A greater understanding of the peripheral skeletal muscle vascular adaptations that occur with physical conditioning may allow for tailored exercise rehabilitation programs. The identification of specific mechanisms that improve whole body and peripheral skeletal muscle oxygen uptake could establish potential therapeutic targets for medical therapies and a means to follow therapeutic response. PMID:24975908

  5. High prevalence of undetected heart failure in long-term care residents: findings from the Heart Failure in Care Homes (HFinCH) study

    PubMed Central

    Hancock, Helen C.; Close, Helen; Mason, James M.; Murphy, Jerry J.; Fuat, Ahmet; Singh, Raj; Wood, Esther; de Belder, Mark; Brennan, Gill; Hussain, Nehal; Kumar, Nitin; Wilson, Doug; Hungin, A. Pali S.

    2013-01-01

    Aims Diagnosis of heart failure in older people in long-term care is challenging because of co-morbidities, cognitive deficit, polypharmacy, immobility, and poor access to services. This study aimed to ascertain heart failure prevalence and clinical management in this population. Methods and results A total of 405 residents, aged 65100 years, in 33 UK care facilities were prospectively enrolled between April 2009 and June 2010. The presence of heart failure was determined using European Society of Cardiology guidelines, modified where necessary for immobility. Evaluation of symptoms and signs, functional capacity, and quality of life, portable on-site echocardiography, and medical record review were completed in 399 cases. The point prevalence of heart failure was 22.8% [n = 91, 95% confidence interval (CI) 18.827.2%]; of these, 62.7% (n = 57, 95% CI 59.666.5%) had heart failure with preserved ejection fraction and 37.3% had left ventricular systolic dysfunction (n = 34, 95% CI 34.840.5%). A total of 76% (n = 61) of previous diagnoses of heart failure were not confirmed, and up to 90% (n = 82) of study cases were new. No symptoms or signs were reliable predictors of heart failure. Conclusion Heart failure was diagnosed in almost a quarter of residents: the prevalence was substantially higher than in other populations. The majority of heart failure cases were undiagnosed, while three-quarters of previously recorded cases were misdiagnosed. Common symptoms and signs appear to have little clinical utility in this population. Early, accurate differential diagnosis is key to the effective management of heart failure; this may be failing in long-term care facilities. Trial registration ISRCTN19781227 PMID:23112002

  6. Coexisting Frailty, Cognitive Impairment, and Heart Failure: Implications for Clinical Care

    PubMed Central

    Butts, Brittany; Gary, Rebecca

    2015-01-01

    Objective To review some of the proposed pathways that increase frailty risk in older persons with heart failure and to discuss tools that may be used to assess for changes in physical and cognitive functioning in this population in order to assist with appropriate and timely intervention. Methods Review of the literature. Results Heart failure is the only cardiovascular disease that is increasing by epidemic proportions, largely due to an aging society and therapeutic advances in disease management. Because heart failure is largely a cardiogeriatric syndrome, age-related syndromes such as frailty and cognitive impairment are common in heart failure patients. Compared with age-matched counterparts, older adults with heart failure 4 to 6 times more likely to be frail or cognitively impaired. The reason for the high prevalence of frailty and cognitive impairment in this population is not well known but may likely reflect the synergistic effects of heart failure and aging, which may heighten vulnerability to stressors and accelerate loss of physiologic reserve. Despite the high prevalence of frailty and cognitive impairment in the heart failure population, these conditions are not routinely screened for in clinical practice settings and guidelines on optimal assessment strategies are lacking. Conclusion Persons with heart failure are at an increased risk for frailty, which may worsen symptoms, impair self-management, and lead to worse heart failure outcomes. Early detection of frailty and cognitive impairment may be an opportunity for intervention and a key strategy for improving clinical outcomes in older adults with heart failure. PMID:26594103

  7. [Surgical heart failure treatment program - the experience of Kazakhstan].

    PubMed

    Bekbossynov, Serik; Medressova, Assel; Murzagaliyev, Muradym; Salov, Roman; Dzhetybayeva, Saltanat; Andossova, Saltanat; Bekbossynova, Makhabbat; Pya, Yuriy

    2014-03-01

    In Kazakhstan, geographical and cultural reasons do not favor the development of heart transplant activity. Thus, a surgical program for treatment of advanced, refractory heart failure was implemented, focusing the efforts on ventricular assist device (VAD) therapy. The program, supported and funded by the national healthcare system, is based on a single, highly specialized surgical Center for the operation, and on a regional infrastructure for outpatient follow-up. Regional VAD coordinators are educated by the National Center. They are in charge of regular patient check, anticoagulant and antiplatelet treatment prescription, and continuing patients' and caregivers' education, mainly regarding driveline exit site dressing and driveline stabilization. From November 2011 to November 2013, 95 patients received 100 devices, mainly for left ventricular support (LVAD): HeartMate II, n=70, HeartWare, n=25. Mean age was 49.5 years, and 87.37% of the patients were males. Most patients had INTERMACS profile 4 (55%), followed by 3 and 2 (17% each). Symptomatic and functional improvement are testified by changes from baseline to month 3 of NYHA functional class (from III-IV to I-II), results of the 6-min walk test (from 152 to 440 m), and NT-proBNP levels (from 6997 to 1126 pg/ml). Overall 1-year survival was 69%, with a trend for outcome improvement over time and a relationship with preoperative INTERMACS profile (1-year survival of 60% in patients with INTERMACS profile 1-2 vs 75% in those with INTERMACS profile 3-4). In summary, where and when a heart transplant program cannot be implemented, LVAD represents a realistic therapeutic alternative. The key points for a successful VAD program are a dedicated, highly specialized multidisciplinary team at the Cardiac Surgery Center, an infrastructure throughout the country for coordinated outpatient follow-up, adequate reimbursement for this activity, and support by the healthcare system. PMID:24770427

  8. Adherence to self-care in patients with heart failure in the HeartCycle study

    PubMed Central

    Stut, Wim; Deighan, Carolyn; Cleland, John G; Jaarsma, Tiny

    2015-01-01

    Purpose The purpose of this study was to evaluate a novel online education and coaching program to promote self-care among patients with heart failure. In this program, education and coaching content is automatically tailored to the knowledge and behavior of the patient. Patients and methods The evaluation of the program took place within the scope of the HeartCycle study. This multi-center, observational study examined the ability of a third generation telehealth system to enhance the management of patients recently (<60 days) admitted to the hospital for worsening heart failure or outpatients with persistent New York Heart Association (NYHA) Functional Classification III/IV symptoms. Self-reported self-care behavior was assessed at baseline and study-end by means of the 9-item European Heart Failure Self-care Behavior scale. Adherence to daily weighing, blood pressure monitoring, and reporting of symptoms was determined by analyzing the systems database. Results Of 123 patients enrolled, the mean age was 6612 years, 66% were in NYHA III and 79% were men. Self-reported self-care behavior scores (n=101) improved during the study for daily weighing, low-salt diet, physical activity (P<0.001), and fluid restriction (P<0.05). Average adherence (n=120) to measuring weight was 90%16%, to measuring blood pressure was 89%17% and to symptom reporting was 66%32%. Conclusion Self-reported self-care behavior scores improved significantly during the period of observation, and the objective evidence of adherence to daily weight and blood pressure measurements was high and remained stable over time. However, adherence to daily reporting of symptoms was lower and declined in the long-term. PMID:26316725

  9. New strategies for heart failure with preserved ejection fraction: the importance of targeted therapies for heart failure phenotypes

    PubMed Central

    Senni, Michele; Paulus, Walter J.; Gavazzi, Antonello; Fraser, Alan G.; Díez, Javier; Solomon, Scott D.; Smiseth, Otto A.; Guazzi, Marco; Lam, Carolyn S. P.; Maggioni, Aldo P.; Tschöpe, Carsten; Metra, Marco; Hummel, Scott L.; Edelmann, Frank; Ambrosio, Giuseppe; Stewart Coats, Andrew J.; Filippatos, Gerasimos S.; Gheorghiade, Mihai; Anker, Stefan D.; Levy, Daniel; Pfeffer, Marc A.; Stough, Wendy Gattis; Pieske, Burkert M.

    2014-01-01

    The management of heart failure with reduced ejection fraction (HF-REF) has improved significantly over the last two decades. In contrast, little or no progress has been made in identifying evidence-based, effective treatments for heart failure with preserved ejection fraction (HF-PEF). Despite the high prevalence, mortality, and cost of HF-PEF, large phase III international clinical trials investigating interventions to improve outcomes in HF-PEF have yielded disappointing results. Therefore, treatment of HF-PEF remains largely empiric, and almost no acknowledged standards exist. There is no single explanation for the negative results of past HF-PEF trials. Potential contributors include an incomplete understanding of HF-PEF pathophysiology, the heterogeneity of the patient population, inadequate diagnostic criteria, recruitment of patients without true heart failure or at early stages of the syndrome, poor matching of therapeutic mechanisms and primary pathophysiological processes, suboptimal study designs, or inadequate statistical power. Many novel agents are in various stages of research and development for potential use in patients with HF-PEF. To maximize the likelihood of identifying effective therapeutics for HF-PEF, lessons learned from the past decade of research should be applied to the design, conduct, and interpretation of future trials. This paper represents a synthesis of a workshop held in Bergamo, Italy, and it examines new and emerging therapies in the context of specific, targeted HF-PEF phenotypes where positive clinical benefit may be detected in clinical trials. Specific considerations related to patient and endpoint selection for future clinical trials design are also discussed. PMID:25104786

  10. New strategies for heart failure with preserved ejection fraction: the importance of targeted therapies for heart failure phenotypes.

    PubMed

    Senni, Michele; Paulus, Walter J; Gavazzi, Antonello; Fraser, Alan G; Díez, Javier; Solomon, Scott D; Smiseth, Otto A; Guazzi, Marco; Lam, Carolyn S P; Maggioni, Aldo P; Tschöpe, Carsten; Metra, Marco; Hummel, Scott L; Edelmann, Frank; Ambrosio, Giuseppe; Stewart Coats, Andrew J; Filippatos, Gerasimos S; Gheorghiade, Mihai; Anker, Stefan D; Levy, Daniel; Pfeffer, Marc A; Stough, Wendy Gattis; Pieske, Burkert M

    2014-10-21

    The management of heart failure with reduced ejection fraction (HF-REF) has improved significantly over the last two decades. In contrast, little or no progress has been made in identifying evidence-based, effective treatments for heart failure with preserved ejection fraction (HF-PEF). Despite the high prevalence, mortality, and cost of HF-PEF, large phase III international clinical trials investigating interventions to improve outcomes in HF-PEF have yielded disappointing results. Therefore, treatment of HF-PEF remains largely empiric, and almost no acknowledged standards exist. There is no single explanation for the negative results of past HF-PEF trials. Potential contributors include an incomplete understanding of HF-PEF pathophysiology, the heterogeneity of the patient population, inadequate diagnostic criteria, recruitment of patients without true heart failure or at early stages of the syndrome, poor matching of therapeutic mechanisms and primary pathophysiological processes, suboptimal study designs, or inadequate statistical power. Many novel agents are in various stages of research and development for potential use in patients with HF-PEF. To maximize the likelihood of identifying effective therapeutics for HF-PEF, lessons learned from the past decade of research should be applied to the design, conduct, and interpretation of future trials. This paper represents a synthesis of a workshop held in Bergamo, Italy, and it examines new and emerging therapies in the context of specific, targeted HF-PEF phenotypes where positive clinical benefit may be detected in clinical trials. Specific considerations related to patient and endpoint selection for future clinical trials design are also discussed. PMID:25104786

  11. Frailty in advanced heart failure: a systematic review.

    PubMed

    Jha, Sunita R; Ha, Hakeem S K; Hickman, Louise D; Hannu, Malin; Davidson, Patricia M; Macdonald, Peter S; Newton, Phillip J

    2015-09-01

    Frailty is a common geriatric syndrome of increased vulnerability to adverse events. The prevalence of frailty among chronic heart failure (CHF) is high and confers a greater risk of adverse events including falls, hospitalisation and mortality. There have been few studies assessing frailty in CHF. A review of the key databases was conducted from 2004 to 2014 including the key search terms 'frail elderly' and 'heart failure'. The following electronic databases were searched: Medline, Cumulative Index for Nursing and Allied Health and Academic Search Complete, with reference lists being manually searched. Articles were included if frailty was assessed using a valid measuring tool in a population with a confirmed diagnosis of CHF. The search yielded a total of 393 articles with 8 articles being selected for review. The prevalence of frailty among those with CHF was high, ranging from 18 to 54%. The frailty phenotype and geriatric assessments tools were the most common frailty measures utilised; high rates of co-morbidity, hospitalisation and mortality were identified. Frailty is common in CHF and is associated with adverse outcomes. PMID:25982016

