Concomitant Wolff-Parkinson-White and Atrioventricular Nodal Reentrant Tachycardia: Which Pathway to Ablate?

PubMed

Sarsam, Sinan; Sidiqi, Ibrahim; Shah, Dipak; Zughaib, Marcel

2015-12-11

Atrioventricular nodal reentrant tachycardia (AVNRT) is the most common form of supraventricular tachycardia. In contrast, Wolff-Parkinson-White (WPW) pattern consists of an accessory pathway, which may result in the development of ventricular arrhythmias. Frequent tachycardia caused by AVNRT and accessory pathways may play a role in left ventricular systolic dysfunction. A 54-year-old man presented with palpitations and acute decompensated congestive heart failure. His baseline EKG showed Wolff-Parkinson-White (WPW) pattern. While hospitalized, he had an episode of atrioventricular nodal reentrant tachycardia (AVNRT). He underwent radiofrequency catheter ablation for AVNRT, and his accessory pathway was also ablated even though its conduction was found to be weak. He was clinically doing well on follow-up visit, with resolution of his heart failure symptoms and normalization of left ventricular function on echocardiography. This case raises the question whether the accessory pathway plays a role in the development of systolic dysfunction, and if there is any role for ablation in patients with asymptomatic WPW pattern.

Ischemic Ventricular Tachycardia Presenting as a Narrow Complex Tachycardia

PubMed Central

Page, Stephen P; Watts, Troy; Yeo, Wee Tiong; Mehul, Dhinoja

2014-01-01

This report describes a patient presenting with a narrow complex tachycardia in the context of prior myocardial infarction and impaired ventricular function. Electrophysiological studies confirmed ventricular tachycardia and activation and entrainment mapping demonstrated a critical isthmus within an area of scar involving the His-Purkinje system accounting for the narrow QRS morphology. This very rare case shares some similarities with upper septal ventricular tachycardia seen in patients with structurally normal hearts, but to our knowledge has not been seen previously in patients with ischemic heart disease. PMID:25057222

Moxonidine-induced central sympathoinhibition improves prognosis in rats with hypertensive heart failure.

PubMed

Honda, Nobuhiro; Hirooka, Yoshitaka; Ito, Koji; Matsukawa, Ryuichi; Shinohara, Keisuke; Kishi, Takuya; Yasukawa, Keiji; Utsumi, Hideo; Sunagawa, Kenji

2013-11-01

Enhanced central sympathetic outflow is an indicator of the prognosis of heart failure. Although the central sympatholytic drug moxonidine is an established therapeutic strategy for hypertension, its benefits for hypertensive heart failure are poorly understood. In the present study, we investigated the effects of central sympathoinhibition by intracerebral infusion of moxonidine on survival in a rat model of hypertensive heart failure and the possible mechanisms involved. As a model of hypertensive heart failure, we fed Dahl salt-sensitive rats an 8% NaCl diet from 7 weeks of age. Intracerebroventricular (ICV) infusion of moxonidine (moxonidine-ICV-treated group [Mox-ICV]) or vehicle (vehicle-ICV-treated group [Veh-ICV]) was performed at 14-20 weeks of age, during the increased heart failure phase. Survival rates were examined, and sympathetic activity, left ventricular function and remodelling, and brain oxidative stress were measured. Hypertension and left ventricular hypertrophy were established by 13 weeks of age. At around 20 weeks of age, Veh-ICV rats exhibited overt heart failure concomitant with increased urinary norepinephrine (uNE) excretion as an index of sympathetic activity, dilated left ventricle, decreased percentage fractional shortening, and myocardial fibrosis. Survival rates at 21 weeks of age (n = 28) were only 23% in Veh-ICV rats, and 76% (n = 17) in Mox-ICV rats with concomitant decreases in uNE, myocardial fibrosis, collagen type I/III ratio, brain oxidative stress, and suppressed left ventricular dysfunction. Moxonidine-induced central sympathoinhibition attenuated brain oxidative stress, prevented cardiac dysfunction and remodelling, and improved the prognosis in rats with hypertensive heart failure. Central sympathoinhibition can be effective for the treatment of hypertensive heart failure.

Pathological alterations in liver injury following congestive heart failure induced by volume overload in rats

PubMed Central

Shaqura, Mohammed; Mohamed, Doaa M.; Aboryag, Noureddin B.; Bedewi, Lama; Dehe, Lukas; Treskatsch, Sascha; Shakibaei, Mehdi; Schäfer, Michael

2017-01-01

Heart failure has emerged as a disease with significant public health implications. Following progression of heart failure, heart and liver dysfunction are frequently combined in hospitalized patients leading to increased morbidity and mortality. Here, we investigated the underlying pathological alterations in liver injury following heart failure. Heart failure was induced using a modified infrarenal aortocaval fistula (ACF) in male Wistar rats. Sham operated and ACF rats were compared for their morphometric and hemodynamic data, for histopathological and ultrastructural changes in the liver as well as differences in the expression of apoptotic factors. ACF-induced heart failure is associated with light microscopic signs of apparent congestion of blood vessels, increased apoptosis and breakdown of hepatocytes and inflammatory cell inifltration were observed. The glycogen content depletion associated with the increased hepatic fibrosis, lipid globule formation was observed in ACF rats. Moreover, cytoplasmic organelles are no longer distinguishable in many ACF hepatocytes with degenerated fragmented rough endoplasmic reticulum, shrunken mitochondria and heavy cytoplasm vacuolization. ACF is associated with the upregulation of the hepatic TUNEL-positive cells and proapoptotic factor Bax protein concomitant with the mitochondrial leakage of cytochrome C into the cell cytoplasm and the transfer of activated caspase 3 from the cytoplasm into the nucleus indicating intrinsic apoptotic events. Taken together, the results demonstrate that ACF-induced congestive heart failure causes liver injury which results in hepatocellular apoptotic cell death mediated by the intrinsic pathway of mitochondrial cytochrome C leakage and subsequent transfer of activated caspase 3 into to the nucleus to initiate overt DNA fragmentation and cell death. PMID:28934226

Cardiac arrhythmia mechanisms in rats with heart failure induced by pulmonary hypertension

PubMed Central

Benoist, David; Stones, Rachel; Drinkhill, Mark J.; Benson, Alan P.; Yang, Zhaokang; Cassan, Cecile; Gilbert, Stephen H.; Saint, David A.; Cazorla, Olivier; Steele, Derek S.; Bernus, Olivier

2012-01-01

Pulmonary hypertension provokes right heart failure and arrhythmias. Better understanding of the mechanisms underlying these arrhythmias is needed to facilitate new therapeutic approaches for the hypertensive, failing right ventricle (RV). The aim of our study was to identify the mechanisms generating arrhythmias in a model of RV failure induced by pulmonary hypertension. Rats were injected with monocrotaline to induce either RV hypertrophy or failure or with saline (control). ECGs were measured in conscious, unrestrained animals by telemetry. In isolated hearts, electrical activity was measured by optical mapping and myofiber orientation by diffusion tensor-MRI. Sarcoplasmic reticular Ca2+ handling was studied in single myocytes. Compared with control animals, the T-wave of the ECG was prolonged and in three of seven heart failure animals, prominent T-wave alternans occurred. Discordant action potential (AP) alternans occurred in isolated failing hearts and Ca2+ transient alternans in failing myocytes. In failing hearts, AP duration and dispersion were increased; conduction velocity and AP restitution were steeper. The latter was intrinsic to failing single myocytes. Failing hearts had greater fiber angle disarray; this correlated with AP duration. Failing myocytes had reduced sarco(endo)plasmic reticular Ca2+-ATPase activity, increased sarcoplasmic reticular Ca2+-release fraction, and increased Ca2+ spark leak. In hypertrophied hearts and myocytes, dysfunctional adaptation had begun, but alternans did not develop. We conclude that increased electrical and structural heterogeneity and dysfunctional sarcoplasmic reticular Ca2+ handling increased the probability of alternans, a proarrhythmic predictor of sudden cardiac death. These mechanisms are potential therapeutic targets for the correction of arrhythmias in hypertensive, failing RVs. PMID:22427523

Protease Activated Receptor-2 Contributes to Heart Failure

PubMed Central

Antoniak, Silvio; Sparkenbaugh, Erica M.; Tencati, Michael; Rojas, Mauricio; Mackman, Nigel; Pawlinski, Rafal

2013-01-01

Heart failure is a major clinical problem worldwide. Previous studies have demonstrated an important role for G protein-coupled receptors, including protease-activated receptors (PARs), in the pathology of heart hypertrophy and failure. Activation of PAR-2 on cardiomyocytes has been shown to induce hypertrophic growth in vitro. PAR-2 also contributes to myocardial infarction and heart remodeling after ischemia/reperfusion injury. In this study, we found that PAR-2 induced hypertrophic growth of cultured rat neonatal cardiomyocytes in a MEK1/2 and p38 dependent manner. In addition, PAR-2 activation on mouse cardiomyocytes increased expression of the pro-fibrotic chemokine MCP-1. Furthermore, cardiomyocyte-specific overexpression of PAR-2 in mice induced heart hypertrophy, cardiac fibrosis, inflammation and heart failure. Finally, in a mouse model of myocardial infarction induced by permanent ligation of the left anterior descending coronary artery, PAR-2 deficiency attenuated heart remodeling and improved heart function independently of its contribution to the size of the initial infarct. Taken together, our data indicate that PAR-2 signaling contributes to the pathogenesis of hypertrophy and heart failure. PMID:24312345

Gallic acid attenuates pulmonary fibrosis in a mouse model of transverse aortic contraction-induced heart failure.

PubMed

Jin, Li; Piao, Zhe Hao; Sun, Simei; Liu, Bin; Ryu, Yuhee; Choi, Sin Young; Kim, Gwi Ran; Kim, Hyung-Seok; Kee, Hae Jin; Jeong, Myung Ho

2017-12-01

Gallic acid, a trihydroxybenzoic acid found in tea and other plants, attenuates cardiac hypertrophy, fibrosis, and hypertension in animal models. However, the role of gallic acid in heart failure remains unknown. In this study, we show that gallic acid administration prevents heart failure-induced pulmonary fibrosis. Heart failure induced in mice, 8weeks after transverse aortic constriction (TAC) surgery, was confirmed by echocardiography. Treatment for 2weeks with gallic acid but not furosemide prevented cardiac dysfunction in mice. Gallic acid significantly inhibited TAC-induced pathological changes in the lungs, such as increased lung mass, pulmonary fibrosis, and damaged alveolar morphology. It also decreased the expression of fibrosis-related genes, including collagen types I and III, fibronectin, connective tissue growth factor (CTGF), and phosphorylated Smad3. Further, it inhibited the expression of epithelial-mesenchymal transition (EMT)-related genes, such as N-cadherin, vimentin, E-cadherin, SNAI1, and TWIST1. We suggest that gallic acid has therapeutic potential for the treatment of heart failure-induced pulmonary fibrosis. Copyright © 2017 Elsevier Inc. All rights reserved.

Hypothyroidism-induced myocardial damage and heart failure: an overlooked entity.

PubMed

Shuvy, Mony; Shifman, Oshrat E Tayer; Nusair, Samir; Pappo, Orit; Lotan, Chaim

2009-01-01

Hypothyroid state may induce cardiac muscle impairment such as diastolic dysfunction and abnormal relaxation time. Advanced heart failure in hypothyroid patients has been described only in severe symptomatic cases, mostly during myxedematous coma. We describe an unusual case of asymptomatic patient with hypothyroidism who presented with severely reduced cardiac function with elevated cardiac enzymes reflecting significant myocardial injury. Comprehensive evaluation for heart failure was suggestive only for long-standing untreated hypothyroidism. Endomyocadial biopsy demonstrated unique histological findings of mucopolysaccharide accumulation attributed to hypothyroid state. Asymptomatic hypothyroidism may cause severe reduction in cardiac function accompanied with elevated cardiac enzymes. To our knowledge, this is the first description of human myocardial biopsy revealing mucopolysaccharide accumulation attributed to hypothyroid state.

Oxymatrine attenuated isoproterenol-induced heart failure in rats via regulation of COX-2/PGI2 pathway.

PubMed

Zhou, Ru; Xu, Qingbin; Xu, Yehua; Xiong, Aiqin; Wang, Yang; Ma, Ping

2016-12-01

Oxymatrine (OMT) is an active constituent of traditional Chinese herb Sophora japonica Ait which has been shown to exert potent anti-inflammatory,anti-oxidant and anti-fibrosis properties. Our previous studies have demonstrated that OMT has protective effects on isoproterenol-induced heart failure in rats through regulation of DDAH/ADMA metabolism pathway.In this study,we further investigated whether OMT could attenuate isoproterenol-induced heart failure through the regulation of COX-2/PGI 2 pathway. Heart failure was induced in Sprague-Dawley rats by 5mg/kg isoproterenol subcutaneous injection for 7days. The rats were maintained on normal diet and randomly divided into five groups: control, isoproterenol, isoproterenol with OMT (50, 100mg/kg), and OMT alone groups (n=12 in each group). Serum brain natruretic peptide (BNP, a heart failure biomarker), histopathological variables, expression of Cytosolic phospholipase A 2 (cPLA 2 ), cyclooxygenase-1 (COX-1), cyclooxygenase-2 (COX-2) and Prostacyclin synthase (PGIS) were analysed. Administration of OMT significantly reduced the increased BNP in plasm of isoproterenol-induced rats, attenuated cardiac fibrosis,suppressed overexpression of myocardial COX-1 expression, up-regulated COX-2 and PGIS expression, but had no effects on isoproterenol-induced elevated protein cPLA 2 . And compared with control group, any indexes in sham rats treated with OMT (100mg/kg) alone were unaltered. These results demonstrated that OMT has cardioprotective effects on isoproterenol-induced heart failure in rats by regulating COX-2/PGI 2 pathway. Copyright © 2016. Published by Elsevier Masson SAS.

[Heart failure as early manifestation of neonatal hyperthyroidism. Case report].

PubMed

Alvarado S, Jorge Luis; Fernández V, Zhirly Andrea

2014-04-01

Neonatal hyperthyroidism is usually a self-limited condition frequently associated with transplacental passage of thyroid stimulating antibodies secondary to maternal autoimmune disorders. To timely detect mothers with this medical antecedents decreases the risk for fetal adverse events. To report a case of neonatal hyperthyroidism associated with intrauterine growth restriction and heart failure. A 36 week-old newborn with birth weight of 1,240 g. Symptoms were tachycardia, distal coldness, exophthalmos, hepatomegaly and tremors. Echocardiogram ruled out structural heart disorders. Due to maternal symptoms suggestive of hyperthyroidism, TSH tests were performed showing 0.01 ulU/ml, free T4 7.7 ng/dl, so the diagnosis of neonatal hyperthyroidism was confirmed. It was treated with methimazole and propanol, alleviating the symptoms and decreasing the levels of free T4. To know the maternal history helps identify and manage neonatal complications of hyperthyroidism. Heart failure and other cardiopulmonary disorders are determinants of mortality during early neonatal period. High-risk newborns should receive follow up assessments.

Mitochondrial proteome remodelling in pressure overload-induced heart failure: the role of mitochondrial oxidative stress

PubMed Central

Dai, Dao-Fu; Hsieh, Edward J.; Liu, Yonggang; Chen, Tony; Beyer, Richard P.; Chin, Michael T.; MacCoss, Michael J.; Rabinovitch, Peter S.

2012-01-01

Aims We investigate the role of mitochondrial oxidative stress in mitochondrial proteome remodelling using mouse models of heart failure induced by pressure overload. Methods and results We demonstrate that mice overexpressing catalase targeted to mitochondria (mCAT) attenuate pressure overload-induced heart failure. An improved method of label-free unbiased analysis of the mitochondrial proteome was applied to the mouse model of heart failure induced by transverse aortic constriction (TAC). A total of 425 mitochondrial proteins were compared between wild-type and mCAT mice receiving TAC or sham surgery. The changes in the mitochondrial proteome in heart failure included decreased abundance of proteins involved in fatty acid metabolism, an increased abundance of proteins in glycolysis, apoptosis, mitochondrial unfolded protein response and proteolysis, transcription and translational control, and developmental processes as well as responses to stimuli. Overexpression of mCAT better preserved proteins involved in fatty acid metabolism and attenuated the increases in apoptotic and proteolytic enzymes. Interestingly, gene ontology analysis also showed that monosaccharide metabolic processes and protein folding/proteolysis were only overrepresented in mCAT but not in wild-type mice in response to TAC. Conclusion This is the first study to demonstrate that scavenging mitochondrial reactive oxygen species (ROS) by mCAT not only attenuates most of the mitochondrial proteome changes in heart failure, but also induces a subset of unique alterations. These changes represent processes that are adaptive to the increased work and metabolic requirements of pressure overload, but which are normally inhibited by overproduction of mitochondrial ROS. PMID:22012956

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 ... and shortness of breath Common causes of heart failure are coronary artery disease, high blood pressure and ...

Contact force monitoring during catheter ablation of intraatrial reentrant tachycardia in patients with congenital heart disease.

PubMed

Krause, Ulrich; Backhoff, David; Klehs, Sophia; Schneider, Heike E; Paul, Thomas

2016-08-01

Monitoring of catheter contact force during catheter ablation of atrial fibrillation has been shown to increase efficacy and safety. However, almost no data exists on the use of this technology in catheter ablation of intraatrial reentrant tachycardia in patients with congenital heart disease. The aim of the present study was to evaluate the impact of contact force monitoring during catheter ablation of intraatrial reentrant tachycardia in those patients. Catheter ablation of intraatrial reentrant tachycardia using monitoring of catheter contact force was performed in 28 patients with congenital heart disease (CHD). Thirty-two patients matched according to gender, age, and body weight with congenital heart disease undergoing catheter ablation without contact force monitoring served as control group. Parameters reflecting acute procedural success, long-term efficacy, and safety were compared. Acute procedural success was statistically not different in both groups (contact force 93 % vs. control 84 %, p = 0.3). Likewise the recurrence rate 1 year after ablation as shown by Kaplan-Meier analysis did not differ (contact force 28 % vs. control 37 %, p = 0.63). Major complications were restricted to groin vessel injuries and occurred in 3 out of 60 patients (contact force n = 1; control n = 2). Complications related to excessive catheter contact force were not observed. The present study did not show superiority of catheter contact force monitoring during ablation of intraatrial reentrant tachycardia in patients with CHD in terms of efficacy and safety. Higher contact force compared to pulmonary vein isolation might therefore be required to increase the efficacy of catheter ablation of intraatrial reentrant tachycardia in patients with congenital heart disease.

Thyroid Echography-induced Thyroid Storm and Exacerbation of Acute Heart Failure.

PubMed

Nakabayashi, Keisuke; Nakazawa, Naomi; Suzuki, Toshiaki; Asano, Ryotaro; Saito, Hideki; Nomura, Hidekimi; Isomura, Daichi; Okada, Hisayuki; Sugiura, Ryo; Oka, Toshiaki

2016-01-01

Hyperthyroidism and thyroid storm affect cardiac circulation in some conditions. Several factors including trauma can induce thyroid storms. We herein describe the case of a 57-year-old woman who experienced a thyroid storm and exacerbation of acute heart failure on thyroid echography. She initially demonstrated a good clinical course after medical rate control for atrial fibrillation; however, thyroid echography for evaluating hyperthyroidism led to a thyroid storm and she collapsed. A multidisciplinary approach stabilized her thyroid hormone levels and hemodynamics. Thus, the medical staff should be prepared for a deterioration in the patient's condition during thyroid echography in heart failure patients with hyperthyroidism.

Heart-rate variability depression in porcine peritonitis-induced sepsis without organ failure.

PubMed

Jarkovska, Dagmar; Valesova, Lenka; Chvojka, Jiri; Benes, Jan; Danihel, Vojtech; Sviglerova, Jitka; Nalos, Lukas; Matejovic, Martin; Stengl, Milan

2017-05-01

Depression of heart-rate variability (HRV) in conditions of systemic inflammation has been shown in both patients and experimental animal models and HRV has been suggested as an early indicator of sepsis. The sensitivity of HRV-derived parameters to the severity of sepsis, however, remains unclear. In this study we modified the clinically relevant porcine model of peritonitis-induced sepsis in order to avoid the development of organ failure and to test the sensitivity of HRV to such non-severe conditions. In 11 anesthetized, mechanically ventilated and instrumented domestic pigs of both sexes, sepsis was induced by fecal peritonitis. The dose of feces was adjusted and antibiotic therapy was administered to avoid multiorgan failure. Experimental subjects were screened for 40 h from the induction of sepsis. In all septic animals, sepsis with hyperdynamic circulation and increased plasma levels of inflammatory mediators developed within 12 h from the induction of peritonitis. The sepsis did not progress to multiorgan failure and there was no spontaneous death during the experiment despite a modest requirement for vasopressor therapy in most animals (9/11). A pronounced reduction of HRV and elevation of heart rate developed quickly (within 5 h, time constant of 1.97 ± 0.80 h for HRV parameter TINN) upon the induction of sepsis and were maintained throughout the experiment. The frequency domain analysis revealed a decrease in the high-frequency component. The reduction of HRV parameters and elevation of heart rate preceded sepsis-associated hemodynamic changes by several hours (time constant of 11.28 ± 2.07 h for systemic vascular resistance decline). A pronounced and fast reduction of HRV occurred in the setting of a moderate experimental porcine sepsis without organ failure. Inhibition of parasympathetic cardiac signaling probably represents the main mechanism of HRV reduction in sepsis. The sensitivity of HRV to systemic inflammation may allow

[Ventricular tachycardia in a patient with rate-responsive cardiac pacemaker].

PubMed

Himbert, C; Lascault, G; Tonet, J; Coutte, R; Busquet, P; Frank, R; Grosgogeat, Y

1992-11-01

The authors report a case of syncopal ventricular tachycardia in a patient with a respiratory-dependent rate responsive pacemaker, followed-up for valvular heart disease with severe left ventricular dysfunction and sustained atrial and ventricular arrhythmias. The introduction of low dose betablocker therapy with reinforcement of the treatment of cardiac failure controlled the ventricular arrhythmia, after suppression of the data responsive function had been shown to be ineffective. The authors discuss the role of the rate responsive function in the triggering of the ventricular tachycardias.

Partially silencing brain toll-like receptor 4 prevents in part left ventricular remodeling with sympathoinhibition in rats with myocardial infarction-induced heart failure.

PubMed

Ogawa, Kiyohiro; Hirooka, Yoshitaka; Kishi, Takuya; Ide, Tomomi; Sunagawa, Kenji

2013-01-01

Left ventricular (LV) remodeling and activation of sympathetic nervous system (SNS) are cardinal features of heart failure. We previously demonstrated that enhanced central sympathetic outflow is associated with brain toll-like receptor 4 (TLR4) probably mediated by brain angiotensin II type 1 receptor in mice with myocardial infarction (MI)-induced heart failure. The purpose of the present study was to examine whether silencing brain TLR4 could prevent LV remodeling with sympathoinhibition in MI-induced heart failure. MI-induced heart failure model rats were created by ligation of left coronary artery. The expression level of TLR4 in brainstem was significantly higher in MI-induced heart failure treated with intracerebroventricular (ICV) injection of hGAPDH-SiRNA than in sham. TLR4 in brainstem was significantly lower in MI-induced heart failure treated with ICV injection of TLR4-SiRNA than in that treated with ICV injection of hGAPDH-SiRNA. Lung weight, urinary norepinephrine excretion, and LV end-diastolic pressure were significantly lower and LV dimension was significantly smaller in MI-induced heart failure treated with TLR4-SiRNA than in that treated with hGAPDH-SiRNA for 2 weeks. Partially silencing brain TLR4 by ICV injection of TLR4-SiRNA for 2 weeks could in part prevent LV remodeling with sympathoinhibition in rats with MI-induced heart failure. Brain TLR4 has a potential to be a target of the treatment for MI-induced heart failure.

Supraventricular tachycardia induced by chocolate: is chocolate too sweet for the heart?

PubMed

Parasramka, Saurabh; Dufresne, Alix

2012-09-01

Conflicting studies have been published concerning the association between chocolate and cardiovascular diseases. Fewer articles have described the potential arrhythmogenic risk related to chocolate intake. We present a case of paroxysmal supraventricular tachycardia in a woman after consumption of large quantity of chocolate. A 53-year-old woman with no significant medical history presented to us with complaints of palpitations and shortness of breath after consuming large amounts of chocolate. Electrocardiogram showed supraventricular tachycardia at 165 beats per minute, which was restored to sinus rhythm after adenosine bolus injection. Electrophysiology studies showed atrioventricular nodal reentry tachycardia, which was treated with radiofrequency ablation. Chocolate contains caffeine and theobromine, which are methylxanthines and are competitive antagonists of adenosine and can have arrhythmogenic potential. Our case very well describes an episode of tachycardia precipitated by large amount of chocolate consumption in a patient with underlying substrate. There are occasional case reports describing association between chocolate, caffeine, and arrhythmias. A large Danish study, however, did not find any association between amount of daily caffeine consumption and risk of arrhythmia.

Cardioprotective Effects of QiShenYiQi Dripping Pills on Transverse Aortic Constriction-Induced Heart Failure in Mice.

PubMed

Ruan, Guoran; Ren, Haojin; Zhang, Chi; Zhu, Xiaogang; Xu, Chao; Wang, Liyue

2018-01-01

QiShenYiQi dripping pills (QSYQ), a traditional Chinese medicine, are commonly used to treat coronary heart disease, and QSYQ was recently approved as a complementary treatment for ischemic heart failure in China. However, only few studies reported on whether QSYQ exerts a protective effect on heart failure induced by pressure overload. In this study, we explored the role of QSYQ in a mouse model of heart failure induced by transverse aortic constriction (TAC). Twenty-eight C57BL/6J mice were divided into four groups: Sham + NS group, Sham + QSYQ group, TAC + NS group, and TAC + QSYQ group. QSYQ dissolved in normal saline (NS) was administered intragastrically (3.5 mg/100 g/day) in the Sham + QSYQ and TAC + QSYQ groups. In the Sham + NS and TAC + NS groups, NS was provided every day intragastrically. Eight weeks after TAC, echocardiography, and cardiac catheterization were performed to evaluate the cardiac function, and immunofluorescent staining with anti-actinin2 antibody was performed to determine the structure of the myocardial fibers. Moreover, TUNEL staining and Masson trichrome staining were employed to assess the effects of QSYQ on cardiac apoptosis and cardiac fibrosis. Western blots and real-time polymerase chain reaction (PCR) were used to measure the expression levels of vascular endothelial growth factor (VEGF) in the heart, and immunohistochemical staining with anti-CD31 antibody was performed to explore the role of QSYQ in cardiac angiogenesis. Results showed that TAC-induced cardiac dysfunction and disrupted structure of myocardial fibers significantly improved after QSYQ treatment. Moreover, QSYQ treatment also significantly improved cardiac apoptosis and cardiac fibrosis in TAC-induced heart failure, which was accompanied by an increase in VEGF expression levels and maintenance of microvessel density in the heart. In conclusion, QSYQ exerts a protective effect on TAC-induced heart failure, which could be attributed to enhanced cardiac angiogenesis

Impact of tachycardia and sympathetic stimulation by cold pressor test on cardiac diastology and arterial function in elderly females.

PubMed

Johnson, Jonas; Håkansson, Felicia; Shahgaldi, Kambiz; Manouras, Aristomenis; Norman, Mikael; Sahlén, Anders

2013-04-01

Abnormal vascular-ventricular coupling has been suggested to contribute to heart failure with preserved ejection fraction in elderly females. Failure to increase stroke volume (SV) during exercise occurs in parallel with dynamic changes in arterial physiology leading to increased afterload. Such adverse vascular reactivity during stress may reflect either sympathoexcitation or be due to tachycardia. We hypothesized that afterload elevation induces SV failure by transiently attenuating left ventricular relaxation, a phenomenon described in animal research. The respective roles of tachycardia and sympathoexcitation were investigated in n = 28 elderly females (70 ± 4 yr) carrying permanent pacemakers. At rest, during atrial tachycardia pacing (ATP; 100 min(-1)) and during cold pressor test (hand immersed in ice water), we performed Doppler echocardiography (maximal untwist rate analyzed by speckle tracking imaging of rotational mechanics) and arterial tonometry (arterial stiffness estimated as augmentation index). Estimation of arterial compliance was based on an exponential relationship between arterial pressure and volume. We found that ATP produced central hypovolemia and a reduction in SV which was larger in patients with stiffer arteries (higher augmentation index). There was an associated adverse response of arterial compliance and vascular resistance during ATP and cold pressor test, causing an overall increase in afterload, but nonetheless enhanced maximal rate of untwist and no evidence of afterload-dependent failure of relaxation. In conclusion, tachycardia and cold provocation in elderly females produces greater vascular reactivity and SV failure in the presence of arterial stiffening, but SV failure does not arise secondary to afterload-dependent attenuation of relaxation.

Sildenafil ameliorates left ventricular T-tubule remodeling in a pressure overload-induced murine heart failure model

PubMed Central

Huang, Chun-kai; Chen, Bi-yi; Guo, Ang; Chen, Rong; Zhu, Yan-qi; Kutschke, William; Hong, Jiang; Song, Long-sheng

2016-01-01

Aim: Sildenafil, a phosphodiesterase 5 (PDE5) inhibitor, has been shown to exert beneficial effects in heart failure. The purpose of this study was to test whether sildenafil suppressed transverse-tubule (T-tubule) remodeling in left ventricular (LV) failure and thereby providing the therapeutic benefits. Methods: A pressure overload-induced murine heart failure model was established in mice by thoracic aortic banding (TAB). One day after TAB, the mice received sildenafil (100 mg·kg−1·d−1, sc) or saline for 5 weeks. At the end of treatment, echocardiography was used to examine LV function. Then the intact hearts were dissected out and placed in Langendorff-perfusion chamber for in situ confocal imaging of T-tubule ultrastructure from epicardial myocytes. Results: TAB surgery resulted in heart failure accompanied by remarkable T-tubule remodeling. Sildenafil treatment significantly attenuated TAB-induced cardiac hypertrophy and congestive heart failure, improved LV contractile function, and preserved T-tubule integrity in LV cardiomyocytes. But sildenafil treatment did not significantly affect the chamber dilation. The integrity of LV T-tubule structure was correlated with cardiac hypertrophy (R2=0.74, P<0.01) and global LV function (R2=0.47, P<0.01). Conclusion: Sildenafil effectively ameliorates LV T-tubule remodeling in TAB mice, revealing a novel mechanism underlying the therapeutic benefits of sildenafil in heart failure. PMID:26972492

Pulmonary hypertension and isolated right heart failure complicating amiodarone induced hyperthyroidism.

PubMed

Wong, Sean-Man; Tse, Hung-Fat; Siu, Chung-Wah

2012-03-01

Hyperthyroidism is a common side effect encountered in patients prescribed long-term amiodarone therapy for cardiac arrhythmias. We previously studied 354 patients prescribed amiodarone in whom the occurrence of hyperthyroidism was associated with major adverse cardiovascular events including heart failure, myocardial infarction, ventricular arrhythmias, stroke and even death [1]. We now present a case of amiodarone-induced hyperthyroidism complicated by isolated right heart failure and pulmonary hypertension that resolved with treatment of hyperthyroidism. Detailed quantitative echocardiography enables improved understanding of the haemodynamic mechanisms underlying the condition. Copyright © 2011 Australian and New Zealand Society of Cardiac and Thoracic Surgeons (ANZSCTS) and the Cardiac Society of Australia and New Zealand (CSANZ). Published by Elsevier B.V. All rights reserved.

Incretin-related drug therapy in heart failure.

PubMed

Vest, Amanda R

2015-02-01

The new pharmacological classes of GLP-1 agonists and DPP-4 inhibitors are now widely used in diabetes and have been postulated as beneficial in heart failure. These proposed benefits arise from the inter-related pathophysiologies of diabetes and heart failure (diabetes increases the risk of heart failure, and heart failure can induce insulin resistance) and also in light of the dysfunctional myocardial energetics seen in heart failure. The normal heart utilizes predominantly fatty acids for energy production, but there is some evidence to suggest that increased myocardial glucose uptake may be beneficial for the failing heart. Thus, GLP-1 agonists, which stimulate glucose-dependent insulin release and enhance myocardial glucose uptake, have become a focus of investigation in both animal models and humans with heart failure. Limited pilot data for GLP-1 agonists shows potential improvements in systolic function, hemodynamics, and quality of life, forming the basis for current phase II trials.

[Understanding heart failure].

PubMed

Boo, José Fernando Guadalajara

2006-01-01

Heart failure is a disease with several definitions. The term "heart failure" is used by has brougth about confusion in the terminology. For this reason, the value of the ejection fraction (< 0.40 or < 0.35) is used in most meganalyses on the treatment of heart failure, avoiding the term "heart failure" that is a confounding concept. In this paper we carefully analyze the meaning of contractility, ventricular function or performance, preload, afterload, heart failure, compensation mechanisms in heart failure, myocardial oxygen consumption, inadequate, adequate and inappropriate hypertrophy, systole, diastole, compliance, problems of relaxation, and diastolic dysfunction. Their definitions are supported by the original scientific descriptions in an attempt to clarify the concepts about ventricular function and heart failure and, in this way, use the same scientific language about the meaning of ventricular function, heart failure, and diastolic dysfunction.

Heart failure.

PubMed

Metra, Marco; Teerlink, John R

2017-10-28

Heart failure is common in adults, accounting for substantial morbidity and mortality worldwide. Its prevalence is increasing because of ageing of the population and improved treatment of acute cardiovascular events, despite the efficacy of many therapies for patients with heart failure with reduced ejection fraction, such as angiotensin converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs), β blockers, and mineralocorticoid receptor antagonists, and advanced device therapies. Combined angiotensin receptor blocker neprilysin inhibitors (ARNIs) have been associated with improvements in hospital admissions and mortality from heart failure compared with enalapril, and guidelines now recommend substitution of ACE inhibitors or ARBs with ARNIs in appropriate patients. Improved safety of left ventricular assist devices means that these are becoming more commonly used in patients with severe symptoms. Antidiabetic therapies might further improve outcomes in patients with heart failure. New drugs with novel mechanisms of action, such as cardiac myosin activators, are under investigation for patients with heart failure with reduced left ventricular ejection fraction. Heart failure with preserved ejection fraction is a heterogeneous disorder that remains incompletely understood and will continue to increase in prevalence with the ageing population. Although some data suggest that spironolactone might improve outcomes in these patients, no therapy has conclusively shown a significant effect. Hopefully, future studies will address these unmet needs for patients with heart failure. Admissions for acute heart failure continue to increase but, to date, no new therapies have improved clinical outcomes. Copyright © 2017 Elsevier Ltd. All rights reserved.

Zebrafish heart failure models: opportunities and challenges.

PubMed

Shi, Xingjuan; Chen, Ru; Zhang, Yu; Yun, Junghwa; Brand-Arzamendi, Koroboshka; Liu, Xiangdong; Wen, Xiao-Yan

2018-05-03

Heart failure is a complex pathophysiological syndrome of pumping functional failure that results from injury, infection or toxin-induced damage on the myocardium, as well as genetic influence. Gene mutations associated with cardiomyopathies can lead to various pathologies of heart failure. In recent years, zebrafish, Danio rerio, has emerged as an excellent model to study human cardiovascular diseases such as congenital heart defects, cardiomyopathy, and preclinical development of drugs targeting these diseases. In this review, we will first summarize zebrafish genetic models of heart failure arose from cardiomyopathy, which is caused by mutations in sarcomere, calcium or mitochondrial-associated genes. Moreover, we outline zebrafish heart failure models triggered by chemical compounds. Elucidation of these models will improve the understanding of the mechanism of pathogenesis and provide potential targets for novel therapies.

Alterations in left ventricular diastolic function in conscious dogs with pacing-induced heart failure

NASA Technical Reports Server (NTRS)

Komamura, K.; Shannon, R. P.; Pasipoularides, A.; Ihara, T.; Lader, A. S.; Patrick, T. A.; Bishop, S. P.; Vatner, S. F.

1992-01-01

We investigated in conscious dogs (a) the effects of heart failure induced by chronic rapid ventricular pacing on the sequence of development of left ventricular (LV) diastolic versus systolic dysfunction and (b) whether the changes were load dependent or secondary to alterations in structure. LV systolic and diastolic dysfunction were evident within 24 h after initiation of pacing and occurred in parallel over 3 wk. LV systolic function was reduced at 3 wk, i.e., peak LV dP/dt fell by -1,327 +/- 105 mmHg/s and ejection fraction by -22 +/- 2%. LV diastolic dysfunction also progressed over 3 wk of pacing, i.e., tau increased by +14.0 +/- 2.8 ms and the myocardial stiffness constant by +6.5 +/- 1.4, whereas LV chamber stiffness did not change. These alterations were associated with increases in LV end-systolic (+28.6 +/- 5.7 g/cm2) and LV end-diastolic stresses (+40.4 +/- 5.3 g/cm2). When stresses and heart rate were matched at the same levels in the control and failure states, the increases in tau and myocardial stiffness were no longer observed, whereas LV systolic function remained depressed. There were no increases in connective tissue content in heart failure. Thus, pacing-induced heart failure in conscious dogs is characterized by major alterations in diastolic function which are reversible with normalization of increased loading condition.

Four faces of baroreflex failure: hypertensive crisis, volatile hypertension, orthostatic tachycardia, and malignant vagotonia

NASA Technical Reports Server (NTRS)

Ketch, Terry; Biaggioni, Italo; Robertson, RoseMarie; Robertson, David

2002-01-01

BACKGROUND: The baroreflex normally serves to buffer blood pressure against excessive rise or fall. Baroreflex failure occurs when afferent baroreceptive nerves or their central connections become impaired. In baroreflex failure, there is loss of buffering ability, and wide excursions of pressure and heart rate occur. Such excursions may derive from endogenous factors such as stress or drowsiness, which result in quite high and quite low pressures, respectively. They may also derive from exogenous factors such as drugs or environmental influences. METHODS AND RESULTS: Impairment of the baroreflex may produce an unusually broad spectrum of clinical presentations; with acute baroreflex failure, a hypertensive crisis is the most common presentation. Over succeeding days to weeks, or in the absence of an acute event, volatile hypertension with periods of hypotension occurs and may continue for many years, usually with some attenuation of pressor surges and greater prominence of depressor valleys during long-term follow-up. With incomplete loss of baroreflex afferents, a mild syndrome of orthostatic tachycardia or orthostatic intolerance may appear. Finally, if the baroreflex failure occurs without concomitant destruction of the parasympathetic efferent vagal fibers, a resting state may lead to malignant vagotonia with severe bradycardia and hypotension and episodes of sinus arrest. CONCLUSIONS: Although baroreflex failure is not the most common cause of the above conditions, correct differentiation from other cardiovascular disorders is important, because therapy of baroreflex failure requires specific strategies, which may lead to successful control.

A Case of Refractory Heart Failure in Becker Muscular Dystrophy Improved With Corticosteroid Therapy.