  12. Translational success stories: angiotensin receptor 1 antagonists in heart failure.

    PubMed

    Dell'Italia, Louis J

    2011-08-01

    The title of the proposed series of reviews is Translational Success Stories. The definition of "translation" according to Webster is, "an act, process, or instance of translating as a rendering of one language into another." In the context of this inaugural review, it is the translation of Tigerstedt's and Bergman's(1) discovery in 1898 of the vasoconstrictive effects of an extract of rabbit kidney to the treatment of heart failure. As recounted by Marks and Maxwell,(2) their discovery was heavily influenced by the original experiments of the French physiologist Brown-Séquard, who was the author of the doctrine that "many organs dispense substances into the blood which are not ordinary waste products, but have specific functions." They were also influenced by Bright's(3) original observation that linked kidney disease with hypertension with the observation that patients dying with contracted kidneys often exhibited a hard, full pulse and cardiac hypertrophy. However, from Tigerstedt's initial discovery, there was a long and arduous transformation of ideas and paradigms that eventually translated to clinical applications. Although the role of the renin-angiotensin system in the pathophysiology of hypertension and heart failure was suspected through the years, beneficial effects from its blockade were not realized until the early 1970s. Thus, this story starts with a short historical perspective that provides the reader some insight and appreciation into the long delay in translation. PMID:21817164

  13. Mechanisms and management of diuretic resistance in congestive heart failure

    PubMed Central

    De Bruyne, L K M

    2003-01-01

    Diuretic drugs are used almost universally in patients with congestive heart failure, most frequently the potent loop diuretics. Despite their unproven effect on survival, their indisputable efficacy in relieving congestive symptoms makes them first line therapy for most patients. In the treatment of more advanced stages of heart failure diuretics may fail to control salt and water retention despite the use of appropriate doses. Diuretic resistance may be caused by decreased renal function and reduced and delayed peak concentrations of loop diuretics in the tubular fluid, but it can also be observed in the absence of these pharmacokinetic abnormalities. When the effect of a short acting diuretic has worn off, postdiuretic salt retention will occur during the rest of the day. Chronic treatment with a loop diuretic results in compensatory hypertrophy of epithelial cells downstream from the thick ascending limb and consequently its diuretic effect will be blunted. Strategies to overcome diuretic resistance include restriction of sodium intake, changes in dose, changes in timing, and combination diuretic therapy. PMID:12782772

  14. Nonlinear dynamics of congestive heart failure (Invited Paper)

    NASA Astrophysics Data System (ADS)

    Bernjak, Alan; Clarkson, Peter B. M.; McClintock, Peter V. E.; Stefanovska, Aneta

    2005-05-01

    Preliminary results are reported from a research project analysing congestive heart failure in terms a stochastic coupled-oscillator model of the cardiovascular system. Measurements of blood flow by laser Doppler flowmetry (LDF) have been processed by use of the wavelet transform to separate its oscillatory components, which number at least five. Particular attention was concentrated on the frequency content near 0.01 Hz, which is known to be associated with endothelial function. The LDF was carried out in conjunction with iontophoretically administered acetylcholine (ACh) and sodium nitroprusside (SNP) in order to evaluate endothelial reactivity. Measurements were made on 17 congestive heart failure (CHF) patients (a) on first diagnosis, and (b) again several weeks later after their treatment with a β-blocker had been stabilised. The results of these two sets of measurements are being compared with each other, and with data from an age and sex-matched group of healthy controls. It is confirmed that endothelial reactivity is reduced in CHF patients, as compared to healthy controls, and it is found that one effect of the Beta-blocker is to ameliorate the loss of endothelial function in CHF. The implications of these results are discussed.

  15. Measurement of thirst in chronic heart failure- a review.

    PubMed

    Allida, Sabine M; Inglis, Sally C; Davidson, Patricia M; Hayward, Christopher S; Newton, Phillip J

    2014-07-19

    Abstract Background: Thirst is a bothersome symptom of chronic heart failure (CHF) which impacts adversely on quality of life. Despite this, limited work has been done to investigate thirst as a symptom or to develop reliable and valid measures of thirst in CHF. The purpose of this manuscript is to establish which tools have been used in research to measure thirst in CHF. Methods: Medline, PubMed, CINAHL, and Scopus were searched using following key words thirst, heart failure, measure, scale, randomised controlled trials and multicentre studies. Results: The search discovered 37 studies of which 6 studies met the inclusion criteria. One study was a research abstract and five were full- text studies. To date, there are only three measurement tools utilised in studies examining thirst in CHF patients (Visual Analogue Scale, Numeric Rating Scale and Thirst Distress Scale). Conclusion: Thirst in CHF is measured in a non- systematic way. In recent studies, the VAS has been used to measure thirst intensity. While this measurement tool is very easy and quick to administer, using a uni-dimensional tool in conjunction with a multi-dimensional tool may be beneficial to capture all dimensions of thirst. In order to manage thirst efficiently, consistent measurement of thirst in CHF is vital. PMID:25041254

  16. Complement C3c as a Biomarker in Heart Failure

    PubMed Central

    Frey, A.; Ertl, G.; Angermann, C. E.; Hofmann, U.; Strk, S.; Frantz, S.

    2013-01-01

    Introduction. Experimental data indicates an important role of the innate immune system in cardiac remodeling and heart failure (HF). Complement is a central effector pathway of the innate immune system. Animals lacking parts of the complement system are protected from adverse remodeling. Based on these data, we hypothesized that peripheral complement levels could be a good marker for adverse remodeling and prognosis in patients with HF. Methods and Results. Since complement activation converges on the complement factor C3, we measured serum C3c, a stable C3-conversion product, in 197 patients with stable systolic HF. Subgroups with normal and elevated C3c levels were compared. C3c levels were elevated in 17% of the cohort. Patients with elevated C3c levels exhibited a trend to better survival, slightly higher LVEF, and lower NTpro-BNP values in comparison to patients with normal C3c values. No differences were found regarding NYHA functional class. Significantly more patients with elevated C3c had preexisting diabetes. The prevalence of CAD, arterial hypertension, and atrial fibrillation was not increased in patients with elevated C3c. Conclusion. Elevated C3c levels are associated with less adverse remodeling and improved survival in patients with stable systolic heart failure. PMID:24489446

  17. Experiences of air travel in patients with chronic heart failure

    PubMed Central

    Ingle, Lee; Hobkirk, James; Damy, Thibaud; Nabb, Samantha; Clark, Andrew L.; Cleland, John G.F.

    2012-01-01

    Aim To conduct a survey in a representative cohort of ambulatory patients with stable, well managed chronic heart failure (CHF) to discover their experiences of air travel. Methods An expert panel including a cardiologist, an exercise scientist, and a psychologist developed a series of survey questions designed to elicit CHF patients' experiences of air travel (Appendix1). The survey questions, information sheets and consent forms were posted out in a self-addressed envelope to 1293 CHF patients. Results 464 patients (response rate 39%) completed the survey questionnaires. 54% of patients had travelled by air since their heart failure diagnosis. 20% of all patients reported difficulties acquiring travel insurance. 65% of patients who travelled by air experienced no health-related problems. 35% of patients who travelled by air experienced health problems, mainly at the final destination, going through security and on the aircraft. 27% of all patients would not travel by air in the future. 38% of patients would consider flying again if there were more leg room on the aeroplane, if their personal health improved (18%), if they could find cheaper travel insurance (19%), if there were less waiting at the airport (11%), or if there were less walking/fewer stairs to negotiate at the airport (7%). Conclusion For most patients in this sample of stable, well managed CHF, air travel was safe. PMID:21256607

  18. Acute heart failure: inotropic agents and their clinical uses.

    PubMed

    Endoh, Masao; Hori, Masatsugu

    2006-11-01

    Inotropic agents are indispensable for the improvement of cardiac contractile dysfunction in acute or decompensated heart failure. Clinically available agents, including sympathomimetic amines (dopamine, dobutamine, noradrenaline) and selective phosphodiesterase-3 inhibitors (amrinone, milrinone, olprinone and enoximone) act via cAMP/protein kinase A (PKA)-mediated facilitation of intracellular Ca2+ mobilisation. Phosphodiesterase-3 inhibitors also have a vasodilatory action, which plays a role in improving haemodynamic parameters in certain patients, and are termed inodilators. The available inotropic agents suffer from risks of Ca2+ overload leading to arrhythmias, myocardial cell injury and ultimately, cell death. In addition, they are energetically disadvantageous because of an increase in activation energy and cellular metabolism. Furthermore, they lose their effectiveness under pathophysiological conditions, such as acidosis, stunned myocardium and heart failure. Pimobendan and levosimendan (that act by a combination of an increase in Ca2+ sensitivity and phosphodiesterase-3 inhibition) appear to be more beneficial among existing agents. Novel Ca2+ sensitisers that are under basic research warrant clinical trials to replace available inotropic agents. PMID:17059376

  19. Investigational positive inotropic agents for acute heart failure.

    PubMed

    Tamargo, Juan; Caballero, Ricardo; Gmez, Ricardo; Barana, Adriana; Amors, Irene; Delpn, Eva

    2009-09-01

    Acute heart failure represents a major public health problem due to its high prevalence, high rates of mortality and readmissions and significant healthcare costs. Patients with AHF and low cardiac output represent a small subgroup of patients with very high mortality rates that require inotropic support to improve cardiac systolic function. Classical inotropic agents, such as beta1-adrenergic agonists (dobutamine, dopamine) and phosphodiesterase III inhibitors (milrinone, enoximone) improve symptoms and hemodynamics by increasing free intracellular Ca(2+) levels, but also increase myocardial O(2) demands and exert arrhythmogenic effects. These actions explain why these drugs increase both short- and long-term mortality, particularly in patients with AHF and coronary artery disease. Thus, we need new inotropic agents that do not increase cytosolic Ca(2+) or myocardial oxygen demands or produce arrhythmogenesis for the treatment of high-risk patients with acute heart failure and low cardiac output. This review describes three new classes of investigational agents: levosimendan, a calcium sensitizer and potassium channel opener, istaroxime, the first new luso-inotropic agent and cardiac myosin activators. PMID:19534658

  20. Mortality in heart failure: clinical variables of prognostic value.

    PubMed Central

    Cleland, J G; Dargie, H J; Ford, I

    1987-01-01

    One hundred and fifty two patients with chronic heart failure caused primarily by left ventricular dysfunction were followed prospectively in an open study for a mean period of 21 months. The effects of several clinical variables on subsequent outcome were examined, including the effects of treatment, which was determined by the clinician caring for the patient and was not randomly allocated. In order of importance, frequent ventricular extrasystoles, non-treatment with amiodarone, low mean arterial pressure, and a diagnosis of coronary artery disease were associated with a poor prognosis, with each of these variables providing extra predictive information independently of the others. Initial serum potassium concentration and treadmill exercise time also carried further weak but independent prognostic information. Neither treatment with angiotensin converting enzyme inhibitors nor digoxin appeared to affect outcome. Left ventricular function (as reflected by M mode echocardiography) and the dose of diuretic also failed to predict outcome. There did, however, appear to be a reduction in the frequency of sudden death when angiotension converting enzyme inhibitors were given. Further studies are required to confirm the adverse prognostic significance of ventricular arrhythmias in patients with heart failure and the possible benefit associated with amiodarone treatment. PMID:2447925

  1. Using EHRs and Machine Learning for Heart Failure Survival Analysis.

    PubMed

    Panahiazar, Maryam; Taslimitehrani, Vahid; Pereira, Naveen; Pathak, Jyotishman

    2015-01-01

    "Heart failure (HF) is a frequent health problem with high morbidity and mortality, increasing prevalence and escalating healthcare costs" [1]. By calculating a HF survival risk score based on patient-specific characteristics from Electronic Health Records (EHRs), we can identify high-risk patients and apply individualized treatment and healthy living choices to potentially reduce their mortality risk. The Seattle Heart Failure Model (SHFM) is one of the most popular models to calculate HF survival risk that uses multiple clinical variables to predict HF prognosis and also incorporates impact of HF therapy on patient outcomes. Although the SHFM has been validated across multiple cohorts [1-5], these studies were primarily done using clinical trials databases that do not reflect routine clinical care in the community. Further, the impact of contemporary therapeutic interventions, such as beta-blockers or defibrillators, was incorporated in SHFM by extrapolation from external trials. In this study, we assess the performance of SHFM using EHRs at Mayo Clinic, and sought to develop a risk prediction model using machine learning techiniques that applies routine clinical care data. Our results shows the models which were built using EHR data are more accurate (11% improvement in AUC) with the convenience of being more readily applicable in routine clinical care. Furthermore, we demonstrate that new predictive markers (such as co-morbidities) when incorporated into our models improve prognostic performance significantly (8% improvement in AUC). PMID:26262006

  2. MINERALOCORTICOID RECEPTOR ANTAGONISM CONFERS CARDIOPROTECTION IN HEART FAILURE

    PubMed Central

    Seawell, Michael R.; Darazi, Fahed Al; Farah, Victor; Ramanathan, Kodangudi B.; Newman, Kevin P.; Bhattacharya, Syamal K.; Weber, Karl T.