PubMed

Nakamura, Makiko; Sunagawa, Osahiko; Hokama, Ryo; Tsuchiya, Hiroyuki; Miyara, Takafumi; Taba, Yoji; Touma, Takashi

2016-09-28

The patient was a 26 year-old man who was referred to our hospital in June 2011 because of severe heart failure. At age 24 years, he was found to have Becker muscular dystrophy. He received enalapril for cardiac dysfunction; however, he had worsening heart failure and was thus referred to our hospital. Echocardiography showed enlargement of the left ventricle, with a diastolic dimension of 77 mm and ejection fraction of 19%. His condition improved temporarily after an infusion of dobutamine and milrinone. He was then administered amiodarone for ventricular tachycardia; however, he subsequently developed hemoptysis. Amiodarone was discontinued and corticosteroid pulse therapy was administered followed by oral prednisolone (PSL). His creatinine phosphokinase (CPK) level and cardiomegaly improved after the corticosteroid therapy. The PSL dose was reduced gradually, bisoprolol was introduced, and the catecholamine infusion was tapered. A cardiac resynchronization device was implanted; however, the patient's condition gradually worsened, which necessitated dobutamine infusion for heart failure. We readministered 30 mg PSL, which decreased the CPK level and improved the cardiomegaly. The dobutamine infusion was discontinued, and the patient was discharged. He was given 7.5 mg PSL as an outpatient, and he returned to normal life without exacerbation of the heart failure. There are similar reports showing that corticosteroids are effective for skeletal muscle improvement in Duchenne muscular dystrophy; however, their effectiveness for heart failure has been rarely reported. We experienced a case of Becker muscular dystrophy in which corticosteroid therapy was effective for refractory heart failure.

Paroxysmal supraventricular tachycardia (PSVT)

MedlinePlus

PSVT; Supraventricular tachycardia; Abnormal heart rhythm - PSVT; Arrhythmia - PSVT; Rapid heart rate - PSVT; Fast heart rate - PSVT ... Normally, the chambers of the heart (atria and ventricles) contract in ... are caused by an electrical signal that begins in an area ...

Determinants of the development of mitral regurgitation in pacing-induced heart failure.

PubMed

Takagaki, Masami; McCarthy, Patrick M; Goormastic, Marlene; Ochiai, Yoshie; Doi, Kazuyoshi; Kopcak, Michael W; Tabata, Tomotsugu; Cardon, Lisa A; Thomas, James D; Fukamachi, Kiyotaka

2003-01-01

The pacing-induced heart failure model provides an opportunity to assess the structural and functional determinants of mitral regurgitation (MR) in dilated cardiomyopathy. This study aimed to evaluate MR to better understand the multitude of factors contributing to its development. Heart failure was induced by rapid ventricular pacing (230 beats/min) in 40 mongrel dogs. Left ventricular (LV) size and MR were evaluated echocardiographically. LV contractility was analyzed using a conductance catheter. MR increased to mild in 12 animals (regurgitant orifice area, 0.06+/-0.05 cm(2)), moderate in 15 (0.14+/-0.07 cm(2)), and severe in 13 (0.34+/-0.16 cm(2)). The grade of MR had an inverse relationships with E(max) (the slope of the end-systolic pressure-volume relationship, p<0.01) and dE/dt (the slope of the maximum rate of change of pressure-end-diastolic volume [V(ED)] relationship, p<0.01) and positive relationships with V(ED) and end-diastolic cross-sectional areas and lengths (p<0.05) by univariate analysis. The dE/dt had an independently significant (p<0.01) relationship by multivariable logistic regression. Many factors influence the development of MR and because of its similarity to the clinical situation, this model can be used to investigate MR and heart failure, as well as new surgical therapies.

Heart Failure as an Aging-Related Phenotype.

PubMed

Morita, Hiroyuki; Komuro, Issei

2018-01-27

The molecular pathophysiology of heart failure, which is one of the leading causes of mortality, is not yet fully understood. Heart failure can be regarded as a systemic syndrome of aging-related phenotypes. Wnt/β-catenin signaling and the p53 pathway, both of which are key regulators of aging, have been demonstrated to play a critical role in the pathogenesis of heart failure. Circulating C1q was identified as a novel activator of Wnt/β-catenin signaling, promoting systemic aging-related phenotypes including sarcopenia and heart failure. On the other hand, p53 induces the apoptosis of cardiomyocytes in the failing heart. In these molecular mechanisms, the cross-talk between cardiomyocytes and non-cardiomyocytes (e,g,. endothelial cells, fibroblasts, smooth muscle cells, macrophages) deserves mentioning. In this review, we summarize recent advances in the understanding of the molecular pathophysiology underlying heart failure, focusing on Wnt/β-catenin signaling and the p53 pathway.

Activation of PPAR-α in the early stage of heart failure maintained myocardial function and energetics in pressure-overload heart failure.

PubMed

Kaimoto, Satoshi; Hoshino, Atsushi; Ariyoshi, Makoto; Okawa, Yoshifumi; Tateishi, Shuhei; Ono, Kazunori; Uchihashi, Motoki; Fukai, Kuniyoshi; Iwai-Kanai, Eri; Matoba, Satoaki

2017-02-01

Failing heart loses its metabolic flexibility, relying increasingly on glucose as its preferential substrate and decreasing fatty acid oxidation (FAO). Peroxisome proliferator-activated receptor α (PPAR-α) is a key regulator of this substrate shift. However, its role during heart failure is complex and remains unclear. Recent studies reported that heart failure develops in the heart of myosin heavy chain-PPAR-α transgenic mice in a manner similar to that of diabetic cardiomyopathy, whereas cardiac dysfunction is enhanced in PPAR-α knockout mice in response to chronic pressure overload. We created a pressure-overload heart failure model in mice through transverse aortic constriction (TAC) and activated PPAR-α during heart failure using an inducible transgenic model. After 8 wk of TAC, left ventricular (LV) function had decreased with the reduction of PPAR-α expression in wild-type mice. We examined the effect of PPAR-α induction during heart failure using the Tet-Off system. Eight weeks after the TAC operation, LV construction was preserved significantly by PPAR-α induction with an increase in PPAR-α-targeted genes related to fatty acid metabolism. The increase of expression of fibrosis-related genes was significantly attenuated by PPAR-α induction. Metabolic rates measured by isolated heart perfusions showed a reduction in FAO and glucose oxidation in TAC hearts, but the rate of FAO preserved significantly owing to the induction of PPAR-α. Myocardial high-energy phosphates were significantly preserved by PPAR-α induction. These results suggest that PPAR-α activation during pressure-overloaded heart failure improved myocardial function and energetics. Thus activating PPAR-α and modulation of FAO could be a promising therapeutic strategy for heart failure. NEW & NOTEWORTHY The present study demonstrates the role of PPAR-α activation in the early stage of heart failure using an inducible transgenic mouse model. Induction of PPAR-α preserved heart

[Chronic heart failure].

PubMed

Gosch, Markus

2008-08-01

As a consequence of the increasing life expectancy the number of patients suffering from chronic heart failure has been growing continuously in the past few decades, especially in the group of the old and oldest. Frailty is a clinical syndrome that geriatricians attach great importance to. Like many other diseases chronic heart failure can cause frailty. Based on the experience that we see only a small correlation between the functional capacity of patients with heart failure and the results of cardiological findings, the model of peripheral myopathy in chronic heart failure was developed. Different pathophysiological changes may cause the increasing exercise intolerance in patients with chronic heart failure. We can already consider different experimental approaches to the therapy of frailty caused by chronic heart failure. At the moment we have to focus our efforts on an optimal therapy of heart failure, especially with angiotensin-converting-enzyme inhibitors and beta-blockers, and on individual endurance and strength training.

Rodent heart failure models do not reflect the human circulating microRNA signature in heart failure.

PubMed

Vegter, Eline L; Ovchinnikova, Ekaterina S; Silljé, Herman H W; Meems, Laura M G; van der Pol, Atze; van der Velde, A Rogier; Berezikov, Eugene; Voors, Adriaan A; de Boer, Rudolf A; van der Meer, Peter

2017-01-01

We recently identified a set of plasma microRNAs (miRNAs) that are downregulated in patients with heart failure in comparison with control subjects. To better understand their meaning and function, we sought to validate these circulating miRNAs in 3 different well-established rat and mouse heart failure models, and correlated the miRNAs to parameters of cardiac function. The previously identified let-7i-5p, miR-16-5p, miR-18a-5p, miR-26b-5p, miR-27a-3p, miR-30e-5p, miR-199a-3p, miR-223-3p, miR-423-3p, miR-423-5p and miR-652-3p were measured by means of quantitative real time polymerase chain reaction (qRT-PCR) in plasma samples of 8 homozygous TGR(mREN2)27 (Ren2) transgenic rats and 8 (control) Sprague-Dawley rats, 6 mice with angiotensin II-induced heart failure (AngII) and 6 control mice, and 8 mice with ischemic heart failure and 6 controls. Circulating miRNA levels were compared between the heart failure animals and healthy controls. Ren2 rats, AngII mice and mice with ischemic heart failure showed clear signs of heart failure, exemplified by increased left ventricular and lung weights, elevated end-diastolic left ventricular pressures, increased expression of cardiac stress markers and reduced left ventricular ejection fraction. All miRNAs were detectable in plasma from rats and mice. No significant differences were observed between the circulating miRNAs in heart failure animals when compared to the healthy controls (all P>0.05) and no robust associations with cardiac function could be found. The previous observation that miRNAs circulate in lower levels in human patients with heart failure could not be validated in well-established rat and mouse heart failure models. These results question the translation of data on human circulating miRNA levels to experimental models, and vice versa the validity of experimental miRNA data for human heart failure.

Rapid-rate nonsustained ventricular tachycardia found on implantable cardioverter-defibrillator interrogation: relationship to outcomes in the SCD-HeFT (Sudden Cardiac Death in Heart Failure Trial).

PubMed

Chen, Jay; Johnson, George; Hellkamp, Anne S; Anderson, Jill; Mark, Daniel B; Lee, Kerry L; Bardy, Gust H; Poole, Jeanne E

2013-05-28

The aim of this study was to examine rapid-rate nonsustained ventricular tachycardia (RR-NSVT) during routine implantable cardioverter-defibrillator (ICD) evaluation in patients with heart failure and its relationship to outcomes. The clinical implications of RR-NSVT identified during routine ICD interrogation are unclear. In this study, the occurrence of RR-NSVT and its association with ICD shocks and mortality in SCD-HeFT (Sudden Cardiac Death in Heart Failure Trial) were examined. The 811 patients who received ICDs in SCD-HeFT constituted the study population. The occurrence of RR-NSVT and its association with ICD shocks and mortality in SCD-HeFT were examined. RR-NSVT was documented on ICD interrogation in 186 of 811 patients (22.9%). The mean duration of RR-NSVT was 26.4 ± 9.1 beats (7.5 ± 2.6 s), with a mean cycle length of 259 ± 32 ms. Polymorphic RR-NSVT accounted for 56% of episodes. Compared with patients without RR-NSVT, those with RR-NSVT were less likely to be taking beta-blockers, statins, or aspirin at enrollment. After adjusting for other known predictors of mortality in SCD-HeFT, RR-NSVT was independently associated with appropriate ICD shocks (hazard ratio: 4.25; 95% confidence interval: 2.94 to 6.14; p < 0.0001), with all-cause mortality (hazard ratio: 2.40; 95% confidence interval: 1.62 to 3.54; p < 0.0001), and with a composite of all-cause mortality and appropriate ICD shocks (hazard ratio: 3.03; 95% confidence interval: 2.21 to 4.15; p < 0.0001). RR-NSVT identified on routine ICD interrogation should be considered an important clinical event. RR-NSVT during ICD interrogation is associated with appropriate ICD shocks and all-cause mortality. The clinical evaluation of patients with RR-NSVT should include intensification of medical therapy, particularly beta-blockers, or other appropriate clinical interventions. (Sudden Cardiac Death in Heart Failure Trial [SCD-HeFT]; NCT00000609). Copyright © 2013 American College of Cardiology Foundation

Rapid recovery from congestive heart failure following successful radiofrequency catheter ablation in a patient with late onset of Wolff-Parkinson-White syndrome.

PubMed

Yodogawa, Kenji; Ono, Norihiko; Seino, Yoshihiko

2012-01-01

A 56-year-old man was admitted because of palpitations and dyspnea. A 12-lead electrocardiogram showed irregular wide QRS complex tachycardia with a slur at the initial portion of the QRS complex. He had preexisting long-standing persistent atrial fibrillation, but early excitation syndrome had never been noted. Chest X-ray showed heart enlargement and pulmonary congestion. He was diagnosed with late onset of Wolff-Parkinson-White syndrome, and congestive heart failure was probably caused by rapid ventricular response of atrial fibrillation through the accessory pathway. Emergency catheter ablation for the accessory pathway was undertaken, and heart failure was dramatically improved.

Understanding chronic heart failure

PubMed Central

Fenton, Matthew; Burch, Michael

2007-01-01

The key principles of chronic heart failure and the development of clinical management strategies are described. The physiological changes in chronic heart failure and the clinical management of children with heart failure are considered, but the treatment of heart failure related to congenital heart disease or the intensive care management of heart failure are not mentioned as both topics require consideration in their own right. A greater understanding of the maladaptive responses to chronic heart failure has enabled targeted therapy to be introduced with consequent improvement in symptoms, reduction in hospitalisation and lower mortality. PMID:17715446

Altered LV inotropic reserve and mechanoenergetics early in the development of heart failure.

PubMed

Prabhu, S D; Freeman, G L

2000-03-01

To test the hypothesis that alterations in left ventricular (LV) mechanoenergetics and the LV inotropic response to afterload manifest early in the evolution of heart failure, we examined six anesthetized dogs instrumented with LV micromanometers, piezoelectric crystals, and coronary sinus catheters before and after 24 h of rapid ventricular pacing (RVP). After autonomic blockade, the end-systolic pressure-volume relation (ESPVR), myocardial O(2) consumption (MVO(2)), and LV pressure-volume area (PVA) were defined at several different afterloads produced by graded infusions of phenylephrine. Short-term RVP resulted in reduced preload with proportionate reductions in stroke work and the maximum first derivative of LV pressure but with no significant reduction in baseline LV contractile state. In response to increased afterload, the baseline ESPVR shifted to the left with maintained end-systolic elastance (E(es)). In contrast, after short-term RVP, in response to comparable increases in afterload, the ESPVR displayed reduced E(es) (P < 0.05) and significantly less leftward shift compared with control (P < 0.05). Compared with the control MVO(2)-PVA relation, short-term RVP significantly increased the MVO(2) intercept (P < 0.05) with no change in slope. These results indicate that short-term RVP produces attenuation of afterload-induced enhancement of LV performance and increases energy consumption for nonmechanical processes with maintenance of contractile efficiency, suggesting that early in the development of tachycardia heart failure, there is blunting of length-dependent activation and increased O(2) requirements for excitation-contraction coupling, basal metabolism, or both. Rather than being adaptive mechanisms, these abnormalities may be primary defects involved in the progression of the heart failure phenotype.

ELABELA-APJ axis protects from pressure overload heart failure and angiotensin II-induced cardiac damage.

PubMed

Sato, Teruki; Sato, Chitose; Kadowaki, Ayumi; Watanabe, Hiroyuki; Ho, Lena; Ishida, Junji; Yamaguchi, Tomokazu; Kimura, Akinori; Fukamizu, Akiyoshi; Penninger, Josef M; Reversade, Bruno; Ito, Hiroshi; Imai, Yumiko; Kuba, Keiji

2017-06-01

Elabela/Toddler/Apela (ELA) has been identified as a novel endogenous peptide ligand for APJ/Apelin receptor/Aplnr. ELA plays a crucial role in early cardiac development of zebrafish as well as in maintenance of self-renewal of human embryonic stem cells. Apelin was the first identified APJ ligand, and exerts positive inotropic heart effects and regulates the renin-angiotensin system. The aim of this study was to investigate the biological effects of ELA in the cardiovascular system. Continuous infusion of ELA peptide significantly suppressed pressure overload-induced cardiac hypertrophy, fibrosis and impaired contractility in mice. ELA treatment reduced mRNA expression levels of genes associated with heart failure and fibrosis. The cardioprotective effects of ELA were diminished in APJ knockout mice, indicating that APJ is the key receptor for ELA in the adult heart. Mechanistically, ELA downregulated angiotensin-converting enzyme (ACE) expression in the stressed hearts, whereas it showed little effects on angiotensin-converting enzyme 2 (ACE2) expression, which are distinct from the effects of Apelin. FoxM1 transcription factor, which induces ACE expression in the stressed hearts, was downregulated by ELA but not by Apelin. ELA antagonized angiotensin II-induced hypertension, cardiac hypertrophy, and fibrosis in mice. The ELA-APJ axis protects from pressure overload-induced heart failure possibly via suppression of ACE expression and pathogenic angiotensin II signalling. The different effects of ELA and Apelin on the expression of ACE and ACE2 implicate fine-tuned mechanisms for a ligand-induced APJ activation and downstream signalling. Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2017. For permissions please email: journals.permissions@oup.com.

Hemodynamic-GUIDEd Management of Heart Failure

ClinicalTrials.gov

2018-03-29

Heart Failure; Heart Failure, Systolic; Heart Failure, Diastolic; Heart Failure NYHA Class II; Heart Failure NYHA Class III; Heart Failure NYHA Class IV; Heart Failure，Congestive; Heart Failure With Reduced Ejection Fraction; Heart Failure With Normal Ejection Fraction; Heart Failure; With Decompensation

Plasma microRNAs serve as biomarkers of therapeutic efficacy and disease progression in hypertension-induced heart failure.

PubMed

Dickinson, Brent A; Semus, Hillary M; Montgomery, Rusty L; Stack, Christianna; Latimer, Paul A; Lewton, Steven M; Lynch, Joshua M; Hullinger, Thomas G; Seto, Anita G; van Rooij, Eva

2013-06-01

Recent studies have shown that microRNAs (miRNAs), besides being potent regulators of gene expression, can additionally serve as circulating biomarkers of disease. The aim of this study is to determine if plasma miRNAs can be used as indicators of disease progression or therapeutic efficacy in hypertension-induced heart disease. In order to define circulating miRNAs that change during hypertension-induced heart failure and that respond to therapeutic treatment, we performed miRNA arrays on plasma RNA from hypertensive rats that show signs of heart failure. Array analysis indicated that approximately one-third of the miRNAs on the array are detectable in plasma. Quantitative real-time polymerase chain reaction (PCR) analysis for a selected panel of miRNAs indicated that circulating levels of miR-16, miR-20b, miR-93, miR-106b, miR-223, and miR-423-5p were significantly increased in response to hypertension-induced heart failure, while this effect was blunted in response to treatment with antimiR-208a as well as an ACE inhibitor. Moreover, treatment with antimiR-208a resulted in a dramatic increase in one miRNA, miR-19b. A time course study indicated that several of these miRNA changes track with disease progression. Circulating levels of miRNAs are responsive to therapeutic interventions and change during the progression of hypertension-induced heart disease.

Heart Failure

MedlinePlus

... cause heart failure, such as coronary artery disease, high blood pressure, diabetes or obesity. Symptoms Heart failure can be ongoing ( ... include: Not smoking Controlling certain conditions, such as high blood pressure and diabetes Staying physically active Eating healthy foods Maintaining a ...

The serine/threonine-protein kinase/endoribonuclease IRE1α protects the heart against pressure overload-induced heart failure.

PubMed

Steiger, DeAnna; Yokota, Tomohiro; Li, Jin; Ren, Shuxun; Minamisawa, Susumu; Wang, Yibin

2018-05-16

Heart failure is associated with induction of endoplasmic reticulum (ER) stress and the unfolded protein response (UPR). The serine/threonine protein kinase/endoribonuclease IRE1α is a key protein in ER stress signal transduction. IRE1α activity can induce both protective UPR and apoptotic downstream signaling events, but the specific role for IRE1α activity in the heart is unknown. A major aim of this study was to characterize the specific contribution of IRE1α in cardiac physiology and pathogenesis. We used both cultured myocytes and a transgenic mouse line with inducible and cardiomyocyte-specific IRE1α overexpression as experimental models to achieve targeted IRE1α activation. IRE1α expression induced a potent but transient ER stress response in cardiomyocytes and did not cause significant effects in the intact heart under normal physiological condition. Furthermore, the IRE1α-activated transgenic heart responding to pressure overload exhibited preserved function and reduced fibrotic area, associated with increased adaptive UPR signaling and with blunted inflammatory and pathological gene expression. Therefore, we conclude that IRE1α induces transient ER stress signaling and confers a protective effect against pressure overload-induced pathological remodeling in the heart. To our knowledge, this report provides first direct evidence of a specific and protective role for IRE1α in the heart and reveals an interaction between ER stress signaling and inflammatory regulation in the pathologically stressed heart. Published under license by The American Society for Biochemistry and Molecular Biology, Inc.

Optimizing Nutrition in Pediatric Heart Failure: The Crisis Is Over and Now It's Time to Feed.

PubMed

Lewis, Kylie D; Conway, Jennifer; Cunningham, Chentel; Larsen, Bodil M K

2018-06-01

Pediatric heart failure is a complex disease occurring when cardiac output is unable to meet the metabolic demands of the body. With improved surgical interventions and medical therapies, survival rates have improved, and care has shifted from focusing on survival to optimizing quality of life and health outcomes. Based on current literature, this review addresses the nutrition needs of infants and children in heart failure and describes the pathophysiology and metabolic implications of this disease. The prevalence of wasting in pediatric heart failure has been reported to be as high as 86%, highlighting the importance of nutrition assessment through all stages of treatment to provide appropriate intake of energy, protein, and micronutrients. The etiology of malnutrition in pediatric heart failure is multifactorial and involves hypermetabolism, decreased intake, increased nutrient losses, inefficient utilization of nutrients, and malabsorption. Children in heart failure often present with tachypnea, tachycardia, fatigue, nausea, and vomiting and consequently may not be able to meet their nutrition requirements through oral intake alone. Nutrition support, including enteral nutrition and parenteral nutrition, should be considered an essential part of routine care. The involvement of multiple allied health professionals may be needed to create a feeding therapy plan to support patients and their families. With appropriate nutrition interventions, clinical outcomes and quality of life can be significantly improved. © 2017 American Society for Parenteral and Enteral Nutrition.

Intracellular calcium dynamics and acetylcholine-induced triggered activity in the pulmonary veins of dogs with pacing-induced heart failure

PubMed Central

Chou, Chung-Chuan; Nguyen, Bich Lien; Tan, Alex Y.; Chang, Po-Cheng; Lee, Hui-Ling; Lin, Fun-Chung; Yeh, San-Jou; Fishbein, Michael C.; Lin, Shien-Fong; Wu, Delon; Wen, Ming-Shien; Chen, Peng-Sheng

2009-01-01

BACKGROUND Heart failure increases autonomic nerve activities and changes intracellular calcium (Cai) dynamics. OBJECTIVE The purpose of this study was to investigate the hypothesis that abnormal Cai dynamics are responsible for triggered activity in the pulmonary veins (PVs) during acetylcholine infusion in a canine model of heart failure. METHODS Simultaneous optical mapping of and membrane Cai potential was performed in isolated Langendorff-perfused PV–left atrial (LA) preparations from nine dogs with ventricular pacing-induced heart failure. Mapping was performed at baseline, during acetylcholine (1 μmol/L) infusion (N = 9), and during thapsigargin and ryanodine infusion (N = 6). RESULTS Acetylcholine abbreviated the action potential. In four tissues, long pauses were followed by elevated diastolic Cai, late phase 3 early afterdepolarizations, and atrial fibrillation (AF). The incidence of PV focal discharges during AF was increased by acetylcholine from 2.4 ± 0.6 beats/s (N = 4) to 6.5 ± 2.2 beats/s (N = 8; P = .003). PV focal discharge and PV–LA microreentry coexisted in 6 of 9 preparations. The spatial distribution of dominant frequency demonstrated a focal source pattern, with the highest dominant frequency areas colocalized with PV focal discharge sites in 35 (95%) of 37 cholinergic AF episodes (N = 8). Thapsigargin and ryanodine infusion eliminated focal discharges in 6 of 6 preparations and suppressed the inducibility of AF in 4 of 6 preparations. PVs with focal discharge have higher densities of parasympathetic nerves than do PVs without focal discharges (P = .01), and periodic acid–Schiff (PAS)-positive cells were present at the focal discharge sites. CONCLUSION Cai dynamics are important in promoting triggered activity during acetylcholine infusion in PVs from pacing-induced heart failure. PV focal discharge sites have PAS-positive cells and high densities of parasympathetic nerves. PMID:18554987

Mitochondria and heart failure.

PubMed

Murray, Andrew J; Edwards, Lindsay M; Clarke, Kieran

2007-11-01

Energetic abnormalities in cardiac and skeletal muscle occur in heart failure and correlate with clinical symptoms and mortality. It is likely that the cellular mechanism leading to energetic failure involves mitochondrial dysfunction. Therefore, it is crucial to elucidate the causes of mitochondrial myopathy, in order to improve cardiac and skeletal muscle function, and hence quality of life, in heart failure patients. Recent studies identified several potential stresses that lead to mitochondrial dysfunction in heart failure. Chronically elevated plasma free fatty acid levels in heart failure are associated with decreased metabolic efficiency and cellular insulin resistance. Tissue hypoxia, resulting from low cardiac output and endothelial impairment, can lead to oxidative stress and mitochondrial DNA damage, which in turn causes dysfunction and loss of mitochondrial mass. Therapies aimed at protecting mitochondrial function have shown promise in patients and animal models with heart failure. Despite current therapies, which provide substantial benefit to patients, heart failure remains a relentlessly progressive disease, and new approaches to treatment are necessary. Novel pharmacological agents are needed that optimize substrate metabolism and maintain mitochondrial integrity, improve oxidative capacity in heart and skeletal muscle, and alleviate many of the clinical symptoms associated with heart failure.

Heart Failure in Women

PubMed Central

Bozkurt, Biykem; Khalaf, Shaden

2017-01-01

Heart failure is an important cause of morbidity and mortality in women, and they tend to develop it at an older age compared to men. Heart failure with preserved ejection fraction is more common in women than in men and accounts for at least half the cases of heart failure in women. When comparing men and women who have heart failure and a low left ventricular ejection fraction, the women are more symptomatic and have a similarly poor outcome. Overall recommendations for guideline-directed medical therapies show no differences in treatment approaches between men and women. Overall, women are generally underrepresented in clinical trials for heart failure. Further studies are needed to shed light into different mechanisms, causes, and targeted therapies of heart failure in women. PMID:29744014

Cardiac Metabolism in Heart Failure - Implications beyond ATP production

PubMed Central

Doenst, Torsten; Nguyen, T. Dung; Abel, E. Dale

2013-01-01

The heart has a high rate of ATP production and turnover which is required to maintain its continuous mechanical work. Perturbations in ATP generating processes may therefore affect contractile function directly. Characterizing cardiac metabolism in heart failure revealed several metabolic alterations termed metabolic remodeling, ranging from changes in substrate utilization to mitochondrial dysfunction, ultimately resulting in ATP deficiency and impaired contractility. However, ATP depletion is not the only relevant consequence of metabolic remodeling during heart failure. By providing cellular building blocks and signaling molecules, metabolic pathways control essential processes such as cell growth and regeneration. Thus, alterations in cardiac metabolism may also affect the progression to heart failure by mechanisms beyond ATP supply. Our aim is therefore to highlight that metabolic remodeling in heart failure not only results in impaired cardiac energetics, but also induces other processes implicated in the development of heart failure such as structural remodeling and oxidative stress. Accordingly, modulating cardiac metabolism in heart failure may have significant therapeutic relevance that goes beyond the energetic aspect. PMID:23989714

p53-mediated miR-18 repression activates HSF2 for IGF-IIR-dependent myocyte hypertrophy in hypertension-induced heart failure.

PubMed

Huang, Chih-Yang; Pai, Pei-Ying; Kuo, Chia-Hua; Ho, Tsung-Jung; Lin, Jing-Ying; Lin, Ding-Yu; Tsai, Fu-Jen; Padma, V Vijaya; Kuo, Wei-Wen; Huang, Chih-Yang

2017-08-10

Hypertension-induced cardiac hypertrophy and attenuated cardiac function are the major characteristics of early stage heart failure. Cardiomyocyte death in pathological cardiac conditions is the primary cause of heart failure and mortality. Our previous studies found that heat shock factor 1 (HSF1) protected cardiomyocytes from death by suppressing the IGF-IIR signaling pathway, which is critical for hypertensive angiotensin II-induced cardiomyocyte apoptosis. However, the role of heat shock factor 2 (HSF2) in hypertension-induced cardiac hypertrophy is unknown. We identified HSF2 as a miR-18 target for cardiac hypertrophy. p53 activation in angiotensin II (ANG II)-stimulated NRVMs is responsible for miR-18 downregulation both in vitro and in vivo, which triggers HSF2 expression and the activation of IGF-IIR-induced cardiomyocyte hypertrophy. Finally, we provide genetic evidence that miR-18 is required for cardiomyocyte functions in the heart based on the gene transfer of cardiac-specific miR-18 via adenovirus-associated virus 2 (AAV2). Transgenic overexpression of miR-18 in cardiomyocytes is sufficient to protect against dilated cardiomyopathy during hypertension-induced heart failure. Our results demonstrated that the p53-miR-18-HSF2-IGF-IIR axis was a critical regulatory pathway of cardiomyocyte hypertrophy in vitro and in vivo, suggesting that miR-18 could be a therapeutic target for the control of cardiac functions and the alleviation of cardiomyopathy during hypertension-induced heart failure.

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 ...

Nurses' decision making in heart failure management based on heart failure certification status.

PubMed

Albert, Nancy M; Bena, James F; Buxbaum, Denise; Martensen, Linda; Morrison, Shannon L; Prasun, Marilyn A; Stamp, Kelly D

Research findings on the value of nurse certification were based on subjective perceptions or biased by correlations of certification status and global clinical factors. In heart failure, the value of certification is unknown. Examine the value of certification based nurses' decision-making. Cross-sectional study of nurses who completed heart failure clinical vignettes that reflected decision-making in clinical heart failure scenarios. Statistical tests included multivariable linear, logistic and proportional odds logistic regression models. Of nurses (N = 605), 29.1% were heart failure certified, 35.0% were certified in another specialty/job role and 35.9% were not certified. In multivariable modeling, nurses certified in heart failure (versus not heart failure certified) had higher clinical vignette scores (p = 0.002), reflecting higher evidence-based decision making; nurses with another specialty/role certification (versus no certification) did not (p = 0.62). Heart failure certification, but not in other specialty/job roles was associated with decisions that reflected delivery of high-quality care. Copyright © 2018 Elsevier Inc. All rights reserved.

TRPC6 counteracts TRPC3-Nox2 protein complex leading to attenuation of hyperglycemia-induced heart failure in mice.

PubMed

Oda, Sayaka; Numaga-Tomita, Takuro; Kitajima, Naoyuki; Toyama, Takashi; Harada, Eri; Shimauchi, Tsukasa; Nishimura, Akiyuki; Ishikawa, Tatsuya; Kumagai, Yoshito; Birnbaumer, Lutz; Nishida, Motohiro

2017-08-08

Excess production of reactive oxygen species (ROS) caused by hyperglycemia is a major risk factor for heart failure. We previously reported that transient receptor potential canonical 3 (TRPC3) channel mediates pressure overload-induced maladaptive cardiac fibrosis by forming stably functional complex with NADPH oxidase 2 (Nox2). Although TRPC3 has been long suggested to form hetero-multimer channels with TRPC6 and function as diacylglycerol-activated cation channels coordinately, the role of TRPC6 in heart is still obscure. We here demonstrated that deletion of TRPC6 had no impact on pressure overload-induced heart failure despite inhibiting interstitial fibrosis in mice. TRPC6-deficient mouse hearts 1 week after transverse aortic constriction showed comparable increases in fibrotic gene expressions and ROS production but promoted inductions of inflammatory cytokines, compared to wild type hearts. Treatment of TRPC6-deficient mice with streptozotocin caused severe reduction of cardiac contractility with enhancing urinary and cardiac lipid peroxide levels, compared to wild type and TRPC3-deficient mice. Knockdown of TRPC6, but not TRPC3, enhanced basal expression levels of cytokines in rat cardiomyocytes. TRPC6 could interact with Nox2, but the abundance of TRPC6 was inversely correlated with that of Nox2. These results strongly suggest that Nox2 destabilization through disrupting TRPC3-Nox2 complex underlies attenuation of hyperglycemia-induced heart failure by TRPC6.

A rare case of supraventricular tachycardia induced by Infliximab: a case report

PubMed Central

2009-01-01

Background Infliximab, a chimeric monoclonal immunoglobulin antibody to tumor necrosis factor-α, has been established as a safe and effective treatment of rheumatoid arthritis, active and fistulising crohn's disease. Infliximab is generally well tolerated drug. The commonly reported cardiac side effects of Infliximab include exacerbation of congestive heart failure, hypotension and syncope. Symptomatic disorders of cardiac rhythm have been reported only rarely in few case reports and to the best of our knowledge, no tachyarrhythmia has been reported in past. Case report We report the case of a supraventricular tachycardia that occurred within three hours of Infliximab infusion in a patient with rheumatoid arthritis. Conclusion It is interesting to note that prior infusions in this patient did not precipitate similar consequences, thus, emphasising the importance of careful monitoring of patients on Infliximab therapy for possible reactions, even if prior exposures have been uneventful. PMID:19946518

Hippo pathway deficiency reverses systolic heart failure after infarction.

PubMed

Leach, John P; Heallen, Todd; Zhang, Min; Rahmani, Mahdis; Morikawa, Yuka; Hill, Matthew C; Segura, Ana; Willerson, James T; Martin, James F

2017-10-12

Mammalian organs vary widely in regenerative capacity. Poorly regenerative organs, such as the heart are particularly vulnerable to organ failure. Once established, heart failure commonly results in mortality. The Hippo pathway, a kinase cascade that prevents adult cardiomyocyte proliferation and regeneration, is upregulated in human heart failure. Here we show that deletion of the Hippo pathway component Salvador (Salv) in mouse hearts with established ischaemic heart failure after myocardial infarction induces a reparative genetic program with increased scar border vascularity, reduced fibrosis, and recovery of pumping function compared with controls. Using translating ribosomal affinity purification, we isolate cardiomyocyte-specific translating messenger RNA. Hippo-deficient cardiomyocytes have increased expression of proliferative genes and stress response genes, such as the mitochondrial quality control gene, Park2. Genetic studies indicate that Park2 is essential for heart repair, suggesting a requirement for mitochondrial quality control in regenerating myocardium. Gene therapy with a virus encoding Salv short hairpin RNA improves heart function when delivered at the time of infarct or after ischaemic heart failure following myocardial infarction was established. Our findings indicate that the failing heart has a previously unrecognized reparative capacity involving more than cardiomyocyte renewal.

Global left atrial failure in heart failure.

PubMed

Triposkiadis, Filippos; Pieske, Burkert; Butler, Javed; Parissis, John; Giamouzis, Gregory; Skoularigis, John; Brutsaert, Dirk; Boudoulas, Harisios

2016-11-01

The left atrium plays an important role in the maintenance of cardiovascular and neurohumoral homeostasis in heart failure. However, with progressive left ventricular dysfunction, left atrial (LA) dilation and mechanical failure develop, which frequently culminate in atrial fibrillation. Moreover, LA mechanical failure is accompanied by LA endocrine failure [deficient atrial natriuretic peptide (ANP) processing-synthesis/development of ANP resistance) and LA regulatory failure (dominance of sympathetic nervous system excitatory mechanisms, excessive vasopressin release) contributing to neurohumoral overactivity, vasoconstriction, and volume overload (global LA failure). The purpose of the present review is to describe the characteristics and emphasize the clinical significance of global LA failure in patients with heart failure. © 2016 The Authors. European Journal of Heart Failure © 2016 European Society of Cardiology.

Combined Inhibition of the Renin-Angiotensin System and Neprilysin Positively Influences Complex Mitochondrial Adaptations in Progressive Experimental Heart Failure

PubMed Central

Reinders, Jörg; Schröder, Josef; Dietl, Alexander; Schmid, Peter M.; Jungbauer, Carsten; Resch, Markus; Maier, Lars S.; Luchner, Andreas; Birner, Christoph

2017-01-01

Background Inhibitors of the renin angiotensin system and neprilysin (RAS-/NEP-inhibitors) proved to be extraordinarily beneficial in systolic heart failure. Furthermore, compelling evidence exists that impaired mitochondrial pathways are causatively involved in progressive left ventricular (LV) dysfunction. Consequently, we aimed to assess whether RAS-/NEP-inhibition can attenuate mitochondrial adaptations in experimental heart failure (HF). Methods and Results By progressive right ventricular pacing, distinct HF stages were induced in 15 rabbits, and 6 animals served as controls (CTRL). Six animals with manifest HF (CHF) were treated with the RAS-/NEP-inhibitor omapatrilat. Echocardiographic studies and invasive blood pressure measurements were undertaken during HF progression. Mitochondria were isolated from LV tissue, respectively, and further worked up for proteomic analysis using the SWATH technique. Enzymatic activities of citrate synthase and the electron transfer chain (ETC) complexes I, II, and IV were assessed. Ultrastructural analyses were performed by transmission electron microscopy. During progression to overt HF, intricate expression changes were mainly detected for proteins belonging to the tricarboxylic acid cycle, glucose and fat metabolism, and the ETC complexes, even though ETC complex I, II, or IV enzymatic activities were not significantly influenced. Treatment with a RAS-/NEP-inhibitor then reversed some maladaptive metabolic adaptations, positively influenced the decline of citrate synthase activity, and altered the composition of each respiratory chain complex, even though this was again not accompanied by altered ETC complex enzymatic activities. Finally, ultrastructural evidence pointed to a reduction of autophagolytic and degenerative processes with omapatrilat-treatment. Conclusions This study describes complex adaptations of the mitochondrial proteome in experimental tachycardia-induced heart failure and shows that a combined RAS

Heart failure in South America.

PubMed

Bocchi, Edimar Alcides

2013-05-01

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.

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

Zebrafish Heart Failure Models for the Evaluation of Chemical Probes and Drugs

PubMed Central

Monte, Aaron; Cook, James M.; Kabir, Mohd Shahjahan; Peterson, Karl P.

2013-01-01

Abstract Heart failure is a complex disease that involves genetic, environmental, and physiological factors. As a result, current medication and treatment for heart failure produces limited efficacy, and better medication is in demand. Although mammalian models exist, simple and low-cost models will be more beneficial for drug discovery and mechanistic studies of heart failure. We previously reported that aristolochic acid (AA) caused cardiac defects in zebrafish embryos that resemble heart failure. Here, we showed that cardiac troponin T and atrial natriuretic peptide were expressed at significantly higher levels in AA-treated embryos, presumably due to cardiac hypertrophy. In addition, several human heart failure drugs could moderately attenuate the AA-induced heart failure by 10%–40%, further verifying the model for drug discovery. We then developed a drug screening assay using the AA-treated zebrafish embryos and identified three compounds. Mitogen-activated protein kinase kinase inhibitor (MEK-I), an inhibitor for the MEK-1/2 known to be involved in cardiac hypertrophy and heart failure, showed nearly 60% heart failure attenuation. C25, a chalcone derivative, and A11, a phenolic compound, showed around 80% and 90% attenuation, respectively. Time course experiments revealed that, to obtain 50% efficacy, these compounds were required within different hours of AA treatment. Furthermore, quantitative polymerase chain reaction showed that C25, not MEK-I or A11, strongly suppressed inflammation. Finally, C25 and MEK-I, but not A11, could also rescue the doxorubicin-induced heart failure in zebrafish embryos. In summary, we have established two tractable heart failure models for drug discovery and three potential drugs have been identified that seem to attenuate heart failure by different mechanisms. PMID:24351044

Elucidation of the Strongest Predictors of Cardiovascular Events in Patients with Heart Failure.