    2012-01-01

    The symptoms and signs constituting the congestive heart failure (CHF) syndrome have their pathophysiologic origins rooted in a salt-avid renal state mediated by effector hormones of the renin-angiotensin-aldosterone and adrenergic nervous systems. Controlled clinical trials, conducted over the past decade in patients having minimally to markedly severe symptomatic heart failure, have demonstrated the efficacy of a pharmacologic regimen that interferes with these hormones, including aldosterone receptor binding with either spironolactone or eplerenone. Potential pathophysiologic mechanisms which have not hitherto been considered involved for the salutary responses and cardioprotection provided by these mineralocorticoid receptor antagonists are reviewed herein. In particular, we focus on the less well-recognized impact of catecholamines and aldosterone on mono- and divalent cation dyshomeostasis which leads to hypokalemia, hypomagnesemia, ionized hypocalcemia with secondary hyperparathyroidism and hypozincemia. Attendant adverse cardiac consequences include a delay in myocardial repolarization with increased propensity for supra- and ventricular arrhythmias and compromised antioxidant defenses with increased susceptibility to nonischemic cardiomyocyte necrosis. PMID:23114591

  3. Progression of heart failure after myocardial infarction in the rat.

    PubMed

    Francis, J; Weiss, R M; Wei, S G; Johnson, A K; Felder, R B

    2001-11-01

    This study examined the early neurohumoral events in the progression of congestive heart failure (CHF) after myocardial infarction (MI) in rats. Immediately after MI was induced by coronary artery ligation, rats had severely depressed left ventricular systolic function and increased left ventricular end-diastolic volume (LVEDV). Both left ventricular function and the neurohumoral indicators of CHF underwent dynamic changes over the next 6 wk. LVEDV increased continuously over the study interval, whereas left ventricular stroke volume increased but reached a plateau at 4 wk. Plasma renin activity (PRA), arginine vasopressin, and atrial natriuretic factor all increased, but with differing time courses. PRA declined to a lower steady-state level by 4 wk. Six to 8 wk after MI, CHF rats had enhanced renal sympathetic nerve activity and blunted baroreflex regulation. These findings demonstrate that the early course of heart failure is characterized not by a simple "switching on" of neurohumoral drive, but rather by dynamic fluctuations in neurohumoral regulation that are linked to the process of left ventricular remodeling. PMID:11641147

  4. Optimization of pharmacotherapy in chronic heart failure: is heart rate adequately addressed?

    PubMed

    Franke, Jennifer; Wolter, Jan Sebastian; Meme, Lillian; Keppler, Jeannette; Tschierschke, Ramon; Katus, Hugo A; Zugck, Christian

    2013-01-01

    The aim of the study is to evaluate the use of beta-blockers in chronic heart failure (CHF) and the extent of heart rate reduction achieved in clinical practice and to determine differences in outcome of patients who fulfilled select inclusion criteria of the SHIFT study according to resting heart rate modulated by beta-blocker therapy. We evaluated an all-comer population of our dedicated CHF outpatient clinic between 2006 and 2010. For inclusion, individually optimized doses of guideline-recommended pharmacotherapy including beta-blockers had to be maintained for at least 3 months and routine follow-up performed at our outpatient CHF-clinic thereafter. Treatment dosages of beta-blockers, and demographic and clinical profiles including resting heart rate were assessed. The outcome of patients who fulfilled select inclusion criteria of the SHIFT study (left-ventricular ejection fraction (LVEF) ≤35 %, sinus rhythm, NYHA II-IV) and were followed-up for at least 1 year was stratified according to resting heart rates: ≥75 versus <75 bpm and ≥70 versus <70 bpm. The composite primary endpoint was defined as all-cause death or hospital admission for worsening heart failure during 12-month follow-up. In total, 3,181 patients were assessed in regard to treatment dosages of beta-blockers, and demographic and clinical profiles including resting heart rate. Of the overall studied population, 443 patients fulfilled all inclusion criteria and entered outcome analysis. Median observation time of survivors was 27.5 months with 1,039.7 observation-years in total. Up-titration to at least half the evidence-based target dose of beta-blockers was achieved in 69 % and full up-titration in 29 % of these patients. Patients with increased heart rates were younger, more often male, exhibited a higher NYHA functional class and lower LVEF. The primary endpoint occurred in 21 % of patients in the ≥70 bpm group versus 9 % of patients in the group with heart rates <70 bpm (p <0.01). Likewise, comparing the groups ≥75 and <75 bpm, the primary endpoint was significantly increased in the group of patients with heart rates ≥75 bpm 27 vs. 12.2 %; p < 0.01). 5-year event-free survival was significantly lower among patients with heart rates ≥70 bpm as compared to those with <70 bpm (log-rank test p < 0.05) and among patients in the ≥75 bpm group versus <75 bpm group (log-rank test p < 0.01). In conclusion, in clinical practice, 53 % of CHF patients have inadequate heart rate control (heart rates ≥75 bpm) despite concomitant beta-blocker therapy. In this non-randomized cohort, adequate heart rate control under individually optimized beta-blocker therapy was associated with improved mid- and long-term clinical outcome up to 5 years. As further up titration of beta-blockers is not achievable in many patients, the administration of a selective heart rate lowering agent, such as ivabradine adjuvant to beta-blockers may pose an opportunity to further modulate outcome. PMID:22760479

  5. Micronutrient deficiencies an unmet need in heart failure.

    PubMed

    Soukoulis, Victor; Dihu, Jamil B; Sole, Michael; Anker, Stefan D; Cleland, John; Fonarow, Gregg C; Metra, Marco; Pasini, Evasio; Strzelczyk, Theresa; Taegtmeyer, Heinrich; Gheorghiade, Mihai

    2009-10-27

    Heart failure (HF) is a common, disabling, and costly disease. Despite major advances in medical therapy, morbidity and mortality remain high, in part because current pharmacological regimens may not fully address some unique requirements of the heart for energy. The heart requires a continuous supply of energy-providing substrates and amino acids in order to maintain its function. In HF, defects in substrate metabolism and cardiac energy and substrate utilization may contribute to contractile dysfunction. HF is often accompanied by a deficiency in key micronutrients required for unimpeded energy transfer. Correcting these deficits has been proposed as a method to limit or even reverse the progressive myocyte dysfunction and/or necrosis in HF. This review summarizes the existing HF literature with respect to supplementation trials of key micronutrients involved in cardiac metabolism: coenzyme Q10, l-carnitine, thiamine, and amino acids, including taurine. Studies using a broader approach to supplementation are also considered. Although some of the results are promising, none are conclusive. There is a need for a prospective trial to examine the effects of micronutrient supplementation on morbidity and mortality in patients with HF. PMID:19850206

  6. Molecular risk stratification in advanced heart failure patients.

    PubMed

    Lamirault, Guillaume; Meur, Nolwenn Le; Roussel, Jean-Christian; Cunff, Marie-France Le; Baron, Daniel; Bihoue, Audrey; Guisle, Isabelle; Raharijaona, Mahatsangy; Ramstein, Grard; Teusan, Raluca; Chevalier, Catherine; Gueffet, Jean-Pierre; Trochu, Jean-Nol; Lger, Jean J; Houlgatte, Rmi; Steenman, Marja

    2010-06-01

    Risk stratification in advanced heart failure (HF) is crucial for the individualization of therapeutic strategy, in particular for heart transplantation and ventricular assist device implantation. We tested the hypothesis that cardiac gene expression profiling can distinguish between HF patients with different disease severity. We obtained tissue samples from both left (LV) and right (RV) ventricle of explanted hearts of 44 patients undergoing cardiac transplantation or ventricular assist device placement. Gene expression profiles were obtained using an in-house microarray containing 4217 muscular organ-relevant genes. Based on their clinical status, patients were classified into three HF-severity groups: deteriorating (n= 12), intermediate (n= 19) and stable (n= 13). Two-class statistical analysis of gene expression profiles of deteriorating and stable patients identified a 170-gene and a 129-gene predictor for LV and RV samples, respectively. The LV molecular predictor identified patients with stable and deteriorating status with a sensitivity of 88% and 92%, and a specificity of 100% and 96%, respectively. The RV molecular predictor identified patients with stable and deteriorating status with a sensitivity of 100% and 96%, and a specificity of 100% and 100%, respectively. The molecular prediction was reproducible across biological replicates in LV and RV samples. Gene expression profiling has the potential to reproducibly detect HF patients with highest HF severity with high sensitivity and specificity. In addition, not only LV but also RV samples could be used for molecular risk stratification with similar predictive power. PMID:19793385

  7. Metabolomic Fingerprint of Heart Failure with Preserved Ejection Fraction

    PubMed Central

    Zordoky, Beshay N.; Sung, Miranda M.; Ezekowitz, Justin; Mandal, Rupasri; Han, Beomsoo; Bjorndahl, Trent C.; Bouatra, Souhaila; Anderson, Todd; Oudit, Gavin Y.; Wishart, David S.; Dyck, Jason R. B.

    2015-01-01

    Background Heart failure (HF) with preserved ejection fraction (HFpEF) is increasingly recognized as an important clinical entity. Preclinical studies have shown differences in the pathophysiology between HFpEF and HF with reduced ejection fraction (HFrEF). Therefore, we hypothesized that a systematic metabolomic analysis would reveal a novel metabolomic fingerprint of HFpEF that will help understand its pathophysiology and assist in establishing new biomarkers for its diagnosis. Methods and Results Ambulatory patients with clinical diagnosis of HFpEF (n = 24), HFrEF (n = 20), and age-matched non-HF controls (n = 38) were selected for metabolomic analysis as part of the Alberta HEART (Heart Failure Etiology and Analysis Research Team) project. 181 serum metabolites were quantified by LC-MS/MS and 1H-NMR spectroscopy. Compared to non-HF control, HFpEF patients demonstrated higher serum concentrations of acylcarnitines, carnitine, creatinine, betaine, and amino acids; and lower levels of phosphatidylcholines, lysophosphatidylcholines, and sphingomyelins. Medium and long-chain acylcarnitines and ketone bodies were higher in HFpEF than HFrEF patients. Using logistic regression, two panels of metabolites were identified that can separate HFpEF patients from both non-HF controls and HFrEF patients with area under the receiver operating characteristic (ROC) curves of 0.942 and 0.981, respectively. Conclusions The metabolomics approach employed in this study identified a unique metabolomic fingerprint of HFpEF that is distinct from that of HFrEF. This metabolomic fingerprint has been utilized to identify two novel panels of metabolites that can separate HFpEF patients from both non-HF controls and HFrEF patients. Clinical Trial Registration ClinicalTrials.gov NCT02052804 PMID:26010610

  8. Management of chronic heart failure in the older population

    PubMed Central

    Azad, Nahid; Lemay, Genevieve

    2014-01-01

    Chronic heart failure (CHF) is the leading cause of hospitalization for those over the age of 65 and represents a significant clinical and economic burden. About half of hospital re-admissions are related to co-morbidities, polypharmacy and disabilities associated with CHF. Moreover, CHF also has an enormous cost in terms of poor prognosis with an average one year mortality of 33%35%. While more than half of patients with CHF are over 75 years, most clinical trials have included younger patients with a mean age of 61 years. Inadequate data makes treatment decisions challenging for the providers. Older CHF patients are more often female, have less cardiovascular diseases and associated risk factors, but higher rates of non-cardiovascular conditions and diastolic dysfunction. The prevalence of CHF with reduced ejection fraction, ischemic heart disease, and its risk factors declines with age, whereas the prevalence of non-cardiac co-morbidities, such as chronic renal failure, dementia, anemia and malignancy increases with age. Diabetes and hypertension are among the strongest risk factors as predictors of CHF particularly among women with coronary heart disease. This review paper will focus on the specific consideration for CHF assessment in the older population. Management strategies will be reviewed, including non-pharmacologic, pharmacologic, quality care indicators, quality improvement in care transition and lastly, end-of-life issues. Palliative care should be an integral part of an interdisciplinary team approach for a comprehensive care plan over the whole disease trajectory. In addition, frailty contributes valuable prognostic insight incremental to existing risk models and assists clinicians in defining optimal care pathways for their patients. PMID:25593582