PubMed

Fukuda, Hiroki; Shindo, Kazuhiro; Sakamoto, Mari; Ide, Tomomi; Kinugawa, Shintaro; Fukushima, Arata; Tsutsui, Hiroyuki; Ito, Shin; Ishii, Akira; Washio, Takashi; Kitakaze, Masafumi

2018-06-20

In previous retrospective studies, we identified the 50 most influential clinical predictors of cardiovascular outcomes in patients with heart failure (HF). The present study aimed to use the novel limitless-arity multiple-testing procedure to filter these 50 clinical factors and thus yield combinations of no more than four factors that could potentially predict the onset of cardiovascular events. A Kaplan-Meier analysis was used to investigate the importance of the combinations. In a multi-centre observational trial, we prospectively enrolled 213 patients with HF who were hospitalized because of exacerbation, discharged according to HF treatment guidelines and observed to monitor cardiovascular events. After the observation period, we stratified patients according to whether they experienced cardiovascular events (rehospitalisation or cardiovascular death). Among 77,562 combinations of fewer than five clinical parameters, we identified 151 combinations that could potentially explain the occurrence of cardiovascular events. Of these, 145 combinations included the use of inotropic agents, whereas the remaining 6 included the use of diuretics without bradycardia or tachycardia, suggesting that the high probability of cardiovascular events is exclusively determined by these two clinical factors. Importantly, Kaplan-Meier curves demonstrated that the use of inotropes or of diuretics without bradycardia or tachycardia were independent predictors of a markedly worse cardiovascular prognosis. Patients treated with either inotropic agents or diuretics without bradycardia or tachycardia were at a higher risk of cardiovascular events. The uses of these drugs, regardless of heart rate, are the strongest clinical predictors of cardiovascular events in patients with HF. Copyright © 2018 The Authors. Published by Elsevier B.V. All rights reserved.

Urocortin-2 infusion in acute decompensated heart failure: findings from the UNICORN study (urocortin-2 in the treatment of acute heart failure as an adjunct over conventional therapy).

PubMed

Chan, W Y Wandy; Frampton, Christopher M; Crozier, Ian G; Troughton, Richard W; Richards, A Mark

2013-10-01

The purpose of this study is to investigate the effects of urocortin-2 as adjunct therapy in acute decompensated heart failure (ADHF). Urocortin-2 produced favorable integrated effects in experimental heart failure but there are no equivalent human data. We describe the first therapeutic study of urocortin-2 infusion in ADHF. Fifty-three patients with ADHF were randomly assigned to 5 ng/kg/min of urocortin-2 or placebo infusion for 4 h as an adjunct therapy. Changes in vital signs, plasma neurohormonal and renal indices during treatment were compared using repeated-measures analysis of covariance. Ten patients in each arm underwent more detailed invasive hemodynamic evaluation. Urocortin-2 produced greater falls in systolic blood pressure compared to placebo (16 ± 5.8 mm Hg, p < 0.001) with nonsignificant increases in heart rate (5.7 ± 3.8 beats/min, p = 0.07) and increased cardiac output (2.1 ± 0.4 l/min vs. -0.1 ± 0.4 l/min, p < 0.001) associated with a 47% reduction in calculated total peripheral resistance (p = 0.015). Falls in pulmonary artery and pulmonary capillary wedge pressures did not differ significantly between groups. Urocortin-2 reduced urine volume and creatinine clearance during infusion but these returned to above baseline level in the 8 h after infusion. Plasma renin activity rose briefly with urocortin-2 coinciding with reductions in blood pressure (p < 0.001). B-type natriuretic peptide levels fell significantly over 24 h with urocortin-2 (p < 0.01) but not with placebo. Urocortin-2 infusion in ADHF markedly augmented cardiac output without significant reflex tachycardia. Renal indices fell transiently concurrent with urocortin-2-induced reductions in blood pressure. Further investigations are required to uncover the full potential of urocortin-2 in treating ADHF. Copyright © 2013 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.

ACONITE-INDUCED VENTRICULAR TACHYCARDIA DURING RADIATION SICKNESS (in French)

DOE Office of Scientific and Technical Information (OSTI.GOV)

Jurkovic, V.; Vokrouhlicky, L.; Belobradek, Z.

1962-10-01

In order to study cardiac excitability and the effects of procaine, ventricular tachycardia was induced by intramyocardial injection of 0.05 ml 50% aconite solution in irradiated and nonirradiated rabbits of both sexes. Tracheotomy and thoracotomy were performed to facilitate access to the heart and to establish artificial respiration through a tracheal tube. Narcosis was induced by urethane. Electrocardiograms were made at various stages in both control and irradiated animals; the former showed no change in preliminary phases of the experiment. Procaine was administered by subcutaneous injection, bilateral vagosympathetic infiltration, or slow intravenous infusion. Its therapeutic effect was determined by givingmore » it 5 min after trachycardia occurred, and its preventive action by giving it 5 min before. The x irradiation rate was 16.6 r/min, to a total dose of 1000 r. On the 3rd day after irradiation, the therapeutic effect of procaine after intramuscular injection was seen as a 50% normalization of heart action, with less by other routes of administration; its preventive effect was seen as a 58% normalization following slow intravenous infusion but was insignificant by other routes. Six days after irradiation, at the peak of radiation sickness, procaine's therapeutic and preventive actions had almost disappeared; its intravenous therapeutic application gave 25% normalization and its intramuscular preventive action provided 20% normalization of heart rate. However, on the 6th day, a profibrillatory effect was observed, especially in the therapeutic vagosympathetic infiltration technique and the preventive use by slow intravenous infusion. Suggested explanations of the reversal are: change in excitability of myocardium when it is irradiated, or change in effect of procaine when the whole organism is irradiated. Results favor the first explanation. (BBB)« less

Psychobiology of depression/distress in congestive heart failure

PubMed Central

Hassan, Mustafa; Sheps, David S.

2011-01-01

Heart failure affects millions of Americans and new diagnosis rates are expected to almost triple over the next 30 years as our population ages. Affective disorders including clinical depression and anxiety are common in patients with congestive heart failure. Furthermore, the presence of these disorders significantly impacts quality of life, medical outcomes, and healthcare service utilization. In recent years, the literature has attempted to describe potential pathophysiologic mechanisms relating affective disorders and psychosocial stress to heart failure. Several potential mechanisms have been proposed including autonomic nervous system dysfunction, inflammation, cardiac arrhythmias, and altered platelet function. These mechanisms are reviewed in this article. Additional novel mechanisms such as mental stress-induced myocardial ischemia are also discussed. PMID:18368481

Palliative Care in Heart Failure.

PubMed

Sood, Abhinav; Dobbie, Krista; Wilson Tang, W H

2018-04-19

This review illustrates the dynamic role of palliative care in heart failure management and encapsulates the commonly utilized pharmacologic and non-pharmacologic therapeutic strategies for symptom palliation in heart failure. In addition, we provide our experience regarding patient care issues common to the domain of heart failure and palliative medicine which are commonly encountered by heart failure teams. Addition of palliative care to conventional heart failure management plan results in improvement in quality of life, anxiety, depression, and spiritual well-being among patients. Palliative care should not be confused with hospice care. Palliative care teams should be involved early in the care of heart failure patients with the aims of improving symptom palliation, discussing goals of care and improving quality of life without compromising utilization of evidence-based heart failure therapies. A consensus on the appropriate timing of involvement and evidence for many symptom palliation therapies is still emerging.

Drp1-Dependent Mitochondrial Autophagy Plays a Protective Role Against Pressure Overload-Induced Mitochondrial Dysfunction and Heart Failure.

PubMed

Shirakabe, Akihiro; Zhai, Peiyong; Ikeda, Yoshiyuki; Saito, Toshiro; Maejima, Yasuhiro; Hsu, Chiao-Po; Nomura, Masatoshi; Egashira, Kensuke; Levine, Beth; Sadoshima, Junichi

2016-03-29

Mitochondrial autophagy is an important mediator of mitochondrial quality control in cardiomyocytes. The occurrence of mitochondrial autophagy and its significance during cardiac hypertrophy are not well understood. Mice were subjected to transverse aortic constriction (TAC) and observed at multiple time points up to 30 days. Cardiac hypertrophy developed after 5 days, the ejection fraction was reduced after 14 days, and heart failure was observed 30 days after TAC. General autophagy was upregulated between 1 and 12 hours after TAC but was downregulated below physiological levels 5 days after TAC. Mitochondrial autophagy, evaluated by electron microscopy, mitochondrial content, and Keima with mitochondrial localization signal, was transiently activated at ≈3 to 7 days post-TAC, coinciding with mitochondrial translocation of Drp1. However, it was downregulated thereafter, followed by mitochondrial dysfunction. Haploinsufficiency of Drp1 abolished mitochondrial autophagy and exacerbated the development of both mitochondrial dysfunction and heart failure after TAC. Injection of Tat-Beclin 1, a potent inducer of autophagy, but not control peptide, on day 7 after TAC, partially rescued mitochondrial autophagy and attenuated mitochondrial dysfunction and heart failure induced by overload. Haploinsufficiency of either drp1 or beclin 1 prevented the rescue by Tat-Beclin 1, suggesting that its effect is mediated in part through autophagy, including mitochondrial autophagy. Mitochondrial autophagy is transiently activated and then downregulated in the mouse heart in response to pressure overload. Downregulation of mitochondrial autophagy plays an important role in mediating the development of mitochondrial dysfunction and heart failure, whereas restoration of mitochondrial autophagy attenuates dysfunction in the heart during pressure overload. © 2016 American Heart Association, Inc.

Protective effects of low-dose rosuvastatin on isoproterenol-induced chronic heart failure in rats by regulation of DDAH-ADMA-NO pathway.

PubMed

Zhou, Ru; Ma, Ping; Xiong, Aiqin; Xu, Yehua; Wang, Yang; Xu, Qingbin

2017-04-01

Cardiovascular disease is the leading cause of death with high morbidity and mortality, and chronic heart failure is the terminal phase of it. This study aimed to investigate the protective effects of the low-dose rosuvastatin on isoproterenol-induced chronic heart failure and to explore the possible related mechanisms. Male Sprague Dawley rats were given isoproterenol 5 mg/kg once a day for 7 days to establish heart failure model by subcutaneous injection. Simultaneously, low-dose rosuvastatin (5 mg/kg) was orally administrated from day 1 to day 14. Protective effects were evaluated by hemodynamic parameter, histopathological variables, serum asymmetric dimethylarginine (ADMA), cardiac troponin I (cTnI), brain natriuretic peptide (BNP) and myocardial nitric oxide (NO), and the levels of dimethylarginine dimethylaminohydrolase 2 (DDAH2), arginine methyltransferases 1 (PRMT1) and endothelial nitric oxide synthase (eNOS) expression were analyzed. Therapeutic rosuvastatin (5 mg/kg) significantly attenuated isoproterenol-induced hypertrophy, remodeling and dysfunction of ventricle, reduced the increased serum content of ADMA, cTnI, and BNP, and elevated myocardial NO in rats (P<.05). Besides, rosuvastatin also significantly inhibited fibrosis of myocardium, normalized the increased PRMT1 and decreased DDAH2 expression. Low-dose rosuvastatin exerted cardioprotective effects on isoproterenol-induced heart failure in rats by modulating DDAH-ADMA-NO pathway, and it may present the new therapeutic value in ameliorating chronic heart failure. © 2016 John Wiley & Sons Ltd.

Lungs in Heart Failure

PubMed Central

Apostolo, Anna; Giusti, Giuliano; Gargiulo, Paola; Bussotti, Maurizio; Agostoni, Piergiuseppe

2012-01-01

Lung function abnormalities both at rest and during exercise are frequently observed in patients with chronic heart failure, also in the absence of respiratory disease. Alterations of respiratory mechanics and of gas exchange capacity are strictly related to heart failure. Severe heart failure patients often show a restrictive respiratory pattern, secondary to heart enlargement and increased lung fluids, and impairment of alveolar-capillary gas diffusion, mainly due to an increased resistance to molecular diffusion across the alveolar capillary membrane. Reduced gas diffusion contributes to exercise intolerance and to a worse prognosis. Cardiopulmonary exercise test is considered the “gold standard” when studying the cardiovascular, pulmonary, and metabolic adaptations to exercise in cardiac patients. During exercise, hyperventilation and consequent reduction of ventilation efficiency are often observed in heart failure patients, resulting in an increased slope of ventilation/carbon dioxide (VE/VCO2) relationship. Ventilatory efficiency is as strong prognostic and an important stratification marker. This paper describes the pulmonary abnormalities at rest and during exercise in the patients with heart failure, highlighting the principal diagnostic tools for evaluation of lungs function, the possible pharmacological interventions, and the parameters that could be useful in prognostic assessment of heart failure patients. PMID:23365739

Heart Failure - Multiple Languages

MedlinePlus

... Heart Failure - العربية (Arabic) Bilingual PDF Health Information Translations Bosnian (bosanski) Expand Section Heart Failure - bosanski (Bosnian) Bilingual PDF Health Information Translations Chinese, Simplified (Mandarin dialect) (简体中文) Expand Section Heart ...

Vascular capacitance and cardiac output in pacing-induced canine models of acute and chronic heart failure.

PubMed

Ogilvie, R I; Zborowska-Sluis, D

1995-11-01

The relationship between stressed and total blood volume, total vascular capacitance, central blood volume, cardiac output (CO), and pulmonary capillary wedge pressure (Ppcw) was investigated in pacing-induced acute and chronic heart failure. Acute heart failure was induced in anesthetized splenectomized dogs by a volume load (20 mL/kg over 10 min) during rapid right ventricular pacing at 250 beats/min (RRVP) for 60 min. Chronic heart failure was induced by continuous RRVP for 2-6 weeks (average 24 +/- 2 days). Total vascular compliance and capacitance were calculated from the mean circulatory filling pressure (Pmcf) during transient circulatory arrest after acetylcholine at three different circulating volumes. Stressed blood volume was calculated as a product of compliance and Pmcf, with the total blood volume measured by a dye dilution. Central blood volume (CBV) and CO were measured by thermodilution. Central (heart and lung) vascular capacitance was estimated from the plot of Ppcw against CBV. Acute volume loading without RRVP increased capacitance and CO, whereas after volume loading with RRVP, capacitance and CO were unaltered from baseline. Chronic RRVP reduced capacitance and CO. All interventions, volume +/- RRVP or chronic RRVP, increased stressed and central blood volumes and Ppcw. Acute or chronic RRVP reduced central vascular capacitance. Cardiac output was increased when stressed and unstressed blood volumes increased proportionately as during volume loading alone. When CO was reduced and Ppcw increased, as during chronic RRVP or acute RRVP plus a volume load, stressed blood volume was increased and unstressed blood volume was decreased. Thus, interventions that reduced CO and increased Ppcw also increased stressed and reduced unstressed blood volume and total vascular capacitance.

Intramyocardial injection of SERCA2a-expressing lentivirus improves myocardial function in doxorubicin-induced heart failure.

PubMed

Mattila, Minttu; Koskenvuo, Juha; Söderström, Mirva; Eerola, Kim; Savontaus, Mikko

2016-07-01

Doxorubicin is an effective anticancer drug. The major limitation to its use is the induction of dose-dependent cardiomyopathy. No specific treatment exists for doxorubicin-induced cardiomyopathy and treatments used for other forms of heart failure have only limited beneficial effects. The contraction-relaxation cycle of the heart is controlled by cytosolic calcium concentrations, which, in turn, are critically regulated by the activity of the sarcoplasmic reticulum Ca(2) (+) ATPase (SERCA2a) pump. We hypothesized that SERCA2a gene transfer would ameliorate doxorubicin-induced cardiomyopathy. Lentiviral vectors LV-SERCA2a-GFP and LV-GFP were constructed and in vitro gene transfer of LV-SERCA2a-GFP confirmed SERCA2a expression by western blot analysis. Heart failure was induced by giving a single intraperitoneal injection of doxorubicin. LV-SERCA2a-GFP, LV-GFP vectors and phosphate-buffered saline (PBS) were injected under echocardiographic control to the anterior wall of the left ventricle. Echocardiography analyses were performed on the injection day and 28 days postinjection. On the injection day, there were no significant differences in the average ejection fractions (EFs) among SERCA2a (40.0%), GFP (41.1%) and PBS (39.4%) injected animals. On day 28, EF in the SERCA2a group had increased by 16.6 ± 6.7% to 46.4 ± 2.1%. By contrast, EFs in the GFP (40.2 ± 1.3%) and PBS (40.6 ± 1.4%) groups remained at pre-injection levels. In addition, end systolic and end diastolic left ventricle volumes were significantly smaller in the SERCA2a group compared to controls. SERCA2a gene transfer significantly improves left ventricle function and dimensions in doxorubicin-induced cardiomyopathy, thus making LV-SERCA2a gene transfer an attractive treatment modality for doxorubicin-induced heart failure. Copyright © 2016 John Wiley & Sons, Ltd. Copyright © 2016 John Wiley & Sons, Ltd.

Disease management programs for heart failure: not just for the 'sick' heart failure population.

PubMed

McDonald, Ken; Conlon, Carmel; Ledwidge, Mark

2007-02-01

The development of disease management programs has been a major advance in heart failure care, bringing about significant improvements for the heart failure population, with reduction in readmission, better use of guideline therapy and improved survival. However, at present, the majority of such programs focus their attention only on the sicker segment of this population, with little application of this important service to the broader heart failure population, where potentially benefits may be even more impressive. This has led to an imbalance in the care of patients with heart failure, where aspects of management such as regular structured review and education are preferentially given to the group at the later stages of the natural history of the syndrome. This paper argues for a far wider application of the disease management program concept in heart failure care so as to bring the benefits of specialist care, patient education and follow-up to patients at an earlier stage in the natural history of heart failure.

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

PubMed

Plácido, 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. Copyright © 2015 Sociedad Española de Cardiología. Published by Elsevier España, S.L.U. All rights reserved.

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. Copyright © 2015 Sociedad Española de Cardiología. Published by Elsevier España, S.L.U. All rights reserved.

Aldosterone antagonists in heart failure.

PubMed

Miller, Susan E; Alvarez, René J

2013-01-01

Chronic, systolic heart failure is an increasing and costly health problem, and treatments based on pathophysiology have evolved that include the use of aldosterone antagonists. Advances in the understanding of neurohormonal responses to heart failure have led to better pharmacologic treatments. The steroid hormone aldosterone has been associated with detrimental effects on the cardiovascular system, such as ventricular remodeling and endothelial dysfunction. This article will review the literature and guidelines that support the use of aldosterone antagonists in the treatment of chronic, systolic heart failure. Aldosterone antagonists are life-saving drugs that have been shown to decrease mortality in patients with New York Heart Association class III to IV heart failure and in patients with heart failure after an acute myocardial infarction. Additional studies are being conducted to determine if the role of aldosterone antagonists can be expanded to patients with less severe forms of heart failure. Aldosterone antagonists are an important pharmacologic therapy in the neurohormonal blockade necessary in the treatment of systolic heart failure. These drugs have been shown to decrease mortality and reduce hospital readmission rates. The major complication of aldosterone antagonists is hyperkalemia, which can be avoided with appropriate patient selection and diligent monitoring.

New Medications for Heart Failure

PubMed Central

Gordin, Jonathan S.; Fonarow, Gregg C.

2016-01-01

Heart failure is common and results in substantial morbidity and mortality. Current guideline-based therapies for heart failure with reduced ejection fraction, including beta-blockers, angiotensin converting enzyme (ACE) inhibitors, and aldosterone antagonists aim to interrupt deleterious neurohormonal pathways and have shown significant success in reducing morbidity and mortality associated with heart failure. Continued efforts to further improve outcomes in patients with heart failure with reduced ejection fraction have led to the first new-in-class medications approved for heart failure since 2005, ivabradine and sacubitril/valsartan. Ivabradine targets the If channels in the sinoatrial node of the heart, decreasing heart rate. Sacubitril/valsartan combines a neprilysin inhibitor that increases levels of beneficial vasodilatory peptides with an angiotensin receptor antagonist. On a background of previously approved, guideline-directed medical therapies for heart failure, these medications have shown improved clinical outcomes ranging from decreased hospitalizations in a select group of patients to a reduction in all-cause mortality across all pre-specified subgroups. In this review, we will discuss the previously established guideline-directed medical therapies for heart failure with reduced ejection fraction, the translational research that led to the development of these new therapies, and the results from the major clinical trials of ivabradine and sacubitril/valsartan. PMID:27038558

Mitochondrial reactive oxygen species production and respiratory complex activity in rats with pressure overload-induced heart failure

PubMed Central

Schwarzer, Michael; Osterholt, Moritz; Lunkenbein, Anne; Schrepper, Andrea; Amorim, Paulo; Doenst, Torsten

2014-01-01

We investigated the impact of cardiac reactive oxygen species (ROS) during the development of pressure overload-induced heart failure. We used our previously described rat model where transverse aortic constriction (TAC) induces compensated hypertrophy after 2 weeks, heart failure with preserved ejection fraction at 6 and 10 weeks, and heart failure with systolic dysfunction after 20 weeks. We measured mitochondrial ROS production rates, ROS damage and assessed the therapeutic potential of in vivo antioxidant therapies. In compensated hypertrophy (2 weeks of TAC) ROS production rates were normal at both mitochondrial ROS production sites (complexes I and III). Complex I ROS production rates increased with the appearance of diastolic dysfunction (6 weeks of TAC) and remained high thereafter. Surprisingly, maximal ROS production at complex III peaked at 6 weeks of pressure overload. Mitochondrial respiratory capacity (state 3 respiration) was elevated 2 and 6 weeks after TAC, decreased after this point and was significantly impaired at 20 weeks, when contractile function was also impaired and ROS damage was found with increased hydroxynonenal. Treatment with the ROS scavenger α-phenyl-N-tert-butyl nitrone or the uncoupling agent dinitrophenol significantly reduced ROS production rates at 6 weeks. Despite the decline in ROS production capacity, no differences in contractile function between treated and untreated animals were observed. Increased ROS production occurs early in the development of heart failure with a peak at the onset of diastolic dysfunction. However, ROS production may not be related to the onset of contractile dysfunction. PMID:24951621

Vitamin D and Heart Failure.

PubMed

Marshall Brinkley, D; Ali, Omair M; Zalawadiya, Sandip K; Wang, Thomas J

2017-10-01

Vitamin D is principally known for its role in calcium homeostasis, but preclinical studies implicate multiple pathways through which vitamin D may affect cardiovascular function and influence risk for heart failure. Many adults with cardiovascular disease have low vitamin D status, making it a potential therapeutic target. We review the rationale and potential role of vitamin D supplementation in the prevention and treatment of chronic heart failure. Substantial observational evidence has associated low vitamin D status with the risk of heart failure, ventricular remodeling, and clinical outcomes in heart failure, including mortality. However, trials assessing the influence of vitamin D supplementation on surrogate markers and clinical outcomes in heart failure have generally been small and inconclusive. There are insufficient data to recommend routine assessment or supplementation of vitamin D for the prevention or treatment of chronic heart failure. Prospective trials powered for clinical outcomes are warranted.

Development of porcine model of chronic tachycardia-induced cardiomyopathy.

PubMed

Paslawska, Urszula; Gajek, Jacek; Kiczak, Liliana; Noszczyk-Nowak, Agnieszka; Skrzypczak, Piotr; Bania, Jacek; Tomaszek, Alicja; Zacharski, Maciej; Sambor, Izabela; Dziegiel, Piotr; Zysko, Dorota; Banasiak, Waldemar; Jankowska, Ewa A; Ponikowski, Piotr

2011-11-17

There are few experimental models of heart failure (HF) in large animals, despite structural and functional similarities to human myocardium. We have developed a porcine model of chronic tachycardia-induced cardiomyopathy. Homogenous siblings of White Large breed swine (n=6) underwent continuous right ventricular (RV) pacing at 170 bpm; 2 subjects served as controls. In the course of RV pacing, animals developed a clinical picture of HF and were presented for euthanasia at subsequent stages: mild, moderate and end-stage HF. Left ventricle (LV) sections were analyzed histologically and relative ANP, BNP, phospholamban and sarcoplasmic reticulum calcium ATPase 2a transcript levels in LV were quantified by real time RT-PCR. In the course of RV pacing, animals demonstrated reduced exercise capacity (time of running until being dyspnoeic: 6.6 ± 0.5 vs. 2.4 ± 1.4 min), LV dilatation (LVEDD: 4.9 ± 0.4 vs. 6.7 ± 0.4 cm), impaired LV systolic function (LVEF: 69 ± 8 vs. 32 ± 7 %), (all baseline vs. before euthanasia, all p<0.001). LV tissues from animals with moderate and end-stage HF demonstrated local foci of interstitial fibrosis, congestion, cardiomyocyte hypertrophy and atrophy, which was not detected in controls and mild HF animals. The up-regulation of ANP and BNP and a reduction in a ratio of sarcoplasmic reticulum calcium ATPase 2a and phospholamban in failing myocardium were observed as compared to controls. In pigs, chronic RV pacing at relatively low rate can be used as an experimental model of HF, as it results in a gradual deterioration of exercise tolerance accompanied by myocardial remodeling confirmed at subcellular level. Copyright © 2010 Elsevier Ireland Ltd. All rights reserved.

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

[Chronic heart failure and depression].

PubMed

Herrmann-Lingen, C

2018-05-01

Depression is a frequent comorbidity in chronic heart failure. It can be triggered by the experience of suffering from heart disease, but it can also play a causal role in accelerated development and poor prognosis of heart failure. The aim of this study was to investigate the interrelationships between heart failure and depression and the psychophysiological and behavioral mechanisms involved in this association. The effects of comorbid depression on quality of life in patients with heart failure were also examined and therapeutic options reviewed. A narrative review of the literature was undertaken. Several psychophysiological and behavioral mechanisms have been identified as mediators of the association between depression and heart failure and the adverse prognostic effects of this comorbidity. Comorbid depression leads to substantial reductions in health-related quality of life. These effects are only incompletely antagonized by exercise training and cognitive behavioral therapy. No specific effect of antidepressant medication has been demonstrated as yet in patients with heart failure. While current guidelines recommend the identification and treatment of depressive comorbidity in patients with heart failure, the available evidence provides no convincing rationale for specific treatment recommendations beyond the guideline-based treatment of heart failure itself, lifestyle interventions and patient-centered medical care. If available, psychotherapy should be offered, ideally cognitive behavioral therapy. For patients that do not improve sufficiently under outpatient treatment, the German health care system offers dedicated psychocardiological inpatient treatment programs.

Does load-induced ventricular hypertrophy progress to systolic heart failure?

PubMed

Berenji, Kambeez; Drazner, Mark H; Rothermel, Beverly A; Hill, Joseph A

2005-07-01

Ventricular hypertrophy develops in response to numerous forms of cardiac stress, including pressure or volume overload, loss of contractile mass from prior infarction, neuroendocrine activation, and mutations in genes encoding sarcomeric proteins. Hypertrophic growth is believed to have a compensatory role that diminishes wall stress and oxygen consumption, but Framingham and other studies established ventricular hypertrophy as a marker for increased risk of developing chronic heart failure, suggesting that hypertrophy may have maladaptive features. However, the relative contribution of comorbid disease to hypertrophy-associated systolic failure is unknown. For instance, coronary artery disease is induced by many of the same risk factors that cause hypertrophy and can itself lead to systolic dysfunction. It is uncertain, therefore, whether ventricular hypertrophy commonly progresses to systolic dysfunction without the contribution of intervening ischemia or infarction. In this review, we summarize findings from epidemiologic studies, preclinical experiments in animals, and clinical trials to lay out what is known-and not known-about this important question.

Development of heart failure is independent of K+ channel-interacting protein 2 expression

PubMed Central

Speerschneider, Tobias; Grubb, Søren; Metoska, Artina; Olesen, Søren-Peter; Calloe, Kirstine; Thomsen, Morten B

2013-01-01

Abnormal ventricular repolarization in ion channelopathies and heart disease is a major cause of ventricular arrhythmias and sudden cardiac death. K+ channel-interacting protein 2 (KChIP2) expression is significantly reduced in human heart failure (HF), contributing to a loss of the transient outward K+ current (Ito). We aim to investigate the possible significance of a changed KChIP2 expression on the development of HF and proarrhythmia. Transverse aortic constrictions (TAC) and sham operations were performed in wild-type (WT) and KChIP2−/− mice. Echocardiography was performed before and every 2 weeks after the operation. Ten weeks post-surgery, surface ECG was recorded and we paced the heart in vivo to induce arrhythmias. Afterwards, tissue from the left ventricle was used for immunoblotting. Time courses of HF development were comparable in TAC-operated WT and KChIP2−/− mice. Ventricular protein expression of KChIP2 was reduced by 70% after 10 weeks TAC in WT mice. The amplitudes of the J and T waves were enlarged in KChIP2−/− control mice. Ventricular effective refractory period, RR, QRS and QT intervals were longer in mice with HF compared to sham-operated mice of either genotype. Pacing-induced ventricular tachycardia (VT) was observed in 5/10 sham-operated WT mice compared with 2/10 HF WT mice with HF. Interestingly, and contrary to previously published data, sham-operated KChIP2−/− mice were resistant to pacing-induced VT resulting in only 1/10 inducible mice. KChIP2−/− with HF mice had similar low vulnerability to inducible VT (1/9). Our results suggest that although KChIP2 is downregulated in HF, it is not orchestrating the development of HF. Moreover, KChIP2 affects ventricular repolarization and lowers arrhythmia susceptibility. Hence, downregulation of KChIP2 expression in HF may be antiarrhythmic in mice via reduction of the fast transient outward K+ current. PMID:24099801

Insomnia Self-Management in Heart Failure

ClinicalTrials.gov

2018-01-05

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

Modulation of fatty acid metabolism is involved in the alleviation of isoproterenol-induced rat heart failure by fenofibrate

PubMed Central

LI, PING; LUO, SHIKE; PAN, CHUNJI; CHENG, XIAOSHU

2015-01-01

Heart failure is a disease predominantly caused by an energy metabolic disorder in cardiomyocytes. The present study investigated the inhibitory effects of fenofibrate (FF) on isoproterenol (ISO)-induced hear failure in rats, and examined the underlying mechanisms. The rats were divided into CON, ISO (HF model), FF and FF+ISO (HF animals pretreated with FF) groups. The cardiac structure and function of the rats were assessed, and contents of free fatty acids and glucose metabolic products were determined. In addition, myocardial cells were isolated from neonatal rats and used in vitro to investigate the mechanisms by which FF relieves heart failure. Western blot analysis was performed to quantify the expression levels of peroxisome proliferator-activated receptor (PPAR)α and uncoupling protein 2 (UCP2). FF effectively alleviated the ISO-induced cardiac structural damage, functional decline, and fatty acid and carbohydrate metabolic abnormalities. Compared with the ISO group, the serum levels of brain natriuretic peptide (BNP), free fatty acids, lactic acid and pyruvic acid were decreased in the FF animals. In the cultured myocardial cells, lactic acid and pyruvic acid contents were lower in the supernatants obtained from the FF animals, with lower levels of mitochondrial ROS production and cell necrosis, compared with the ISO group, whereas PPARα upregulation and UCP2 downregulation occurred in the FF+ISO group. The results demonstrated that FF efficiently alleviated heart failure in the ISO-induced rat model, possibly via promoting fatty acid oxidation. PMID:26497978

[Is iron important in heart failure?].

PubMed

Murín, Ján; Pernický, Miroslav

2015-01-01

Iron deficiency is a frequent comorbidity in a patient with chronic heart failure, and it associates with a worse pro-gnosis of that patient. Mainly worse quality of life and more rehospitalizations are in these iron deficient patients. Iron metabolism is rather complex and there is some new information concerning this complexity in heart failure. We distinquish an absolute and a functional iron deficiency in heart failure. It is this deficit which is important and not as much is anemia important here. Prevalence of anaemia in heart failure is about 30-50 %, higher it is in patients suffering more frequently heart failure decompensations. Treatment of iron deficiency is important and it improves prognosis of these patients. Most experiences there are with i.v. iron treatment (FERRIC HF, FAIR HF and CONFIRM HF studies), less so with per oral treatment. There are no clinical trials which analysed mortality influences. heart failure - iron metabolism in heart failure - prevalence of iron deficit - treatment of iron deficiency in heart failure.

Newborn infant with maternal anti-SSA antibody-induced complete heart block accompanying cardiomyopathy.

PubMed

Iida, Midori; Inamura, Noboru; Takeuchi, Makoto

2006-01-01

Newborn case of maternal anti-SSA antibody-induced congenital complete heart block (CCHB) accompanying cardiomyopathy is presented. Unexpectedly, she died of ventricular tachycardia, not bradycardia, 6 days after birth. Autopsy revealed left ventricular cardiomyopathy with endocardial fibroelastosis. Thus, when evaluating fetal cardiac performance in cases of maternal anti-SSA antibody-induced CCHB, it is necessary to pay attention to myocardial attributes such as endocardial hyperplasia.

Prediction of mode of death in heart failure: the Seattle Heart Failure Model.

PubMed

Mozaffarian, Dariush; Anker, Stefan D; Anand, Inder; Linker, David T; Sullivan, Mark D; Cleland, John G F; Carson, Peter E; Maggioni, Aldo P; Mann, Douglas L; Pitt, Bertram; Poole-Wilson, Philip A; Levy, Wayne C

2007-07-24

Prognosis and mode of death in heart failure patients are highly variable in that some patients die suddenly (often from ventricular arrhythmia) and others die of progressive failure of cardiac function (pump failure). Prediction of mode of death may facilitate decisions about specific medications or devices. We used the Seattle Heart Failure Model (SHFM), a validated prediction model for total mortality in heart failure, to assess the mode of death in 10,538 ambulatory patients with New York Heart Association class II to IV heart failure and predominantly systolic dysfunction enrolled in 6 randomized trials or registries. During 16,735 person-years of follow-up, 2014 deaths occurred, which included 1014 sudden deaths and 684 pump-failure deaths. Compared with a SHFM score of 0, patients with a score of 1 had a 50% higher risk of sudden death, patients with a score of 2 had a nearly 3-fold higher risk, and patients with a score of 3 or 4 had a nearly 7-fold higher risk (P<0.001 for all comparisons; 1-year area under the receiver operating curve, 0.68). Stratification of risk of pump-failure death was even more pronounced, with a 4-fold higher risk with a score of 1, a 15-fold higher risk with a score of 2, a 38-fold higher risk with a score of 3, and an 88-fold higher risk with a score of 4 (P<0.001 for all comparisons; 1-year area under the receiver operating curve, 0.85). The proportion of deaths caused by sudden death versus pump-failure death decreased from a ratio of 7:1 with a SHFM score of 0 to a ratio of 1:2 with a SHFM score of 4 (P trend <0.001). The SHFM score provides information about the likely mode of death among ambulatory heart failure patients. Investigation is warranted to determine whether such information might predict responses to or cost-effectiveness of specific medications or devices in heart failure patients.

Effects of nitric oxide synthase inhibition on sympathetically-mediated tachycardia

NASA Technical Reports Server (NTRS)

Whalen, E. J.; Johnson, A. K.; Lewis, S. J.

1999-01-01

The aim of the present study was to determine whether inhibition of nitric oxide (NO) synthesis directly alters the tachycardia produced by sympathetically-derived norepinephrine. The NO synthase inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME; 50 micromol/kg, i.v.), produced a marked rise in mean arterial blood pressure. This pressor response was associated with a fall in heart rate which involved the withdrawal of cardiac sympathetic nerve activity. The NO-donor, sodium nitroprusside (5 microg/kg, i.v.), produced a pronounced fall in mean arterial blood pressure but only a minor increase in heart rate. The beta-adrenoceptor agonist, isoproterenol (0.5 micromol/kg, i.v.), and the membrane-permeable cAMP analogue, 8-(4-chlorophenylthiol)-cAMP (10 micromol/kg, i.v.), produced falls in mean arterial blood pressure and pronounced increases in heart rate. The indirectly acting sympathomimetic agent, tyramine (0.5 mg/kg, i.v.), produced a pressor response and a tachycardia. The effects of sodium nitroprusside, tyramine, isoproterenol and 8-(4-chlorophenylthiol)-cAMP on mean arterial blood pressure were not markedly affected by L-NAME. However, the tachycardia produced by these agents was considerably exaggerated in the presence of this NO synthesis inhibitor. These findings suggest that L-NAME potentiates the tachycardia produced by sympathetically-derived norepinephrine. The increased responsiveness to norepinephrine may involve (i) a rapid up-regulation of cardiac beta1-adrenoceptors and cAMP signaling in cardiac pacemaker cells due to the loss of the inhibitory influence of cardiac NO, and (ii) the up-regulation of beta1-adrenoceptor-mediated signal transduction processes in response to the L-NAME-induced withdrawal of cardiac sympathetic nerve activity.

RBFox1-mediated RNA splicing regulates cardiac hypertrophy and heart failure.

PubMed

Gao, Chen; Ren, Shuxun; Lee, Jae-Hyung; Qiu, Jinsong; Chapski, Douglas J; Rau, Christoph D; Zhou, Yu; Abdellatif, Maha; Nakano, Astushi; Vondriska, Thomas M; Xiao, Xinshu; Fu, Xiang-Dong; Chen, Jau-Nian; Wang, Yibin

2016-01-01

RNA splicing is a major contributor to total transcriptome complexity; however, the functional role and regulation of splicing in heart failure remain poorly understood. Here, we used a total transcriptome profiling and bioinformatic analysis approach and identified a muscle-specific isoform of an RNA splicing regulator, RBFox1 (also known as A2BP1), as a prominent regulator of alternative RNA splicing during heart failure. Evaluation of developing murine and zebrafish hearts revealed that RBFox1 is induced during postnatal cardiac maturation. However, we found that RBFox1 is markedly diminished in failing human and mouse hearts. In a mouse model, RBFox1 deficiency in the heart promoted pressure overload-induced heart failure. We determined that RBFox1 is a potent regulator of RNA splicing and is required for a conserved splicing process of transcription factor MEF2 family members that yields different MEF2 isoforms with differential effects on cardiac hypertrophic gene expression. Finally, induction of RBFox1 expression in murine pressure overload models substantially attenuated cardiac hypertrophy and pathological manifestations. Together, this study identifies regulation of RNA splicing by RBFox1 as an important player in transcriptome reprogramming during heart failure that influence pathogenesis of the disease.

RBFox1-mediated RNA splicing regulates cardiac hypertrophy and heart failure

PubMed Central

Gao, Chen; Ren, Shuxun; Lee, Jae-Hyung; Qiu, Jinsong; Chapski, Douglas J.; Rau, Christoph D.; Zhou, Yu; Abdellatif, Maha; Nakano, Astushi; Vondriska, Thomas M.; Xiao, Xinshu; Fu, Xiang-Dong; Chen, Jau-Nian; Wang, Yibin

2015-01-01

RNA splicing is a major contributor to total transcriptome complexity; however, the functional role and regulation of splicing in heart failure remain poorly understood. Here, we used a total transcriptome profiling and bioinformatic analysis approach and identified a muscle-specific isoform of an RNA splicing regulator, RBFox1 (also known as A2BP1), as a prominent regulator of alternative RNA splicing during heart failure. Evaluation of developing murine and zebrafish hearts revealed that RBFox1 is induced during postnatal cardiac maturation. However, we found that RBFox1 is markedly diminished in failing human and mouse hearts. In a mouse model, RBFox1 deficiency in the heart promoted pressure overload–induced heart failure. We determined that RBFox1 is a potent regulator of RNA splicing and is required for a conserved splicing process of transcription factor MEF2 family members that yields different MEF2 isoforms with differential effects on cardiac hypertrophic gene expression. Finally, induction of RBFox1 expression in murine pressure overload models substantially attenuated cardiac hypertrophy and pathological manifestations. Together, this study identifies regulation of RNA splicing by RBFox1 as an important player in transcriptome reprogramming during heart failure that influence pathogenesis of the disease. PMID:26619120

Ventricular tachycardia storm originating from interventricular septum successfully treated with surgical cryoablation with electroanatomic and electrophysiological mapping before dual valve replacement.