  9. Thermal therapy: a viable adjunct in the treatment of heart failure?

    PubMed

    Mussivand, Tofy; Alshaer, Hisham; Haddad, Haissam; Beanlands, Donald S; Beanlands, Rob; Chan, Kwan-Leung; Higginson, Lyall; Leenen, Frans; Ruddy, Terrence D; Mesana, Thierry; Silver, Marc A

    2008-01-01

    The aim of this work was to review and provide a summary of published literature on the clinical impact of thermal therapy (ie, warm water immersion, traditional sauna bathing, and dry infrared sauna) in patients with heart failure. Medline and Embase database literature searches were conducted, and studies that included measurement of heart failure-related clinical parameters were reviewed. Thermal therapy was found to have a positive impact on key heart failure-related parameters across multiple studies. Significant improvements were noted across a wide scope of heart failure-related parameters in the areas of (1) endothelial function, (2) hemodynamics, (3) cardiac geometry, (4) neurohormonal markers, and (5) quality of life. Of special note, thermal therapy also conveyed a strong antiarrhythmic effect in heart failure patients. The clinical evidence highlights repeatable and compelling data showing that thermal therapy may provide an important and viable adjunct in the treatment of heart failure. PMID:18772622

  10. Stratification of the Risk of Sudden Death in Nonischemic Heart Failure

    PubMed Central

    Pimentel, Maurcio; Zimerman, Leandro Ioschpe; Rohde, Luis Eduardo

    2014-01-01

    Despite significant therapeutic advancements, heart failure remains a highly prevalent clinical condition associated with significant morbidity and mortality. In 30%-40% patients, the etiology of heart failure is nonischemic. The implantable cardioverter-defibrillator (ICD) is capable of preventing sudden death and decreasing total mortality in patients with nonischemic heart failure. However, a significant number of patients receiving ICD do not receive any kind of therapy during follow-up. Moreover, considering the situation in Brazil and several other countries, ICD cannot be implanted in all patients with nonischemic heart failure. Therefore, there is an urgent need to identify patients at an increased risk of sudden death because these would benefit more than patients at a lower risk, despite the presence of heart failure in both risk groups. In this study, the authors review the primary available methods for the stratification of the risk of sudden death in patients with nonischemic heart failure. PMID:25352509

  11. [Volume assessment in the acute heart and renal failure].

    PubMed

    Vujici?, Bozidar; Ruzi?, Alen; Zaputovi?, Luka; Racki, Sanjin

    2012-10-01

    Acute kidney injury (AKI) is an important clinical issue, especially in the setting of critical care. It has been shown in multiple studies to be a key independent risk factor for mortality, even after adjustment for demographics and severity of illness. There is wide agreement that a generally applicable classification system is required for AKI which helps to standardize estimation of severity of renal disfunction and to predict outcome associated with this condition. That's how RIFLE (Risk-Injury-Failure-Loss-End-stage renal disease), and AKIN (Acute Kidney Injury Network) classifications for AKI were found in 2004 and 2007, respectively. In the clinical setting of heart failure, a positive fluid balance (often expressed in the literature as weight gain) is used by disease management programs as a marker of heart failure decompensation. Oliguria is defined as urine output less than 0,3 ml/kg/h for at least 24 h. Since any delay in treatment can lead to a dangerous progression of the AKI, early recognition of oliguria appears to be crucial. Critically ill patients with oliguric AKI are at increased risk for fluid imbalance due to widespread systemic inflammation, reduced plasma oncotic pressure and increased capillary leak. These patients are particulary at risk of fluid overload and therefore restrictive strategy of fluid administration should be used. Objective, rapid and accurate volume assessment is important in undiagnosed patients presenting with critical illness, as errors may result in interventions with fatal outcomes. The historical tools such as physical exam, and chest radiography suffer from significant limitations. As gold standard, radioisolopic measurement of volume is impractical in the acute care enviroment. Newer technologies offer the promise of both rapid and accurate bedside estimation of volume status with the potential to improve clinical outcomes. Blood assessment with bioimpendance vector analysis, and bedside ultrasound seem to be promising technologies for this need. PMID:23513416

  12. Mitochondrial dynamics and cell death in heart failure.

    PubMed

    Marín-García, José; Akhmedov, Alexander T

    2016-03-01

    The highly regulated processes of mitochondrial fusion (joining), fission (division) and trafficking, collectively called mitochondrial dynamics, determine cell-type specific morphology, intracellular distribution and activity of these critical organelles. Mitochondria are critical for cardiac function, while their structural and functional abnormalities contribute to several common cardiovascular diseases, including heart failure (HF). The tightly balanced mitochondrial fusion and fission determine number, morphology and activity of these multifunctional organelles. Although the intracellular architecture of mature cardiomyocytes greatly restricts mitochondrial dynamics, this process occurs in the adult human heart. Fusion and fission modulate multiple mitochondrial functions, ranging from energy and reactive oxygen species production to Ca(2+) homeostasis and cell death, allowing the heart to respond properly to body demands. Tightly controlled balance between fusion and fission is of utmost importance in the high energy-demanding cardiomyocytes. A shift toward fission leads to mitochondrial fragmentation, while a shift toward fusion results in the formation of enlarged mitochondria and in the fusion of damaged mitochondria with healthy organelles. Mfn1, Mfn2 and OPA1 constitute the core machinery promoting mitochondrial fusion, whereas Drp1, Fis1, Mff and MiD49/51 are the core components of fission machinery. Growing evidence suggests that fusion/fission factors in adult cardiomyocytes play essential noncanonical roles in cardiac development, Ca(2+) signaling, mitochondrial quality control and cell death. Impairment of this complex circuit causes cardiomyocyte dysfunction and death contributing to heart injury culminating in HF. Pharmacological targeting of components of this intricate network may be a novel therapeutic modality for HF treatment. PMID:26872674

  13. Water and Sodium in Heart Failure: A Spotlight on Congestion

    PubMed Central

    Greene, Stephen J.; Torres, Daniele; Alderman, Michael; Bonventre, Joseph Vincent; Di Pasquale, Pietro; Gargani, Luna; Nohria, Anju; Fonarow, Gregg C.; Vaduganathan, Muthiah; Butler, Javed; Paterna, Salvatore; Stevenson, Lynne Warner; Gheorghiade, Mihai

    2015-01-01

    Despite all available therapies, the rates of hospitalization and death from heart failure (HF) remain unacceptably high. The most common reasons for hospital admission are symptoms related to congestion. During hospitalization, most patients respond well to standard therapy and are discharged with significantly improved symptoms. Post-discharge, many patients receive diligent and frequent follow-up. However, rehospitalization rates remain high. One potential explanation is a persistent failure by clinicians to adequately manage congestion in the outpatient setting. The failure to successfully manage these patients post-discharge may represent an unmet need to improve the way congestion is both recognized and treated. A primary aim of future HF management may be to improve clinical surveillance to prevent and manage chronic fluid overload while simultaneously maximizing the use of evidence-based therapies with proven long-term benefit. Improvement in cardiac function is the ultimate goal and maintenance of a dry clinical profile is important to prevent hospital admission and improve prognosis. This paper focuses on methods for monitoring congestion, and strategies for water and sodium management in the context of the complex interplay between the cardiac and renal systems. A rationale for improving recognition and treatment of congestion is also proposed. PMID:24942806

  14. The global health and economic burden of hospitalizations for heart failure: lessons learned from hospitalized heart failure registries.

    PubMed

    Ambrosy, Andrew P; Fonarow, Gregg C; Butler, Javed; Chioncel, Ovidiu; Greene, Stephen J; Vaduganathan, Muthiah; Nodari, Savina; Lam, Carolyn S P; Sato, Naoki; Shah, Ami N; Gheorghiade, Mihai

    2014-04-01

    Heart failure is a global pandemic affecting an estimated 26 million people worldwide and resulting in more than 1 million hospitalizations annually in both the United States and Europe. Although the outcomes for ambulatory HF patients with a reduced ejection fraction (EF) have improved with the discovery of multiple evidence-based drug and device therapies, hospitalized heart failure (HHF) patients continue to experience unacceptably high post-discharge mortality and readmission rates that have not changed in the last 2 decades. In addition, the proportion of HHF patients classified as having a preserved EF continues to grow and may overtake HF with a reduced EF in the near future. However, the prognosis for HF with a preserved EF is similar and there are currently no available disease-modifying therapies. HHF registries have significantly improved our understanding of this clinical entity and remain an important source of data shaping both public policy and research efforts. The authors review global HHF registries to describe the patient characteristics, management, outcomes and their predictors, quality improvement initiatives, regional differences, and limitations of the available data. Moreover, based on the lessons learned, they also propose a roadmap for the design and conduct of future HHF registries. PMID:24491689

  15. Skeletal muscle electrical stimulation improves baroreflex sensitivity and heart rate variability in heart failure rats.

    PubMed

    Lazzarotto Rucatti, Ananda; Jaenisch, Rodrigo Boemo; Rossato, Douglas Dalcin; Poletto Bonetto, Jéssica Hellen; Ferreira, Janaína; Xavier, Leder Leal; Sonza, Anelise; Dal Lago, Pedro

    2015-12-01

    The goal of the current study was to evaluate the effects of electrical stimulation (ES) on the arterial baroreflex sensitivity (BRS) and cardiovascular autonomic control in rats with chronic heart failure (CHF). Male Wistar rats were designated to one of four groups: placebo sham (P-Sham, n=9), ES sham (ES-Sham, n=9), placebo CHF (P-CHF, n=9) or ES CHF (ES-CHF, n=9). The ES was adjusted at a low frequency (30 Hz), duration of 250 μs, with hold and rest time of 8s (4 weeks, 30 min/day, 5 times/week). It was applied on the gastrocnemius muscle with intensity to produce a visible muscle contraction. The rats assigned to the placebo groups performed the same procedures with the equipment turned off. The two-way ANOVA and the post hoc Student-Newman-Keuls tests (P<0.05) were used to data comparison. The BRS was higher in ES-Sham group compared to the P-Sham group and the ES-CHF group compared to the P-CHF group. ES was able to decrease heart rate sympatho-vagal modulation and peripheral sympathetic modulation in ES-CHF compared to P-CHF group. Interestingly, heart rate sympatho-vagal modulation was similar between ES-CHF and P-Sham groups. Thus, ES enhances heart rate parasympathetic modulation on heart failure (ES-CHF) compared to placebo (P-CHF), with consequent decrease of sympatho-vagal balance in the ES-CHF group compared to the P-CHF. The results show that a 4 week ES protocol in CHF rats enhances arterial BRS and cardiovascular autonomic control. PMID:26433753

  16. [Nurse-led heart failure clinics: Swedish experiences of Advanced Nursing Practice during 10 years].

    PubMed

    Strmberg, Anna

    2004-08-01

    This paper aims at describing the development of nurse-led heart failure clinics in Sweden and discusses what effects and possibilities this type of advanced nursing practice gives the patients, the health care system and the nurses. Follow-up at nurse-led heart failure clinics involve patient education, optimised treatment and social support and has been shown to improve survival and self-care behaviour in patients with heart failure and reduce the need for hospital care. This model of care has spread from Sweden to many European countries, but still only a minority of the patients hospitalised due to heart failure receive this type of follow-up. It should be considered for several more patients in Europe. The organisation of the nurse-led follow-up needs to be adapted to the different needs of patients within the heart failure population and to the health care system of each country. Formal competence among heart failure nurses needs to be continuously improved in order to provide high-quality care to heart failure patients. This can be achieved through improved education and increased national and international collaboration among heart failure nurses. Networking among heart failure nurses on a regional, national and international level is crucial. Joint activities such as study visits, national and international working groups, conferences, workshops and research collaboration can be important tools in this development. PMID:15455825

  17. Race-related differences in heart failure therapies: simply black and white or shades of grey?

    PubMed

    Shroff, Gautam R; Taylor, Anne L; Colvin-Adams, Monica

    2007-05-01

    The magnitude of burden imposed by heart failure on society has necessitated the evolution of innovative strategies to identify specific avenues of treatment and the populations at highest risk. Multiple studies have demonstrated a higher burden of cardiovascular disease in black Americans. It has also been shown that the clinical characteristics of heart failure, therapeutic targets, and response to various treatment modalities, are different in blacks as compared with whites. This article explores the unique race-related differences in heart failure with particular emphasis on the currently recommended therapeutic agents in heart failure. PMID:17470329

  18. Influence of sex on treatment and outcome in chronic heart failure.

    PubMed

    Frankenstein, Lutz; Clark, Andrew L; Ribeiro, Jorge P

    2012-06-01

    The population is aging, the prevalence of heart failure increases with age, and on average women live longer than men. There is evidence for sex-specific effects of individual, guideline-recommended drugs used for treatment of chronic heart failure. Women are underrepresented in most clinical trials and only a minority of drug applications to regulatory authorities have included sex analyses. The present review focuses on the potential female survival benefit in heart failure, the influence of sex on medical treatment in a broader sense, and the potential benefit to be derived from guideline recommended treatment and common adjunctive heart failure medication. PMID:21599874

  19. Salt Intake Is Associated with Inflammation in Chronic Heart Failure

    PubMed Central

    Azak, Alper; Huddam, Bulent; Gonen, Namik; Yilmaz, Seref Rahmi; Kocak, Gulay; Duranay, Murat

    2014-01-01

    Background: Chronic Heart Failure (CHF) is highly prevalent and is associated with high morbidity and mortality rates. It has been well established that excessive intake of sodium chloride (salt) induced hypertension in some populations. Although salt seems to induce cardiovascular diseases through elevation of blood pressure, it has also been indicated that salt can induce cardiovascular diseases independently from blood pressure elevation. Objectives: The present study aimed to evaluate the association between salt consumption and inflammation in CHF patients. Patients and Methods: This study was conducted on 86 patients between 18 and 65 years old who were diagnosed with New York Heart Association (NYHA) functional class I and II heart failure. Salt intake was calculated by using 24 hour urine sodium excretion. Besides, the association between inflammation and daily salt intake was evaluated regarding C - reactive protein (CPR), High sensitive CRP (HsCPR), Erythrocyte Sedimentation Rate (ESR), and ferritin and fibrinogen levels using Pearson correlation analysis. Results: Our results showed a statistically significant difference between the low (n = 41) and high (n = 45) salt intake groups in terms of serum HsCRP levels (5.21 2.62 vs. 6.36 2.64) (P < 0.048). Additionally, a significant correlation was observed between the amount of salt consumption and HsCRP levels. In this study, daily salt consumption of the enrolled patients was 8.53 gram/day. The medications and even the blood pressures were similar in the two groups, but daily pill count, prevalence of hypertension, and coronary heart disease were higher in the high salt intake group; however, the differences were not statistically significant (P = 0.065). Also, no significant difference was observed between the groups concerning the inflammation markers, such as CRP, ESR, ferritin, and fibrinogen. Conclusions: Neurohumoral and inflammatory factors are thought to contribute to high mortality and morbidity rates in CHF. Yet, inflammatory markers may early diagnose CHF and predict the prognosis. Excessive salt intake also worsens the inflammation as well as volume control. PMID:25177670

  20. Heart disease in cattle with clinical signs of heart failure: 59 cases

    PubMed Central

    Buczinski, Sbastien; Francoz, David; Fecteau, Gilles; DiFruscia, Rocky

    2010-01-01

    This retrospective study identified clinical signs, underlying cardiac conditions, blood findings, echocardiographic findings, and prognosis for 59 cattle with clinical signs of congestive heart failure. Signalment; history; clinical signs; clinicopathologic, echocardiographic, and radiographic findings; and treatment were determined by reviewing medical records. Follow-up information was obtained by telephone conversation with owners. Most patients were tachycardic (n = 50), and tachypneic (n = 55). Pericarditis of traumatic origin (n = 21), by extension from pleuritis (n = 3), or of idiopathic origin (n = 1) was diagnosed in 25 cases. Other diagnoses were congenital heart defect (n = 13), cardiomyopathy (n = 9), bacterial endocarditis (n = 7), and neoplasm (n = 5). Twelve cases (20%) were discharged. Long-term survival was good in 2 out of 3 cases treated by pericardiostomy. The prognosis is poor in cases of heart failure in cattle and deaths within 1 mo (n = 3) or between 1 to 3 mo after discharge (n = 3) were common in cases for which follow-up was available (n = 8). PMID:21197204

  1. DuraHeart magnetically levitated centrifugal left ventricular assist system for advanced heart failure patients.

    PubMed

    Morshuis, Michiel; Schoenbrodt, Michael; Nojiri, Chisato; Roefe, Daniela; Schulte-Eistrup, Sebastian; Boergermann, Jochen; Gummert, Jan F; Arusoglu, Latif

    2010-03-01

    The implantable left ventricular assist system (LVAS) using pulsatile pump technology has become an established therapeutic option for advanced heart failure patients. However, there have been technological limitations in some older designs, including a high incidence of infection and mechanical failures associated with moving parts, and the large size of both implantable pump and percutaneous cable. A smaller rotary blood pump emerged as a possible alternative to a large pulsatile pump to overcome some of these limitations. The technological advancement that defines the third-generation LVAS was the elimination of all mechanical contacts between the impeller and the drive mechanism. The DuraHeart LVAS is the world's first third-generation implantable LVAS to obtain market approval (CE-mark), which combines a centrifugal pump and active magnetic levitation. The initial clinical experience with the DuraHeart LVAS in Europe demonstrated that it provided significantly improved survival (85% at 6 months and 79% at 1 year), reduced adverse event rates and long-term device reliability (freedom from device replacement at 2 years: 96 +/- 3%) over pulsatile LVAS. PMID:20214423

  2. Transcriptomic profiling of the canine tachycardia-induced heart failure model: global comparison to human and murine heart failure

    PubMed Central

    Gao, Zhong; Xu, Hai; DiSilvestre, Deborah; Halperin, Victoria L.; Tunin, Richard; Tian, Yanli; Yu, Wayne; Winslow, Raimond L.; Tomaselli, Gordon F.

    2006-01-01

    Alterations of cardiac gene expression are central to ventricular dysfunction in human heart failure (HF). The canine tachycardia pacing-induced HF model is known to reproduce the main hemodynamic, echocardiographic and electrophysiological changes observed in human HF. In this study, we use this HF model to compare gene expression profiles in the left and right ventricles (LV, RV) of normal and end-stage failing canine hearts and compare the transcription profiles to those in human and murine models of HF. In end-stage HF, the LV exhibits down regulation of genes involved in energy production, cardiac contraction, and modulation of excitation–contraction coupling as compared with normal LV. The majority of transcriptomic changes between normal and end-stage canine HF were shared by the RV and LV. Genes down regulated only in the LV included those involved in aerobic energy production pathways, regulation of actin filament length, and enzyme-linked receptor protein signaling pathways. In normal canine hearts, genes encoding specific components of the contractile apparatus exhibit LV–RV asymmetric expression patterns; in failing hearts, cardiac fetal transcription factors MEF2 and MITF and the stress-responsive transcription factor ATF4 showed interventricular differences in expression. The comparison among the canine tachypacing, mouse transgenic, and human HF reveals that human disease involves down regulation of genes in a broad range of biological processes while experimentally induced HF is associated with down regulation of energy pathways, and that human ischemic HF and canine HF share a similar over representation of transcriptional pathways in the up regulated genes. This study provides insights into the molecular pathways leading to end-stage tachycardia-induced HF, and into global transcriptomic differences between the animal HF models and human HF. PMID:16236311

  3. Regulation of the renal sympathetic nerves in heart failure

    PubMed Central

    Ramchandra, Rohit; Barrett, Carolyn J.

    2015-01-01

    Heart failure (HF) is a serious debilitating condition with poor survival rates and an increasing level of prevalence. HF is associated with an increase in renal norepinephrine (NE) spillover, which is an independent predictor of mortality in HF patients. The excessive sympatho-excitation that is a hallmark of HF has long-term effects that contribute to disease progression. An increase in directly recorded renal sympathetic nerve activity (RSNA) has also been recorded in animal models of HF. This review will focus on the mechanisms controlling sympathetic nerve activity (SNA) to the kidney during normal conditions and alterations in these mechanisms during HF. In particular the roles of afferent reflexes and central mechanisms will be discussed. PMID:26388778

  4. The role of metabolic syndrome in heart failure.

    PubMed

    Perrone-Filardi, Pasquale; Paolillo, Stefania; Costanzo, Pierluigi; Savarese, Gianluigi; Trimarco, Bruno; Bonow, Robert O

    2015-10-14

    Metabolic syndrome (MS) is a highly prevalent condition in patients affected by heart failure (HF); however, it is still unclear whether, in the setting of cardiac dysfunction, it represents an adverse risk factor for the occurrence of cardiac events. The epidemiologic implications of MS in HF have been studied intensely, as many of its components contribute to the incidence and severity of HF. In particular, insulin resistance, diabetes mellitus, and lipid abnormalities represent the main components that negatively influence disease progression and evolution. Yet, other components of the MS, i.e. overweight/obesity and high blood pressure, are favourably associated with outcome in HF patients. The aim of this review was to report epidemiology and prognostic role of MS in HF and to investigate current clinical implications and future research needs. PMID:26242711

  5. Radionuclide Imaging Applications in Cardiomyopathies and Heart Failure.

    PubMed

    Harinstein, Matthew E; Soman, Prem

    2016-03-01

    Multiple epidemiological factors including population aging and improved survival after acute coronary syndromes have contributed to a heart failure (HF) prevalence in the USA in epidemic proportions. In the absence of transplantation, HF remains a progressive disease with poor prognosis. The structural and functional abnormalities of the myocardium in HF can be assessed by various radionuclide imaging techniques. Radionuclide imaging may be uniquely suited to address several important clinical questions in HF such as identifying etiology and guiding the selection of patients for coronary revascularization. Newer approaches such as autonomic innervation imaging, phase analysis for synchrony assessment, and other molecular imaging techniques continue to expand the applications of radionuclide imaging in HF. In this manuscript, we review established and evolving applications of radionuclide imaging for the diagnosis, risk stratification, and management of HF. PMID:26841785

  6. Obesity and the obesity paradox in heart failure.

    PubMed

    Gupta, Pritha P; Fonarow, Gregg C; Horwich, Tamara B

    2015-02-01

    Obesity has reached epidemic proportions in the general population and is associated with an increased risk for the development of new-onset heart failure (HF). However, in acute and chronic HF, overweight and mild to moderate obesity is associated with substantially improved survival compared with normal weight. This phenomenon has been termed the "obesity paradox" in HF. The majority of data pertaining to the obesity paradox identifies obesity with body mass index; however, the reliability of this method has been questioned. Newer studies have explored the use of other measures of body fat and body composition, including waist circumference, waist-to-hip ratio, skinfold thickness, and bioelectrical impedance analysis of body composition. The relationship between the obesity paradox and cardiorespiratory fitness in HF is also discussed in this review, and we explore the various potential explanations for the obesity paradox and summarize the current evidence and guidelines for intentional weight loss treatments for HF in the obese population. PMID:25661554

  7. Disparities in heart failure and other cardiovascular diseases among women

    PubMed Central

    McSweeney, Jean; Pettey, Christina; Lefler, Leanne L; Heo, Seongkum

    2012-01-01

    This article reviews literature pertinent to cardiovascular disparities in women, focusing primarily on heart failure (HF). It provides an in-depth look at causes, biological influences, self-management and lack of adherence to HF-treatment guidelines in women. Disparities in treatment of causative factors of HF, such as myocardial infarction and hypertension, contribute to women having poorer HF outcomes than men. This article discusses major contributing reasons for nonadherence to medication regimes for HF in women, including advanced age at time of diagnosis, likelihood of multiple comorbidities, lack of social support and low socioeconomic status. Limited inclusion of women in clinical trials and the scarcity of gender analyses for HF and other cardiovascular diseases continues to limit the applicability of research findings to women. PMID:22757737

  8. Multidisciplinary management of heart failure just beginning in Japan.

    PubMed

    Sato, Yukihito

    2015-09-01

    The mortality associated with end-stage heart failure (HF) is high despite the development of new and increasingly effective drugs and non-pharmacological therapies. Repetitive hospitalizations predict fatal outcomes and each hospitalization should prompt individual conversations with the patient, the family, and the caregivers. A multidisciplinary disease management program promotes the education of patients and their families and modifies their behavior, with a view to ultimately improve the prognosis and quality of life. From the early to the late stages of HF, a multidisciplinary disease management program should be implemented. In Western societies this multidisciplinary management has long been debated and endorsed, in contrast to Japan, where it has just begun. In 2012, the Japanese Nursing Association launched a certification in chronic HF nursing. A Japanese version of HF disease management should soon be developed in its own social environment. PMID:25722045

  9. Understanding the Epidemic of Heart Failure: Past, Present, and Future

    PubMed Central

    Dunlay, Shannon M.; Roger, Véronique L.