PubMed

Kawamura, Iwanari; Fukamizu, Seiji; Miyazawa, Satoshi; Hojo, Rintaro; Ito, Fusahiko; Watanabe, Masazumi; Nishizaki, Mitsuhiro; Sakurada, Harumizu; Hiraoka, Masayasu

2018-02-01

A 58-year-old man with dilated cardiomyopathy was admitted with heart failure. He had a history of two catheter ablation procedures for ventricular tachycardia (VT) originating from the intraventricular septum (IVS). Before dual valve replacement (DVR), he suffered a VT storm. An electrophysiological study revealed an extended low-voltage area at the IVS with the exit of the induced VT at the anterior side. Radiofrequency application was performed at the VT exit as a landmark for surgical cryoablation (SA). During the DVR, SA was performed at the IVS using this landmark. After SA, the patient had no ventricular tachyarrhythmia.

Heart Failure with Recovered EF and Heart Failure with Mid-Range EF: Current Recommendations and Controversies.

PubMed

Unkovic, Peter; Basuray, Anupam

2018-04-03

This review explores key features and potential management controversies in two emerging populations in heart failure: heart failure with recovered ejection fraction (HF-recovered EF) and heart failure with mid-range ejection fraction (HFmrEF). While HF-recovered EF patients have better outcomes than heart failure with reduced ejection fraction (HFrEF), they continue to have symptoms, persistent biomarker elevations, and abnormal outcomes suggesting a continued disease process. HFmrEF patients appear to have features of HFrEF and heart failure with preserved ejection fraction (HFpEF), but have a high prevalence of ischemic heart disease and may represent a transitory phase between the HFrEF and HFpEF. Management strategies have insufficient data to warrant standardization at this time. HF-recovered EF and HFmrEF represent new populations with unmet needs and expose the pitfalls of an EF basis for heart failure classification.

Periodontitis in Chronic Heart Failure.

PubMed

Fröhlich, Hanna; Herrmann, Kristina; Franke, Jennifer; Karimi, Alamara; Täger, Tobias; Cebola, Rita; Katus, Hugo A; Zugck, Christian; Frankenstein, Lutz

2016-08-01

Periodontal disease has been associated with an increased risk of cardiovascular events. The purpose of our study was to investigate whether a correlation between periodontitis and chronic heart failure exists, as well as the nature of the underlying cause. We enrolled 71 patients (mean age, 54 ± 13 yr; 56 men) who had stable chronic heart failure; all underwent complete cardiologic and dental evaluations. The periodontal screening index was used to quantify the degree of periodontal disease. We compared the findings to those in the general population with use of data from the 4th German Dental Health Survey. Gingivitis, moderate periodontitis, and severe periodontitis were present in 17 (24%), 17 (24%), and 37 (52%) patients, respectively. Severe periodontitis was more prevalent among chronic heart failure patients than in the general population. In contrast, moderate periodontitis was more prevalent in the general population (P <0.00001). The severity of periodontal disease was not associated with the cause of chronic heart failure or the severity of heart failure symptoms. Six-minute walking distance was the only independent predictor of severe periodontitis. Periodontal disease is highly prevalent in chronic heart failure patients regardless of the cause of heart failure. Prospective trials are warranted to clarify the causal relationship between both diseases.

Periodontitis in Chronic Heart Failure

PubMed Central

Fröhlich, Hanna; Herrmann, Kristina; Franke, Jennifer; Karimi, Alamara; Täger, Tobias; Cebola, Rita; Katus, Hugo A.; Zugck, Christian

2016-01-01

Periodontal disease has been associated with an increased risk of cardiovascular events. The purpose of our study was to investigate whether a correlation between periodontitis and chronic heart failure exists, as well as the nature of the underlying cause. We enrolled 71 patients (mean age, 54 ± 13 yr; 56 men) who had stable chronic heart failure; all underwent complete cardiologic and dental evaluations. The periodontal screening index was used to quantify the degree of periodontal disease. We compared the findings to those in the general population with use of data from the 4th German Dental Health Survey. Gingivitis, moderate periodontitis, and severe periodontitis were present in 17 (24%), 17 (24%), and 37 (52%) patients, respectively. Severe periodontitis was more prevalent among chronic heart failure patients than in the general population. In contrast, moderate periodontitis was more prevalent in the general population (P <0.00001). The severity of periodontal disease was not associated with the cause of chronic heart failure or the severity of heart failure symptoms. Six-minute walking distance was the only independent predictor of severe periodontitis. Periodontal disease is highly prevalent in chronic heart failure patients regardless of the cause of heart failure. Prospective trials are warranted to clarify the causal relationship between both diseases. PMID:27547136

Docosahexaenoic acid supplementation alters key properties of cardiac mitochondria and modestly attenuates development of left ventricular dysfunction in pressure overload-induced heart failure.

PubMed

Dabkowski, Erinne R; O'Connell, Kelly A; Xu, Wenhong; Ribeiro, Rogerio F; Hecker, Peter A; Shekar, Kadambari Chandra; Daneault, Caroline; Des Rosiers, Christine; Stanley, William C

2013-12-01

Supplementation with the n3 polyunsaturated fatty acid docosahexaenoic acid (DHA) is beneficial in heart failure patients, however the mechanisms are unclear. DHA is incorporated into membrane phospholipids, which may prevent mitochondrial dysfunction. Thus we assessed the effects of DHA supplementation on cardiac mitochondria and the development of heart failure caused by aortic pressure overload. Pathological cardiac hypertrophy was generated in rats by thoracic aortic constriction. Animals were fed either a standard diet or were supplemented with DHA (2.3 % of energy intake). After 14 weeks, heart failure was evident by left ventricular hypertrophy and chamber enlargement compared to shams. Left ventricle fractional shortening was unaffected by DHA treatment in sham animals (44.1 ± 1.6 % vs. 43.5 ± 2.2 % for standard diet and DHA, respectively), and decreased with heart failure in both treatment groups, but to a lesser extent in DHA treated animals (34.9 ± 1.7 %) than with the standard diet (29.7 ± 1.5 %, P < 0.03). DHA supplementation increased DHA content in mitochondrial phospholipids and decreased membrane viscosity. Myocardial mitochondrial oxidative capacity was decreased by heart failure and unaffected by DHA. DHA treatment enhanced Ca(2+) uptake by subsarcolemmal mitochondria in both sham and heart failure groups. Further, DHA lessened Ca(2+)-induced mitochondria swelling, an index of permeability transition, in heart failure animals. Heart failure increased hydrogen peroxide-induced mitochondrial permeability transition compared to sham, which was partially attenuated in interfibrillar mitochondria by treatment with DHA. DHA decreased mitochondrial membrane viscosity and accelerated Ca(2+) uptake, and attenuated susceptibility to mitochondrial permeability transition and development of left ventricular dysfunction.

BNP and congestive heart failure.

PubMed

Cowie, Martin R; Mendez, Gustavo F

2002-01-01

Brain natriuretic peptide (BNP), a peptide hormone secreted chiefly by ventricular myocytes, plays a key role in volume homeostasis. The plasma concentration of BNP is raised in various pathological states, especially heart failure. Many studies suggest that measurement of plasma BNP has clinical utility for excluding a diagnosis of heart failure in patients with dyspnea or fluid retention and for providing prognostic information in those with heart failure or other cardiac disease. It may also be of value in identifying patients after myocardial infarction in whom further assessment of cardiac function is likely to be worthwhile. Preliminary evidence suggests that measuring the plasma concentration of BNP may be useful in fine tuning therapy for heart failure. Artificially raising the circulating levels of BNP shows considerable promise as a treatment for heart failure. With simpler assay methods now available, it is likely that many physicians will measure plasma BNP to aid them in the diagnosis, risk stratification, and monitoring of their patients with heart failure or other cardiac dysfunction. Copyright 2002, Elsevier Science.

Autonomic control of heart rate during orthostasis and the importance of orthostatic-tachycardia in the snake Python molurus.

PubMed

Armelin, Vinicius Araújo; da Silva Braga, Victor Hugo; Abe, Augusto Shinya; Rantin, Francisco Tadeu; Florindo, Luiz Henrique

2014-10-01

Orthostasis dramatically influences the hemodynamics of terrestrial vertebrates, especially large and elongated animals such as snakes. When these animals assume a vertical orientation, gravity tends to reduce venous return, cardiac filling, cardiac output and blood pressure to the anterior regions of the body. The hypotension triggers physiological responses, which generally include vasomotor adjustments and tachycardia to normalize blood pressure. While some studies have focused on understanding the regulation of these vasomotor adjustments in ectothermic vertebrates, little is known about regulation and the importance of heart rate in these animals during orthostasis. We acquired heart rate and carotid pulse pressure (P PC) in pythons in their horizontal position, and during 30 and 60° inclinations while the animals were either untreated (control) or upon muscarinic cholinoceptor blockade and a double autonomic blockade. Double autonomic blockade completely eradicated the orthostatic-tachycardia, and without this adjustment, the P PC reduction caused by the tilts became higher than that which was observed in untreated animals. On the other hand, post-inclinatory vasomotor adjustments appeared to be of negligible importance in counterbalancing the hemodynamic effects of gravity. Finally, calculations of cardiac autonomic tones at each position revealed that the orthostatic-tachycardia is almost completely elicited by a withdrawal of vagal drive.

Endoplasmic reticulum stress sensor protein kinase R-like endoplasmic reticulum kinase (PERK) protects against pressure overload-induced heart failure and lung remodeling.

PubMed

Liu, Xiaoyu; Kwak, Dongmin; Lu, Zhongbing; Xu, Xin; Fassett, John; Wang, Huan; Wei, Yidong; Cavener, Douglas R; Hu, Xinli; Hall, Jennifer; Bache, Robert J; Chen, Yingjie

2014-10-01

Studies have reported that development of congestive heart failure is associated with increased endoplasmic reticulum stress. Double stranded RNA-activated protein kinase R-like endoplasmic reticulum kinase (PERK) is a major transducer of the endoplasmic reticulum stress response and directly phosphorylates eukaryotic initiation factor 2α, resulting in translational attenuation. However, the physiological effect of PERK on congestive heart failure development is unknown. To study the effect of PERK on ventricular structure and function, we generated inducible cardiac-specific PERK knockout mice. Under unstressed conditions, cardiac PERK knockout had no effect on left ventricular mass, or its ratio to body weight, cardiomyocyte size, fibrosis, or left ventricular function. However, in response to chronic transverse aortic constriction, PERK knockout mice exhibited decreased ejection fraction, increased left ventricular fibrosis, enhanced cardiomyocyte apoptosis, and exacerbated lung remodeling in comparison with wild-type mice. PERK knockout also dramatically attenuated cardiac sarcoplasmic reticulum Ca(2+)-ATPase expression in response to aortic constriction. Our findings suggest that PERK is required to protect the heart from pressure overload-induced congestive heart failure. © 2014 American Heart Association, Inc.

Metabolic support for the heart: complementary therapy for heart failure?

PubMed

Heggermont, Ward A; Papageorgiou, Anna-Pia; Heymans, Stephane; van Bilsen, Marc

2016-12-01

The failing heart has an increased metabolic demand and at the same time suffers from impaired energy efficiency, which is a detrimental combination. Therefore, therapies targeting the energy-deprived failing heart and rewiring cardiac metabolism are of great potential, but are lacking in daily clinical practice. Metabolic impairment in heart failure patients has been well characterized for patients with reduced ejection fraction, and is coming of age in patients with 'preserved' ejection fraction. Targeting cardiomyocyte metabolism in heart failure could complement current heart failure treatments that do improve cardiovascular haemodynamics, but not the energetic status of the heart. In this review, we discuss the hallmarks of normal cardiac metabolism, typical metabolic disturbances in heart failure, and past and present therapeutic targets that impact on cardiac metabolism. © 2016 The Authors. European Journal of Heart Failure © 2016 European Society of Cardiology.

Humoral immunity in heart failure.

PubMed

Sarkar, Amrita; Rafiq, Khadija

2018-05-17

Cardiovascular disease (CVD) is a class of diseases that involve disorders of heart and blood vessels, including: hypertension, coronary heart disease, cerebrovascular disease, peripheral vascular disease, which finally lead to heart failure (HF). There are several treatments available all over the world, but still CVD and heart failure became the number one problem causing death every year worldwide. Both experimental and clinical studies have shown a role for inflammation in the pathogenesis of heart failure. This seems related to an imbalance between pro-inflammatory and anti-inflammatory cytokines. Cardiac inflammation is major pathophysiological mechanism operating in the failing heart, regardless of HF aetiology. Disturbances of the cellular and humoral immune system are frequently observed in heart failure. This review describes how B-cells play specific role in the heart failure states. There is an urgent need to identify novel therapeutic targets and develop advanced therapeutic strategies to combat the syndrome of HF. Understanding and describing the elements of the humoral immunity function are essential, and may suggest potential new treatment strategies. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.org.

Management of Arrhythmias in Heart Failure

PubMed Central

Masarone, Daniele; Limongelli, Giuseppe; Rubino, Marta; Valente, Fabio; Vastarella, Rossella; Ammendola, Ernesto; Gravino, Rita; Verrengia, Marina; Salerno, Gemma; Pacileo, Giuseppe

2017-01-01

Heart failure patients are predisposed to develop arrhythmias. Supraventricular arrhythmias can exacerbate the heart failure symptoms by decreasing the effective cardiac output and their control require pharmacological, electrical, or catheter-based intervention. In the setting of atrial flutter or atrial fibrillation, anticoagulation becomes paramount to prevent systemic or cerebral embolism. Patients with heart failure are also prone to develop ventricular arrhythmias that can present a challenge to the managing clinician. The management strategy depends on the type of arrhythmia, the underlying structural heart disease, the severity of heart failure, and the range from optimization of heart failure therapy to catheter ablation. Patients with heart failure, irrespective of ejection fraction are at high risk for developing sudden cardiac death, however risk stratification is a clinical challenge and requires a multiparametric evaluation for identification of patients who should undergo implantation of a cardioverter defibrillator. Finally, patients with heart failure can also develop symptomatic bradycardia, caused by sinus node dysfunction or atrio-ventricular block. The treatment of bradycardia in these patients with pacing is usually straightforward but needs some specific issue. PMID:29367535

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

Renin-Angiotensin-Aldosterone Signaling Inhibitors-Losartan, Enalapril, and Cardosten-Prevent Infarction-induced Heart Failure Development in Rats.

PubMed

Kiss, Krisztina; Fekete, Veronika; Pálóczi, János; Sárközy, Márta; Murlasits, Zsolt; Pipis, Judit; Kheyfets, Irina A; Dugina, Julia L; Sergeeva, Svetlana A; Epstein, Oleg I; Csonka, Csaba; Csont, Tamás; Ferdinandy, Péter; Bencsik, Péter

2016-01-01

The activation of the renin-angiotensin-aldosterone system (RAAS) plays an important role in the pathophysiology of congestive heart failure, which is the reason that angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin 2 receptor blockers (ARBs) have become established therapies for heart failure. However, it is still not known whether preventive treatment with losartan or enalapril can reduce symptoms of infarction-induced heart failure. Ultra-low dose (ULD) drug therapy is thought to exert specific activity, with a lower chance of side effects. OBJECTIVES • The research team had hypothesized that preventive treatment with inhibitors of RAAS signaling-losartan, enalapril, and a preparation of a ULD antibody (ie, cardosten), which target the angiotensin type 1 (AT1) receptor-might alleviate pathological hypertrophy and/or functional decline in infarction-induced heart failure. The research team treated male Wistar rats orally for 30 d with 20 mg/kg of losartan, 10 mg/kg enalapril, 5 or 7.5 mL/kg of cardosten, or a control solution, started 1 d prior to permanent coronary occlusion. A sham-operated group functioned as a second control group. The study was conducted at the Department of Biochemistry of the Faculty of Medicine at the University of Szeged in Szeged, Hungary, in cooperation with the Pharmahungary Group, also in Szeged, Hungary, and with OOO "NPF" Materia Medica Holding Ltd in Moscow, Russia. To determine cardiac functional parameters in vivo, the research team inserted a catheter into the left ventricle of the rats and measured the parameters of ventricular pressure, and cardiac output was determined by thermodilution. Morphological parameters were measured after heart isolation in transverse sections by a digital caliper. A total of 30 d after permanent coronary ligation, both losartan and enalapril, significantly decreased mean arterial blood pressure (MABP), attenuated the development of the left-ventricular anterior-wall and septum

CONGESTIVE HEART FAILURE ASSOCIATED WITH PREGNANCY IN OKAPI (OKAPIA JOHNSTONI).

PubMed

Warren, Joshua D; Aitken-Palmer, Copper; Weldon, Alan D; Flanagan, Joseph P; Howard, Lauren L; Garner, Michael M; Citino, Scott B

2017-03-01

Acute signs associated with cardiovascular disease occurred in three pregnant okapi ( Okapia johnstoni ) during early to midgestation and progressed to congestive heart failure. Congestive heart failure was diagnosed antemortem using echocardiography and plasma cardiac troponin levels. Clinical signs included decreased activity, hyporexia, tachypnea, dyspnea, flared nostrils, and productive coughing with copious amounts of foamy nasal discharge. Parenteral and oral treatment with furosemide, enalapril, and spironolactone controlled clinical signs in the three okapi allowing each to carry out one pregnancy to term. Two okapi carried the first pregnancy to term after showing signs, while one okapi aborted the first calf and gave birth to a healthy calf in a subsequent pregnancy. Subsequent pregnancy in one okapi ended with abortion and associated dystocia and endometritis. Following parturition, clinical signs associated with heart failure resolved in all three individuals; serial echocardiography in two individuals showed improvement in fractional shortening and left atrial size and all three okapi showed markedly decreased pleural effusion and resolution of pulmonary edema. However, subsequent pregnancies in all three okapi induced respiratory distress and recurrence of congestive heart failure; one okapi died from congestive heart failure associated with subsequent pregnancy. This case series describes the clinical presentation and pathologic findings of congestive heart failure during pregnancy in adult okapi.

Randomised trial of low-dose amiodarone in severe congestive heart failure. Grupo de Estudio de la Sobrevida en la Insuficiencia Cardiaca en Argentina (GESICA)

PubMed

Doval, H C; Nul, D R; Grancelli, H O; Perrone, S V; Bortman, G R; Curiel, R

1994-08-20

In severe heart failure many deaths are sudden and are presumed to be due to ventricular arrhythmias. The GESICA trial evaluated the effect of low-dose amiodarone on two-year mortality in patients with severe heart failure. Our prospective multicentre trial included 516 patients on optimal standard treatment for heart failure. Patients were randomised to 300 mg/day amiodarone (260) or to standard treatment (256). Intention-to-treat analysis showed 87 deaths in the amiodarone group (33.5%) compared with 106 in the control group (41.4%) (risk reduction 28%; 95% CI 4%-45%; log rank test p = 0.024). There were reductions in both sudden death (risk reduction 27%; p = 0.16) and death due to progressive heart failure (risk reduction 23%; p = 0.16). Fewer patients in the amiodarone group died or were admitted to hospital due to worsening heart failure (119 versus 149 in the control group; risk reduction 31%; 95% CI 13-46%; p = 0.0024). The decrease in mortality and hospital admission was present in all subgroups examined and independent of the presence of non-sustained ventricular tachycardia. Side-effects were reported in 17 patients (6.1%); amiodarone was withdrawn in 12. Low-dose amiodarone proved to be an effective and reliable treatment, reducing mortality and hospital admission in patients with severe heart failure independently of the presence of complex ventricular arrhythmias.

The initial (earliest) report of polymorphous ventricular tachycardia.