    2014-01-01

    Heart failure (HF) is a major public health problem affecting more than 5 million Americans and more than 23 million patients worldwide. The epidemiology of HF is evolving. Data suggests that the incidence of HF peaked in the mid 1990s and has since declined. Survival after HF diagnosis has improved, leading to an increase in prevalence. The case mix is also changing, as a rising proportion of patients with HF have preserved ejection fraction and multimorbidity is increasingly common. After diagnosis, HF can have a profound associated morbidity. Hospitalizations in HF remain both frequent and costly, though they may be declining as a result of preventive efforts. The need for skilled nursing facility care in HF has risen. The role of palliative medicine in the care of patients with advanced HF is evolving as we learn how to best care for this population with a large symptom burden. PMID:25182014

  10. Progress toward genetic tailoring of heart failure therapy

    PubMed Central

    Lillvis, John H; Lanfear, David E

    2010-01-01

    Heart failure (HF) is a modern epidemic and a heterogeneous disorder with many therapeutic options. While the average response to each individual treatment is favorable, significant interindividual variation exists in the response to HF therapeutics. As a result, the optimal regimen for an individual patient or subgroup of patients is elusive, with current treatment being mainly empirical. Pharmacogenetic customization of HF therapy may provide an important opportunity to improve the treatment of HF. Common genetic variations exist in genes related to most classes of HF drugs, many of which have known functional consequences for or established relationships with drug response. This review summarizes the current understanding of the pharmacogenetics of HF therapeutics, including angiotensin-converting enzyme inhibitors and ?-blockers, and focuses on recent advances and medium-term expectations for the field. PMID:20521218

  11. Pulmonary Hypertension and Cardiopulmonary Exercise in Heart Failure

    PubMed Central

    Kim, Chul-Ho; Jae, Sae Young; Johnson, Bruce D.

    2014-01-01

    In heart failure (HF), pulmonary hypertension (PH) is initially associated with a rise in the left ventricular filling pressure. PH is defined by pulmonary hemodynamic measurements including pulmonary capillary wedge pressure, mean pulmonary arterial pressure and pulmonary vascular resistance. Eventually, PH in HF may become more of a reactive process. Although the mechanism of the reactive PH development is not clearly understood, vascular dysfunction induced by remodeling, vasoactive substances and genetic variation appear to contribute significantly to this form of PH. Noninvasive cardiopulmonary exercise testing has been extensively utilized to assess disease severity in HF patients. It provides integrated information that is dependent on cardiopulmonary hemodynamics, lung mechanics, breathing pattern and strategy. In this review, we will discuss the mechanisms of PH development in HF and how noninvasive gas exchange measures obtained with submaximal exercise are influenced by PH in this population. PMID:26389080

  12. Iron deficiency and heart failure: diagnostic dilemmas and therapeutic perspectives

    PubMed Central

    Jankowska, Ewa A.; von Haehling, Stephan; Anker, Stefan D.; Macdougall, Iain C.; Ponikowski, Piotr

    2013-01-01

    Iron is a micronutrient essential for cellular energy and metabolism, necessary for maintaining body homoeostasis. Iron deficiency is an important co-morbidity in patients with heart failure (HF). A major factor in the pathogenesis of anaemia, it is also a separate condition with serious clinical consequences (e.g. impaired exercise capacity) and poor prognosis in HF patients. Experimental evidence suggests that iron therapy in iron-deficient animals may activate molecular pathways that can be cardio-protective. Clinical studies have demonstrated favourable effects of i.v. iron on the functional status, quality of life, and exercise capacity in HF patients. It is hypothesized that i.v. iron supplementation may become a novel therapy in HF patients with iron deficiency. PMID:23100285

  13. Intersections Between Microbiome and Heart Failure: Revisiting the Gut Hypothesis.

    PubMed

    Nagatomo, Yuji; Tang, W H Wilson

    2015-12-01

    Microbes play an important role in human health and disease. In the setting of heart failure (HF), substantial hemodynamic changes, such as hypoperfusion and congestion in the intestines, can alter gut morphology, permeability, function, and possibly the growth and composition of gut microbiota. These changes can disrupt the barrier function of the intestines and exacerbate systemic inflammation via microbial or endotoxin translocation into systemic circulation. Furthermore, cardiorenal alterations via metabolites derived from gut microbiota can potentially mediate or modulate HF pathophysiology. Recently, trimethylamine N-oxide (TMAO) has emerged as a key mediator that provides a mechanistic link between gut microbiota and multiple cardiovascular diseases, including HF. Potential intervention strategies which may target this microbiota-driven pathology include dietary modification, prebiotics/probiotics, and selective binders of microbial enzymes or molecules, but further investigations into their safety and efficacy are warranted. PMID:26435097

  14. BNP and Heart Failure: Preclinical and Clinical Trial Data.

    PubMed

    Egom, Emmanuel E

    2015-04-01

    The B-type natriuretic peptide (BNP), a member of the family of vasoactive peptides, has emerged as an important diagnostic, prognostic, and therapeutic tool in patients with heart failure (HF). The rapid incorporation into clinical practice of bioassays to BNP concentrations and pharmacological agents that augment the biological actions of this peptide such as nesiritide or vasopeptidase inhibitors has shown the potential for translational research to improve patient care. Despite the indirect evidence in support of a potential benefit from raising BNP, accumulating evidence suggests that simply increasing the amount of circulating BNP does not necessarily confer cardiovascular benefits in patient with HF. Moreover, in experimental HF, the response to treatments targeting specific natriuretic peptide receptors (NPRs) signaling seems to be attenuated. A better understanding of the NPRs signaling in HF would be clinically relevant and thus required, in order to devise strategies to develop novel agents and technologies that directly target this signaling pathway. PMID:25771949

  15. Patient and Caregiver Incongruence in Advanced Heart Failure.

    PubMed

    Kitko, Lisa A; Hupcey, Judith E; Pinto, Casey; Palese, Maureen

    2015-08-01

    The important role of caregivers in heart failure (HF) management is well documented, but few studies have explored HF patient-caregiver dyads when dyadic incongruence is evident. The purpose of this study was to determine the prevalence of incongruence between HF patient-caregiver dyads, areas of incongruence, and the impact on individuals in the dyadic relationship. Data were collected as part of a longitudinal qualitative study examining the palliative care needs of HF dyads. Interviews with dyads determined to be incongruent were further analyzed. Of the 100 dyads, 47 were identified as being incongruent. Dyads were found to be incongruent in illness management, health care issues, and end-of-life decisions. Dyads that were incongruent reported more psychosocial issues and distress within the dyad and individually. Further research is needed to determine the impact of incongruence and whether interventions to modify incongruence will lead to improved HF patient and caregiver outcomes and experiences. PMID:24599063

  16. Management of acute heart failure in the emergency department.

    PubMed

    Fenwick, Rob

    2015-12-01

    Acute heart failure (AHF) is a leading cause of hospital admission in the UK and is associated with significant mortality. The National Institute for Health and Care Excellence ( 2014 ) has published guidelines for the management of AHF but, after a clinical event in which a patient's management differed from that recommended in the guidelines occurred in the author's emergency department, he conducted a critical analysis of them. This article provides a case study of the clinical event, reviews the treatment methods adopted and explores the rationale for taking a different approach from that recommended in the guidelines. The evidence base for the use of diuretics, nitrates and non-invasive ventilation in the management of patients with AHF is also appraised. PMID:26638756

  17. New diagnostic modalities in the diagnosis of heart failure.

    PubMed Central

    Mitchell, Judith E.; Palta, Sanjeev

    2004-01-01

    Heart failure (HF) is the one cardiovascular disease that is increasing in prevalence in the United States. As the population continues to age, the incidence will certainly be amplified. However, some studies have shown that HF is correctly diagnosed initially in only 50% of affected patients. Despite the use of history, physical examination, echocardiogram, and chest x-ray, the percentage of correct initial diagnosis of HF is low. Recognizing the symptoms of HF decompensations is often problematic because other diagnoses can mimic them. There are two new diagnostic modalities that offer promise in improving HF diagnostic accuracy and identifying early HF decompensations. These diagnostic modalities include tests utilizing impedance cardiography and the B-type natriuretic peptide assay. They have the potential of increasing the accuracy of HF diagnosis and guide pharmacological treatment in the inpatient and outpatient settings. They may also assist in the recognition (or prediction) of acute HF decompensations. Images Figure 2 PMID:15586645

  18. The future of pharmacogenetics in the treatment of heart failure.

    PubMed

    Anwar, Mohamed Subhan; Iskandar, Muhammad Zaid; Parry, Helen M; Doney, Alex S; Palmer, Colin N; Lang, Chim C

    2015-11-01

    Heart failure is a common disease with high levels of morbidity and mortality. Current treatment comprises ?-blockers, ACE inhibitors, aldosterone antagonists and diuretics. Variation in clinical response seen in patients begs the question of whether there is a pharmacogenetic component yet to be identified. To date, the genes most studied involve the ?-1, ?-2, ?-2 adrenergic receptors and the renin-angiotensin-aldosterone pathway, mainly focusing on SNPs. However results have been inconsistent. Genome-wide association studies and next-generation sequencing are seen as alternative approaches to discovering genetic variations influencing drug response. Hopefully future research will lay the foundations for genotype-led drug management in these patients with the ultimate aim of improving their clinical outcome. PMID:26555119

  19. Palliative Care and Hospice in Advanced Heart Failure

    PubMed Central

    LeMond, Lisa; Allen, Larry A.

    2013-01-01

    Advanced heart failure (HF) is a disease process that carries a high burden of symptoms, suffering, and death. Palliative care can complement traditional care to improve symptom amelioration, patient-caregiver communication, emotional support, and medical decision making. Despite a growing body of evidence supporting the integration of palliative care into the overall care of patients with HF and some recent evidence of increased use, palliative therapies remain underused in the treatment of advanced HF. Review of the literature reveals that although barriers to integrating palliative care are not fully understood, difficult prognostication combined with caregiver inexperience with end-of-life issues specific to advanced HF is likely to contribute. In this review, we have outlined the general need for palliative care in advanced HF, detailed how palliative measures can be integrated into the care of those having this disease, and explored end-of-life issues specific to these patients. PMID:21875515

  20. Complexity in congestive heart failure: A time-frequency approach

    NASA Astrophysics Data System (ADS)

    Banerjee, Santo; Palit, Sanjay K.; Mukherjee, Sayan; Ariffin, MRK; Rondoni, Lamberto

    2016-03-01

    Reconstruction of phase space is an effective method to quantify the dynamics of a signal or a time series. Various phase space reconstruction techniques have been investigated. However, there are some issues on the optimal reconstructions and the best possible choice of the reconstruction parameters. This research introduces the idea of gradient cross recurrence (GCR) and mean gradient cross recurrence density which shows that reconstructions in time frequency domain preserve more information about the dynamics than the optimal reconstructions in time domain. This analysis is further extended to ECG signals of normal and congestive heart failure patients. By using another newly introduced measure—gradient cross recurrence period density entropy, two classes of aforesaid ECG signals can be classified with a proper threshold. This analysis can be applied to quantifying and distinguishing biomedical and other nonlinear signals.

  1. [Optimization of energy metabolism in patients with chronic heart failure].

    PubMed

    Korzh, A N

    2010-01-01

    Nowadays particular interest of clinicians is attracted by metabolic therapy of patients with chronic heart failure (CHF). The objective of this study was to investigate the influence of complex therapy with addition of Vasonat on the dynamics of remodeling indexes of left ventricle and functional class of CHF on classification of NYHA. It has been shown that application of metabolic modulator Vasonat in addition to conventional therapy of CHF facilitated the clinical improvement and significant decline of functional class. Vasonat use resulted in the meaningful improvement of the contractive function of myocardium and increase of tolerance to the physical exercise. Moreover, high efficiency of Vasonat has been demonstrated in the control of the syndrome of oxidizing stress, by decrease in intensity of free-radical processes and activation of the antioxidant defense system. PMID:21265120

  2. Respiratory muscle function and exercise intolerance in heart failure.

    PubMed

    Ribeiro, Jorge P; Chiappa, Gaspar R; Neder, J Alberto; Frankenstein, Lutz

    2009-06-01

    Inspiratory muscle weakness (IMW) is prevalent in patients with chronic heart failure (CHF) caused by left ventricular systolic dysfunction, which contributes to reduced exercise capacity and the presence of dyspnea during daily activities. Inspiratory muscle strength (estimated by maximal inspiratory pressure) has independent prognostic value in CHF. Overall, the results of trials with inspiratory muscle training (IMT) indicate that this intervention improves exercise capacity and quality of life, particularly in patients with CHF and IMW. Some benefit from IMT may be accounted for by the attenuation of the inspiratory muscle metaboreflex. Moreover, IMT results in improved cardiovascular responses to exercise and to those obtained with standard aerobic training. These findings suggest that routine screening for IMW is advisable in patients with CHF, and specific IMT and/or aerobic training are of practical value in the management of these patients. PMID:19486593

  3. Can cognitive behaviour therapy be beneficial for heart failure patients?

    PubMed

    Lundgren, Johan; Andersson, Gerhard; Johansson, Peter

    2015-04-01

    This review aims to summarize the theory of cognitive behavioural therapy (CBT) as well as the current evidence for whether CBT can be beneficial for patients with heart failure (HF). Depression and/or anxiety are common in HF patients. However, participation in disease management programmes does not seem to be beneficial for these problems. CBT, which focuses on the identification and changing of dysfunctional beliefs and thoughts and on behaviour therapy, is a possible treatment option. The number of CBT studies on HF is small and they are often not designed as randomized controlled trials. However, the studies on HF indicate that CBT can decrease depression as well as anxiety and suggest that relaxation exercises with elements of CBT may decrease symptom burden. Before implementation in clinical practice, more knowledge is needed about how CBT programmes should be designed, where CBT should be delivered and who should deliver CBT. PMID:25475179

  4. Right heart failure post left ventricular assist device implantation

    PubMed Central

    Argiriou, Mihalis; Kolokotron, Styliani-Maria; Sakellaridis, Timothy; Argiriou, Orestis; Charitos, Christos; Katsikogiannis, Nikolaos; Kougioumtzi, Ioanna; Machairiotis, Nikolaos; Tsiouda, Theodora; Tsakiridis, Kosmas; Zarogoulidis, Konstantinos

    2014-01-01

    Right heart failure (RHF) is a frequent complication following left ventricular assist device (LVAD) implantation. The incidence of RHF complicates 20-50% (range, 9-44%) of cases and is a major factor of postoperative morbidity and mortality. Unfortunately, despite the fact that many risk factors contributing to the development of RHF after LVAD implantation have been identified, it seems to be extremely difficult to avoid them. Prevention of RHF consists of the management of the preload and the afterload of the right ventricle with optimum inotropic support. The administration of vasodilators designed to reduce pulmonary vascular resistance is standard practice in most centers. The surgical attempt of implantation of a right ventricular assist device does not always resolve the problem and is not available in all cardiac surgery centers. PMID:24672699

  5. The baroreceptor as a therapeutic target for heart failure.

    PubMed

    Gronda, Edoardo; Lovett, Eric G; Tarascio, Michela; Georgakopoulos, Dimitrios; Grassi, Guido; Vanoli, Emilio

    2014-04-01

    Sympathoactivation is a prominent feature of heart failure (HF). Its role in cardiac remodeling and arrhythmogenesis is well-recognized today, although incomplete understanding of autonomic mechanisms was a barrier to development of contemporary medical therapies. Despite widespread availability of drugs and devices, mortality and morbidity in HF remain unacceptably high. Recognition of an additional phenotype, HF with preserved ejection fraction (EF), poses additional challenges. New treatment options are required. Electrical modulation of the central nervous system with baroreflex activation therapy offers a new approach. Activation of this afferent pathway induces the central nervous system to rebalance autonomic modulation of the cardiovascular system. Results in animal models of HF demonstrating increased survival and beneficial cardiac remodeling recently led to a clinical feasibility study in HF with reduced EF wherein the clinical course of patients dramatically improved. Results in resistant hypertension patients further suggest potential for benefit in HF with preserved EF. PMID:24563340

  6. Sleep apnea and cognitive function in heart failure.

    PubMed

    Knecht, Krysten M; Alosco, Michael L; Spitznagel, Mary Beth; Cohen, Ronald; Raz, Naftali; Sweet, Lawrence; Colbert, Lisa H; Josephson, Richard; Hughes, Joel; Rosneck, Jim; Gunstad, John

    2012-01-01

    Background. Prior research indicates that heart failure (HF) patients exhibit significant cognitive deficits on neuropsychological testing. Sleep apnea is associated with both HF and reduced cognitive function, but the combined impact of these conditions on cognitive function is unknown. Methods. In the current study, 172 older adults with a dual diagnosis of HF and sleep apnea or HF alone completed a battery of cognitive tests measuring attention, executive functioning, and memory. Results. Relative to patients with HF alone, persons with both HF and sleep apnea performed worse on measures of attention after adjusting for demographic and medical variables. Conclusions. The current findings suggest that HF patients with comorbid sleep apnea may be at greater risk for cognitive impairment relative to HF patient without such history. Further work is needed to clarify mechanisms for these findings and to determine whether the interactive effects on cognitive function lead to poorer patient outcomes. PMID:22745901

  7. Current perspectives on hydralazine and nitrate therapies in heart failure.

    PubMed

    Cole, Robert T; Gupta, Divya; Butler, Javed

    2014-10-01

    The origins of the hydralazine/isosorbide dinitrate (H+ISDN) combination therapy are rooted in the first large-scale clinical trial in heart failure: V-HeFT I. Initially utilized for the balanced vasodilatory properties of each drug, we now know there is "more to the story." In fact, the maintenance of the nitroso-redox balance may be the true mechanism of benefit. Since the publication of V-HeFT I 30 years ago, H+ISDN has been the subject of much discussion and debate. Regardless of the many controversies surrounding H+ISDN, one thing is clear: therapy is underutilized and many patients who could benefit never receive the drugs. Ongoing physician and patient education are mandatory to improve the rates of H+ISDN use. PMID:25217432

  8. Dietary management of heart failure: room for improvement?

    PubMed

    Butler, Thomas

    2016-04-01

    There is growing awareness of the role of diet in both health and disease management. Much data are available on the cardioprotective diet in the primary and secondary prevention of CVD. However, there is limited information on the role of diet in the management of heart failure (HF). Animal models of HF have provided interesting insight and potential mechanisms by which dietary manipulation may improve cardiac performance and delay the progression of the disease, and small-scale human studies have highlighted beneficial diet patterns. The aim of this review is to summarise the current data available on the role of diet in the management of human HF and to demonstrate that dietary manipulation needs to progress further than the simple recommendation of salt and fluid restriction. PMID:26857032

  9. V2 receptor antagonism with tolvaptan in heart failure.

    PubMed

    Costello-Boerrigter, Lisa C; Boerrigter, Guido; Burnett, John C

    2007-10-01

    The prevalence and incidence of congestive heart failure continues to increase. The two hallmarks of this syndrome, sodium and water retention, are frequently a therapeutic challenge. Most conventional diuretics act primarily as saluretics by inhibiting renal tubular electrolyte reabsorption, which, due to osmotic pressure, promotes excretion of isotonic fluid. The peptide hormone arginine vasopressin vasoconstricts at the V(1A) receptor and promotes water reabsorption via the V(2) receptor in the renal collecting duct by inserting aquaporin-2 water channels into the luminal membrane. Tolvaptan, the first orally available non-peptide V(2) receptor antagonist, acts as a potent aquaretic. In this paper, the authors review the pharmacology of tolvaptan and discuss the results of the initial clinical trials with this potent new drug. PMID:17922627

  10. Oxidative stress and inflammatory markers the future of heart failure diagnostics?

    PubMed Central

    Szczurek, Wioletta

    2015-01-01

    Heart failure remains one of the most important problems in cardiology despite the progress in its treatment. A number of recent studies have demonstrated the relationship between the intensification of oxidative stress and chronic inflammation and the severity of left ventricular dysfunction, development of heart failure symptoms, and prediction of future cardiac events. Early detection of changes developing in the heart is key in improving the treatment's effectiveness. It appears that determining specific, sensitive biomarkers reflecting the complex pathophysiology of heart failure and using them to detect asymptomatic cardiac alterations may become a crucial screening tool, assisting in the identification of patients requiring further diagnostic examinations. This article presents an overview of the current knowledge of the role of oxidative stress and inflammation in heart failure; it also discusses the potential role of oxidative stress and inflammatory markers as prognostic factors in heart failure that may be used in screening tests. PMID:26336497

  11. Update for 2014 on clinical cardiology, geriatric cardiology, and heart failure and transplantation.

    PubMed

    Barn-Esquivias, Gonzalo; Manito, Nicols; Lpez Daz, Javier; Martn Santana, Antonio; Garca Pinilla, Jos Manuel; Gmez Doblas, Juan Jos; Gmez Bueno, Manuel; Barrios Alonso, Vivencio; Lambert, Jos Luis

    2015-04-01

    In the present article, we review publications from the previous year in the following 3 areas: clinical cardiology, geriatric cardiology, and heart failure and transplantation. Among the new developments in clinical cardiology are several contributions from Spanish groups on tricuspid and aortic regurgitation, developments in atrial fibrillation, syncope, and the clinical characteristics of heart disease, as well as various studies on familial heart disease and chronic ischemic heart disease. In geriatric cardiology, the most relevant studies published in 2014 involve heart failure, degenerative aortic stenosis, and data on atrial fibrillation in the geriatric population. In heart failure and transplantation, the most noteworthy developments concern the importance of multidisciplinary units and patients with preserved systolic function. Other notable publications were those related to iron deficiency, new drugs, and new devices and biomarkers. Finally, we review studies on acute heart failure and transplantation, such as inotropic drugs and ventricular assist devices. PMID:25758161

  12. Effect of Selective Heart Rate Slowing in Heart Failure With Preserved Ejection Fraction

    PubMed Central

    Pal, Nikhil; Sivaswamy, Nadiya; Mahmod, Masliza; Yavari, Arash; Rudd, Amelia; Singh, Satnam; Dawson, Dana K.; Francis, Jane M.; Dwight, Jeremy S.; Watkins, Hugh; Neubauer, Stefan; Frenneaux, Michael

    2015-01-01

    Background Heart failure with preserved ejection fraction (HFpEF) is associated with significant morbidity and mortality but is currently refractory to therapy. Despite limited evidence, heart rate reduction has been advocated, on the basis of physiological considerations, as a therapeutic strategy in HFpEF. We tested the hypothesis that heart rate reduction improves exercise capacity in HFpEF. Methods and Results We conducted a randomized, crossover study comparing selective heart rate reduction with the If blocker ivabradine at 7.5 mg twice daily versus placebo for 2 weeks each in 22 symptomatic patients with HFpEF who had objective evidence of exercise limitation (peak oxygen consumption at maximal exercise [o2 peak] <80% predicted for age and sex). The result was compared with 22 similarly treated matched asymptomatic hypertensive volunteers. The primary end point was the change in o2 peak. Secondary outcomes included tissue Dopplerderived E/e? at echocardiography, plasma brain natriuretic peptide, and quality-of-life scores. Ivabradine significantly reduced peak heart rate compared with placebo in the HFpEF (107 versus 129 bpm; P<0.0001) and hypertensive (127 versus 145 bpm; P=0.003) cohorts. Ivabradine compared with placebo significantly worsened the change in o2 peak in the HFpEF cohort (-2.1 versus 0.9 mLkg?1min?1; P=0.003) and significantly reduced submaximal exercise capacity, as determined by the oxygen uptake efficiency slope. No significant effects on the secondary end points were discernable. Conclusion Our observations bring into question the value of heart rate reduction with ivabradine for improving symptoms in a HFpEF population characterized by exercise limitation. Clinical Trial Registration URL: http://www.clinicaltrials.gov. Unique identifier: NCT02354573. PMID:26338956

  13. [New pharmaceuticals in cardiology. Heart failure, anticoagulation, dyslipidemia].

    PubMed

    Czepluch, F S; Hasenfu, G; Jacobshagen, C

    2014-04-01

    Three innovative pharmaceuticals which might play an important role in the field of cardiology in the near future were recently tested in large clinical studies. Serelaxin, a vasoactive hormone peptide that is produced during pregnancy, reduces vessel resistance, increases cardiac output, and improves renal function. Lately, it was demonstrated that serelaxin significantly reduces congestion symptoms in patients with acute heart failure. As a secondary endpoint the mortality at day180 was reduced. Therefore, serelaxin seems to be a promising new drug for the treatment of acute heart failure which might have a prognostic impact. Edoxaban is a selective factorXa inhibitor, which inhibits thrombin production and thrombus formation. Two recently published studies reported that edoxaban is at least as effective as the vitaminK antagonist warfarin in prevention and treatment of venous thromboembolism and in the prevention of stroke and systemic embolism due to nonvalvular atrial fibrillation. Compared to warfarin, edoxaban significantly exhibited less frequent severe bleeding complications. Edoxaban will probably soon be the fourth new oral anticoagulant available for patients. The serine protease proprotein convertase subtilisin/kexin9 (PCSK9) reduces the ability of the liver to bind low-density lipoprotein cholesterol (LDL-C) and to remove it from the circulation. Recently, a monoclonal antibody for PCSK9 was developed which induces a LDL-C plasma level reduction up to 73?% and also decreases lipoprotein(a) and apolipoprotein B. PCSK9 inhibition is a promising new mechanism for LDL-C reduction and the corresponding drug will be presumably approved soon by the regulatory authorities. PMID:24619100

  14. Sodium and water balance in chronic congestive heart failure.

    PubMed Central

    Cody, R J; Covit, A B; Schaer, G L; Laragh, J H; Sealey, J E; Feldschuh, J

    1986-01-01

    As the characteristics of sodium and water balance in heart failure remain undefined, we evaluated the hemodynamic, metabolic, and hormonal effects of balanced sodium intake in 10 patients with chronic congestive heart failure. We discontinued diuretics to avoid their confounding influence, and all patients received 1 wk of 10 meq and 100 meq balanced sodium intake and controlled free water. Comparing sodium intake of 10 with 100 meq, the following observations were made. There was weight gain (2.0 kg) and increased sodium excretion (11 +/- 3 to 63 +/- 15 meq/24 h), unaccompanied by increase of blood volume. Both renin-angiotensin system and sympathetic nervous system activity were greater during the 10 meq diet, and suppressed with the 100 meq sodium diet. For both diets, plasma renin and urinary aldosterone excretion were correlated with urinary sodium excretion (r = -0.768, r = -0.726, respectively; P less than 0.005). Systemic hemodynamics were minimally changed with increased sodium intake. However, reversal of vasoconstriction by captopril during the 10 meq diet, and its ineffectiveness during the 100 meq diet, indicated a renin-dependent mechanism in the former, and a renin-independent mechanism in the latter diet. There were two subgroups of response to the 100 meq diet: one group (n = 5) achieved neutral balance, while the second (n = 5) avidly retained sodium and water. Renin-angiotensin system activity was significantly higher in the latter group, and the mechanism for differences in sodium excretion for the subgroups could not be identified by blood volume or hemodynamic parameters. Orthostatic hypotension during tilt was greater during the 10 meq sodium diet, and in all cases, related to ineffective hemodynamic and hormonal compensatory responses. PMID:3517066

  15. Reduced Regional Brain Cortical Thickness in Patients with Heart Failure

    PubMed Central

    Kumar, Rajesh; Yadav, Santosh K.; Palomares, Jose A.; Park, Bumhee; Joshi, Shantanu H.; Ogren, Jennifer A.; Macey, Paul M.; Fonarow, Gregg C.; Harper, Ronald M.; Woo, Mary A.

    2015-01-01

    Aims Autonomic, cognitive, and neuropsychologic deficits appear in heart failure (HF) subjects, and these compromised functions depend on cerebral cortex integrity in addition to that of subcortical and brainstem sites. Impaired autoregulation, low cardiac output, sleep-disordered-breathing, hypertension, and diabetic conditions in HF offer considerable potential to affect cortical areas by loss of neurons and glia, which would be expressed as reduced cortical thicknesses. However, except for gross descriptions of cortical volume loss/injury, regional cortical thickness integrity in HF is unknown. Our goal was to assess regional cortical thicknesses across the brain in HF, compared to control subjects. Methods and Results We examined localized cortical thicknesses in 35 HF and 61 control subjects with high-resolution T1-weighted images (3.0-Tesla MRI) using FreeSurfer software, and assessed group differences with analysis-of-covariance (covariates; age, gender; p<0.05; FDR). Significantly-reduced cortical thicknesses appeared in HF over controls in multiple areas, including the frontal, parietal, temporal, and occipital lobes, more markedly on the left side, within areas that control autonomic, cognitive, affective, language, and visual functions. Conclusion Heart failure subjects show reduced regional cortical thicknesses in sites that control autonomic, cognitive, affective, language, and visual functions that are deficient in the condition. The findings suggest chronic tissue alterations, with regional changes reflecting loss of neurons and glia, and presumably are related to earlier-described axonal changes. The pathological mechanisms contributing to reduced cortical thicknesses likely include hypoxia/ischemia, accompanying impaired cerebral perfusion from reduced cardiac output and sleep-disordered-breathing and other comorbidities in HF. PMID:25962164

  16. Population pharmacokinetics of levosimendan in patients with congestive heart failure

    PubMed Central

    Jonsson, E Niclas; Antila, Saila; McFadyen, Lynn; Lehtonen, Lasse; Karlsson, Mats O

    2003-01-01

    Aims The aim of this study was to characterize the population pharmacokinetics of levosimendan in patients with heart failure (NYHA grades III and IV) and its relationship to demographic factors, disease severity and concomitant use of digoxin and ?-blocking agents. Methods Data from two efficacy studies with levosimendan administered by intravenous infusion were combined (190 patients in total). The data were analysed using a nonlinear mixed-effects modelling approach as implemented in the NONMEM program. The model development was done in three sequential steps. First the best structural model was determined (e.g. a one-, two- or three-compartment pharmacokinetic model). This was followed by the identification and incorporation of important covariates into the model. Lastly the stochastic part of the model was refined. Results A two-compartment model best described levosimendan pharmacokinetics. Clearance and the central volume of distribution were found to increase linearly with bodyweight. No other covariates, including concomitant use of digoxin and ?-blocking agents, influenced the pharmacokinetics. In the final model, a 76-kg patient was estimated to have a clearance s.e. of 13.3 0.4 l h?1 and a central volume of distribution of 16.8 0.79 l. The interindividual variability was estimated to be 39% and 60% for clearance and central volume of distribution, respectively. Weight changed clearance by 1.5% [95% confidence interval (CI) 0.9%, 2.1%] and the central volume of distribution by 0.9% (95% CI 0.5%, 1.3%) per kg. Conclusions The population pharmacokinetics parameters of levosimendan in this patient group were comparable to those obtained by traditional methods in healthy volunteers and patients with mild heart failure. Bodyweight influenced the clearance and the central volume of distribution, which in practice is accounted for by weight adjusting doses. None of the other covariates, including digoxin and ?-blocking agents, significantly influenced the pharmacokinetics of levosimendan. PMID:12814448

  17. A study of heart diseases without clinical signs of heart failure in 47 cattle

    PubMed Central

    Buczinski, Sbastien; Francoz, David; Fecteau, Gilles; DiFruscia, Rocky

    2010-01-01

    In this retrospective study, features of 47 cattle suffering from heart disease (HD) without clinical signs of heart failure (HF) were reviewed. The most common reasons for referral were respiratory problems (n =14), anorexia (n = 13), fever (n = 10), and lameness (n = 9). Thirty-nine animals were tachypneic. In 31 cases, cardiac auscultation revealed abnormalities. The final diagnoses were bacterial endocarditis (BE; n = 19), congenital heart disease (CHD; n = 18), pericarditis (n = 8), cardiomyopathy (n = 1), and lymphoma (n = 1). Echocardiography was performed in 39 cases. Gross pathology examination confirmed the echocardiographic diagnosis in 4 of 5 cases of pericarditis, 6 of 6 cases of BE, and 4 of 6 cases of CHD. Short-term prognosis was guarded with 19 cases (40.4%) being discharged. Premature death within 2 mo after discharge (n = 5), early culling because of poor breeding performance (n = 5), and normal productive life in the herd (n = 5) were observed in the cases that were followed. Echocardiography may be the most sensitive tool for the antemortem diagnosis of heart disease in cattle. PMID:21286323

  18. Heart failure in adult congenital heart disease: Emerging concepts with a focus on tetralogy of Fallot.

    PubMed

    Wald, Rachel M; Valente, Anne Marie; Marelli, Ariane

    2015-07-01

    Emerging heart failure (HF) concepts in the growing population of adults with congenital heart disease (ACHD) are reviewed in the following article with a focus on individuals with tetralogy of Fallot (TOF), the largest group of adults with repaired cyanotic congenital heart disease (CHD). In the first section, the changing epidemiology of CHD and HF in ACHD patients is described. We demonstrate the challenges health care providers face when caring for this unique population. Emphasis is placed on the importance and difficulty of identifying patients at risk for HF, of which TOF patients comprise a substantial subset, underscoring the benefits of specialized cardiac care. In the second portion of the article, we review underlying mechanisms of HF in adults with TOF. We elaborate on the wide-ranging etiologies of HF that reflect a confluence of factors related to native anatomic substrate, history of surgical intervention(s), and superimposed hemodynamic and/or ischemic burden to the right and left heart. We describe state-of-the-art imaging concepts as they apply to qualifying and quantifying acquired myocardial and valvular dysfunction in adults with repaired TOF. In the final part of the article, we review the current literature pertaining to the management of adults with repaired TOF. Specifically, we explore medical and surgical issues related to pulmonary valve replacement, arrhythmia management, and transplantation. Finally, we highlight current knowledge gaps and propose future directions of much-needed research that will improve the quality of care for this growing population. PMID:25630927

  19. Nitroglycerin in a transdermal therapeutic system in chronic heart failure.

    PubMed

    Sharpe, D N; Coxon, R

    1984-01-01

    Nitroglycerin (NTG) in a transdermal therapeutic system (TTS) was evaluated in 16 patients with severe chronic heart failure. Eight patients were given NTG TTS with an in vivo release rate of 5 mg/24 h. No significant changes in heart rate or blood pressure were observed. Pulmonary capillary wedge (PCW) pressure was reduced significantly from a control value of 29 +/- 4 mm Hg to 17 +/- 2 mm Hg after 1 h (p less than 0.01), and significant reduction was maintained for 24 h. The system was then removed and PCW pressure rose to 27 +/- 2 mm Hg after 2 h. NTG TTS, 10 mg/24 h, was applied and PCW pressure was again reduced significantly. Significant reduction in systemic vascular resistance and increases in cardiac and stroke volume indices occurred on the first day at 4 h but were not maintained. In another eight patients, the haemodynamic effects of NTG TTS (5 mg/24 h), oral isosorbide dinitrate (20 mg), and topical NTG ointment (1 inch) were compared. Significant reductions in PCW pressure were achieved with each method of treatment, but no significant alterations in other haemodynamic measurements were observed. Haemodynamic reevaluation of 10 patients treated with NTG TTS for 3 months showed partial attenuation of the reduction in PCW pressure compared with the initial response. PMID:6199616

  20. Atrial fibrillation in heart failure: what should we do?

    PubMed

    Kotecha, Dipak; Piccini, Jonathan P

    2015-12-01

    Heart failure (HF) and atrial fibrillation (AF) are two conditions that are likely to dominate the next 50 years of cardiovascular (CV) care. Both are increasingly prevalent and associated with high morbidity, mortality, and healthcare cost. They are closely inter-related with similar risk factors and shared pathophysiology. Patients with concomitant HF and AF suffer from even worse symptoms and poorer prognosis, yet evidence-based evaluation and management of this group of patients is lacking. In this review, we evaluate the common mechanisms for the development of AF in HF patients and vice versa, focusing on the evidence for potential treatment strategies. Recent data have suggested that these patients may respond differently than those with HF or AF alone. These results highlight the clear clinical need to identify and treat according to best evidence, in order to prevent adverse outcomes and reduce the huge burden that HF and AF are expected to have on global healthcare systems in the future. We propose an easy-to-use clinical mnemonic to aid the initial management of newly discovered concomitant HF and AF, the CAN-TREAT HFrEF + AF algorithm (Cardioversion if compromised; Anticoagulation unless contraindication; Normalize fluid balance; Target initial heart rate <110 b.p.m.; Renin-angiotensin-aldosterone modification; Early consideration of rhythm control; Advanced HF therapies; Treatment of other CV disease). PMID:26419625