PubMed

Jani, Sonal; Schweitzer, Paul

2006-07-01

In these short historical notes, we describe the early history of polymorphic ventricular tachycardia. Polymorphous ventricular tachycardia was probably first noted in 1918 by Wilson and Robinson. In a publication describing complete heart block and ventriculophasic arrhythmia, they noted a tachyarrhythmia characterized by multiple extrasystoles of different types at a rapid rate. Also, we briefly discuss the earliest recognized torsades de pointes by Dessertenes in 1966 and the first description of catecholaminergic polymorphic ventricular tachycardia, by Reid in 1977.

Hyperkalemia in Heart Failure.

PubMed

Sarwar, Chaudhry M S; Papadimitriou, Lampros; Pitt, Bertram; Piña, Ileana; Zannad, Faiez; Anker, Stefan D; Gheorghiade, Mihai; Butler, Javed

2016-10-04

Disorders of potassium homeostasis can potentiate the already elevated risk of arrhythmia in heart failure. Heart failure patients have a high prevalence of chronic kidney disease, which further heightens the risk of hyperkalemia, especially when renin-angiotensin-aldosterone system inhibitors are used. Acute treatment for hyperkalemia may not be tolerated in the long term. Recent data for patiromer and sodium zirconium cyclosilicate, used to treat and prevent high serum potassium levels on a more chronic basis, have sparked interest in the treatment of hyperkalemia, as well as the potential use of renin-angiotensin-aldosterone system inhibitors in patients who were previously unable to take these drugs or tolerated only low doses. This review discusses the epidemiology, pathophysiology, and outcomes of hyperkalemia in heart failure; provides an overview of traditional and novel ways to approach management of hyperkalemia; and discusses the need for further research to optimally treat heart failure. Copyright © 2016 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.

Pathophysiology of chronic heart failure.

PubMed

Francis, G S

2001-05-07

Heart failure is a changing paradigm. The hemodynamic model, which served our needs well from the 1950s through the early 1980s, has now been largely abandoned, except for the management of decompensated patients in the hospital. The pathophysiology is exceedingly complex and involves structural changes, such as loss of myofilaments, apoptosis and disorganization of the cytoskeleton, as well as disturbances in Ca(2+) homeostasis, alteration in receptor density, signal transduction, and collagen synthesis. A more contemporary working hypothesis is that heart failure is a progressive disorder of left ventricular remodeling, usually resulting from an index event, that culminates in a clinical syndrome characterized by impaired cardiac function and circulatory congestion. This change in the framework of our understanding of the pathophysiology of heart failure is predicated on the results of numerous clinical trials conducted during the past 20 years. New therapies are now evolving that are designed to inhibit neuroendocrine and cytokine activation, whereas drugs specifically designed to heighten cardiac contractility and "unload" the left ventricle have proven to be unhelpful in long-term management of patients with chronic heart failure. However, the hemodynamic model is still relevant for patients in the hospital with decompensated heart failure, where positive inotropic drugs and vasodilators are still widely used. The modern treatment of chronic heart failure is now largely based on the neurohormonal hypothesis, which states that neuroendocrine activation is important in the progression of heart failure and that inhibition of neurohormones is likely to have long-term benefit with regard to morbidity and mortality. Thus, the evolution of treatment for chronic heart failure as a result of clinical trials has provided much enlightenment for our understanding of the fundamental biology of the disorder, a reversal of the usual flow of information from basic science to

Heart failure and the holidays.

PubMed

Shah, Mahek; Bhalla, Vikas; Patnaik, Soumya; Maludum, Obiora; Lu, Marvin; Figueredo, Vincent M

2016-10-01

Studies suggest increased cardiac morbidity and heart failure exacerbations during winter months with a peak around the holiday season. Major sporting events and intense encounters in sports have been shown to affect cardiovascular outcomes amongst its fans. All patients admitted to Einstein Medical Center between January 1, 2003 and December 31, 2013 with a diagnosis of congestive heart failure were included in the study. They were included on the basis of the presence of an ICD-9CM code representing congestive heart failure as the primary diagnosis. Comparisons were made between the rates of heart failure admissions on the holiday, 4 days following the holiday and the rest of the month for 5 specific days: Christmas day, New Year's day, Independence day, Thanksgiving day and Super Bowl Sunday. Our study included 22,727 heart failure admissions at an average of 5.65 admissions per day. The mean patient age was 68 ± 15 years. There was a significant increase in daily heart failure admissions following Independence day (5.65 vs. 5; p = 0.027) and Christmas day (6.5 vs. 5.5; p = 0.046) when compared to the rest of the month. A history of alcohol abuse or dependence did not correlate with the reported+ rise in heart failure admissions immediately following the holidays. The mean number of daily admissions on the holidays were significantly lower for all holidays compared to the following 4 days. All holidays apart from Super Bowl Sunday demonstrated lower admission rates on the holiday compared to the rest of the month. Christmas and Independence day were associated with increased heart failure admissions immediately following the holidays. The holidays themselves saw lower admission rates. Overeating on holidays, associated emotional stressors, lesser exercise and postponing medical around holidays may be among the factors responsible for the findings.

Recent advances in heart failure.

PubMed

Kassi, Mahwash; Hannawi, Bashar; Trachtenberg, Barry

2018-03-01

Acute heart failure continues to be a challenge as there is limited benefit of numerous agents that have been tested. Cardiac resynchronization therapy remains standard of care, yet timing and need for implantable cardiac defibrillator has been brought into question with the recent randomized trials. Several recent advances have been made towards management of heart failure both in drug and device therapy. The purpose of this review is to provide an update on the most important recent studies on heart failure with reduced ejection fraction (HFrEF) and heart failure with preserved ejection fraction (HFpEF). Two new drugs have been added to the armamentarium for HFrEF; ivabradine and angiotensin receptor-neprilysin inhibitors (ARNIs). Initial data from a new left ventricular assist device (LVAD) pump, the HeartMate 3 (HM III), have demonstrated no reports of pump thrombosis at 6 months, but stroke and right ventricle failure continue to be a challenge with comparable rates compared with the HeartMate II. Several large studies in HFpEF failed to show improvement in outcomes and management continues to be geared towards lifestyle modification and symptom relief. Newer therapies and devices have met with great success, yet there are several therapies that provide no benefit and even harm. A careful review of the recent literature remains instrumental to the effective management of patients with heart failure.

Effect of carvedilol on the morbidity of patients with severe chronic heart failure: results of the carvedilol prospective randomized cumulative survival (COPERNICUS) study.

PubMed

Packer, Milton; Fowler, Michael B; Roecker, Ellen B; Coats, Andrew J S; Katus, Hugo A; Krum, Henry; Mohacsi, Paul; Rouleau, Jean L; Tendera, Michal; Staiger, Christoph; Holcslaw, Terry L; Amann-Zalan, Ildiko; DeMets, David L

2002-10-22

Beta-blocking agents improve functional status and reduce morbidity in mild-to-moderate heart failure, but it is not known whether they produce such benefits in severe heart failure. We randomly assigned 2289 patients with symptoms of heart failure at rest or on minimal exertion and with an ejection fraction <25% (but not volume-overloaded) to double-blind treatment with either placebo (n=1133) or carvedilol (n=1156) for an average of 10.4 months. Carvedilol reduced the combined risk of death or hospitalization for a cardiovascular reason by 27% (P=0.00002) and the combined risk of death or hospitalization for heart failure by 31% (P=0.000004). Patients in the carvedilol group also spent 27% fewer days in the hospital for any reason (P=0.0005) and 40% fewer days in the hospital for heart failure (P<0.0001). These differences were as a result of both a decrease in the number of hospitalizations and a shorter duration of each admission. More patients felt improved and fewer patients felt worse in the carvedilol group than in the placebo group after 6 months of maintenance therapy (P=0.0009). Carvedilol-treated patients were also less likely than placebo-treated patients to experience a serious adverse event (P=0.002), especially worsening heart failure, sudden death, cardiogenic shock, or ventricular tachycardia. In euvolemic patients with symptoms at rest or on minimal exertion, the addition of carvedilol to conventional therapy ameliorates the severity of heart failure and reduces the risk of clinical deterioration, hospitalization, and other serious adverse clinical events.

Re-entry using anatomically determined isthmuses: a curable ventricular tachycardia in repaired congenital heart disease.

PubMed

Kapel, Gijsbert F L; Reichlin, Tobias; Wijnmaalen, Adrianus P; Piers, Sebastiaan R D; Holman, Eduard R; Tedrow, Usha B; Schalij, Martin J; Stevenson, William G; Zeppenfeld, Katja

2015-02-01

Ventricular tachycardia (VT) is an important cause of late morbidity and mortality in repaired congenital heart disease. The substrate often includes anatomic isthmuses that can be transected by radiofrequency catheter ablation similar to isthmus block for atrial flutter. This study evaluates the long-term efficacy of isthmus block for treatment of re-entry VT in adults with repaired congenital heart disease. Thirty-four patients (49±13 years; 74% male) with repaired congenital heart disease who underwent radiofrequency catheter ablation of VT in 2 centers were included. Twenty-two (65%) had a preserved left and right ventricular function. Patients were inducible for 1 (interquartile range, 1-2) VT, median cycle length: 295 ms (interquartile range, 242-346). Ablation aimed to transect anatomic isthmuses containing VT re-entry circuit isthmuses. Procedural success was defined as noninducibility of any VT and transection of the anatomic isthmus and was achieved in 25 (74%) patients. During long-term follow-up (46±29 months), all patients with procedural success (18/25 with internal cardiac defibrillators) were free of VT recurrence but 7 of 18 experienced internal cardiac defibrillator-related complications. One patient with procedural success and depressed cardiac function received an internal cardiac defibrillator shock for ventricular fibrillation. None of the 18 patients (12/18 with internal cardiac defibrillators) with complete success and preserved cardiac function experienced any ventricular arrhythmia. In contrast, VT recurred in 4 of 9 patients without procedural success. Four patients died from nonarrhythmic causes. In patients with repaired congenital heart disease with preserved ventricular function and isthmus-dependent re-entry, VT isthmus ablation can be curative. © 2014 American Heart Association, Inc.

Myostatin from the heart: local and systemic actions in cardiac failure and muscle wasting

PubMed Central

Breitbart, Astrid; Auger-Messier, Mannix; Molkentin, Jeffery D.

2011-01-01

A significant proportion of heart failure patients develop skeletal muscle wasting and cardiac cachexia, which is associated with a very poor prognosis. Recently, myostatin, a cytokine from the transforming growth factor-β (TGF-β) family and a known strong inhibitor of skeletal muscle growth, has been identified as a direct mediator of skeletal muscle atrophy in mice with heart failure. Myostatin is mainly expressed in skeletal muscle, although basal expression is also detectable in heart and adipose tissue. During pathological loading of the heart, the myocardium produces and secretes myostatin into the circulation where it inhibits skeletal muscle growth. Thus, genetic elimination of myostatin from the heart reduces skeletal muscle atrophy in mice with heart failure, whereas transgenic overexpression of myostatin in the heart is capable of inducing muscle wasting. In addition to its endocrine action on skeletal muscle, cardiac myostatin production also modestly inhibits cardiomyocyte growth under certain circumstances, as well as induces cardiac fibrosis and alterations in ventricular function. Interestingly, heart failure patients show elevated myostatin levels in their serum. To therapeutically influence skeletal muscle wasting, direct inhibition of myostatin was shown to positively impact skeletal muscle mass in heart failure, suggesting a promising strategy for the treatment of cardiac cachexia in the future. PMID:21421824

Advanced Heart Failure

MedlinePlus

... must be made. Do I want to receive aggressive treatment? Is quality of life more important than ... American Heart Association recommends: An annual heart failure review to discuss how well you are functioning, current ...

Short-term Effects of High-Dose Caffeine on Cardiac Arrhythmias in Patients With Heart Failure: A Randomized Clinical Trial.

PubMed

Zuchinali, Priccila; Souza, Gabriela C; Pimentel, Maurício; Chemello, Diego; Zimerman, André; Giaretta, Vanessa; Salamoni, Joyce; Fracasso, Bianca; Zimerman, Leandro I; Rohde, Luis E

2016-12-01

The presumed proarrhythmic action of caffeine is controversial. Few studies have assessed the effect of high doses of caffeine in patients with heart failure due to left ventricular systolic dysfunction at high risk for ventricular arrhythmias. To compare the effect of high-dose caffeine or placebo on the frequency of supraventricular and ventricular arrhythmias, both at rest and during a symptom-limited exercise test. Double-blinded randomized clinical trial with a crossover design conducted at the heart failure and cardiac transplant clinic of a tertiary-care university hospital. The trial included patients with chronic heart failure with moderate-to-severe systolic dysfunction (left ventricular ejection fraction <45%) and New York Heart Association functional class I to III between March 5, 2013, and October 2, 2015. Caffeine (100 mg) or lactose capsules, in addition to 5 doses of 100 mL decaffeinated coffee at 1-hour intervals, for a total of 500 mg of caffeine or placebo during a 5-hour protocol. After a 1-week washout period, the protocol was repeated. Number and percentage of ventricular and supraventricular premature beats assessed by continuous electrocardiographic monitoring. We enrolled 51 patients (37 [74%] male; mean [SD] age, 60.6 [10.9] years) with predominantly moderate-to-severe left ventricular systolic dysfunction (mean [SD] left ventricular ejection fraction, 29% [7%]); 31 [61%] had an implantable cardioverter-defibrillator device. No significant differences between the caffeine and placebo groups were observed in the number of ventricular (185 vs 239 beats, respectively; P = .47) and supraventricular premature beats (6 vs 6 beats, respectively; P = .44), as well as in couplets, bigeminal cycles, or nonsustained tachycardia during continuous electrocardiographic monitoring. Exercise test-derived variables, such as ventricular and supraventricular premature beats, duration of exercise, estimated peak oxygen consumption, and heart rate

Thioredoxin 1 is Essential for Sodium Sulfide-Mediated Cardioprotection in the Setting of Heart Failure

PubMed Central

Nicholson, Chad K.; Lambert, Jonathan P.; Molkentin, Jeffery D.; Sadoshima, Junichi; Calvert, John W.

2013-01-01

Objective The aim of this study was to determine if thioredoxin-1 (Trx1) mediates the cardioprotective effects of hydrogen sulfide (H2S) in a model of ischemic-induced heart failure. Approach/Results Mice with a cardiac-specific overexpression of a dominant negative mutant of Trx1 (Tg-DN-Trx1) and wild-type littermates were subjected to ischemic-induced heart failure. Treatment with H2S as sodium sulfide (Na2S) not only increased the gene and protein expression of Trx1 in the absence of ischemia, but also augmented the heart failure-induced increase in both. Wild-type mice treated with Na2S experienced less left ventricular (LV) dilatation, improved LV function, and less cardiac hypertrophy after the induction of heart failure. In contrast, Na2S therapy failed to improve any of these parameters in the Tg-DN-Trx1 mice. Studies aimed at evaluating the underlying cardioprotective mechanisms found that Na2S therapy inhibited heart failure-induced apoptosis signaling kinase-1 (ASK1) signaling and nuclear export of histone deacetylase 4 (HDAC4) in a Trx1-dependent manner. Conclusions These findings provide novel information that the upregulation of Trx1 by Na2S therapy in the setting of heart failure sets into motion events, such as the inhibition of ASK1 signaling and HDAC4 nuclear export, which ultimately leads to the attenuation of LV remodeling. PMID:23349187

Junctional ectopic tachycardia after infant heart surgery: incidence and outcomes.

PubMed

Zampi, Jeffrey D; Hirsch, Jennifer C; Gurney, James G; Donohue, Janet E; Yu, Sunkyung; LaPage, Martin J; Hanauer, David A; Charpie, John R

2012-12-01

Junctional ectopic tachycardia (JET) is an arrhythmia observed almost exclusively after open heart surgery in children. Current literature on JET has not focused on patients at the highest risk of both developing and being negatively impacted by JET. The purpose of this study was to determine the overall incidence of JET in an infant patient cohort undergoing open cardiac surgery, to identify patient- and procedure-related factors associated with developing JET, and to assess the clinical impact of JET on patient outcomes. We performed a nested case-control study from the complete cohort of patients at our institution younger than 1 year of age who underwent open heart surgery between 2005 and 2010. JET patients were compared with an age matched control group undergoing open heart surgery without JET regarding potential risk factors and outcomes. The overall incidence of JET in infants after open cardiac surgery was 14.3 %. From multivariate analyses, complete repair of tetralogy of Fallot [adjusted odds ratio (AOR) 2.0, 95 % CI 1.12-3.57] and longer aortic cross clamp times (AOR 1.02, 95 % CI 1.01-1.03) increased the risk of developing JET. Patients with JET had longer length of intubation, intensive care unit stays, and total length of hospitalization, and were more likely to require extracorporeal membrane oxygenation support (13 vs. 4.3 %). JET is a common postoperative arrhythmia in infants after open heart operations. Both anatomic substrate and surgical procedure contribute to the overall risk of developing JET. Developing JET is associated with worse clinical outcomes.

Extracorporeal Ultrafiltration for Fluid Overload in Heart Failure

PubMed Central

Costanzo, Maria Rosa; Ronco, Claudio; Abraham, William T.; Agostoni, Piergiuseppe; Barasch, Jonathan; Fonarow, Gregg C.; Gottlieb, Stephen S.; Jaski, Brian E.; Kazory, Amir; Levin, Allison P.; Levin, Howard R.; Marenzi, Giancarlo; Mullens, Wilfried; Negoianu, Dan; Redfield, Margaret M.; Tang, W.H. Wilson; Testani, Jeffrey M.; Voors, Adriaan A.

2017-01-01

More than 1 million heart failure hospitalizations occur annually, and congestion is the predominant cause. Rehospitalizations for recurrent congestion portend poor outcomes independently of age and renal function. Persistent congestion trumps serum creatinine increases in predicting adverse heart failure outcomes. No decongestive pharmacological therapy has reduced these harmful consequences. Simplified ultrafiltration devices permit fluid removal in lower-acuity hospital settings, but with conflicting results regarding safety and efficacy. Ultrafiltration performed at fixed rates after onset of therapy-induced increased serum creatinine was not superior to standard care and resulted in more complications. In contrast, compared with diuretic agents, some data suggest that adjustment of ultrafiltration rates to patients’ vital signs and renal function may be associated with more effective decongestion and fewer heart failure events. Essential aspects of ultrafiltration remain poorly defined. Further research is urgently needed, given the burden of congestion and data suggesting sustained benefits of early and adjustable ultrafiltration. PMID:28494980

Embryonic Stem Cell Therapy of Heart Failure in Genetic Cardiomyopathy

PubMed Central

Yamada, Satsuki; Nelson, Timothy J.; Crespo-Diaz, Ruben J.; Perez-Terzic, Carmen; Liu, Xiao-Ke; Miki, Takashi; Seino, Susumu; Behfar, Atta; Terzic, Andre

2009-01-01

Pathogenic causes underlying nonischemic cardiomyopathies are increasingly being resolved, yet repair therapies for these commonly heritable forms of heart failure are lacking. A case in point is human dilated cardiomyopathy 10 (CMD10; Online Mendelian Inheritance in Man #608569), a progressive organ dysfunction syndrome refractory to conventional therapies and linked to mutations in cardiac ATP-sensitive K+ (KATP) channel sub-units. Embryonic stem cell therapy demonstrates benefit in ischemic heart disease, but the reparative capacity of this allogeneic regenerative cell source has not been tested in inherited cardiomyopathy. Here, in a Kir6.2-knockout model lacking functional KATP channels, we recapitulated under the imposed stress of pressure overload the gene-environment substrate of CMD10. Salient features of the human malignant heart failure phenotype were reproduced, including compromised contractility, ventricular dilatation, and poor survival. Embryonic stem cells were delivered through the epicardial route into the left ventricular wall of cardiomyopathic stressed Kir6.2-null mutants. At 1 month of therapy, transplantation of 200,000 cells per heart achieved teratoma-free reversal of systolic dysfunction and electrical synchronization and halted maladaptive remodeling, thereby preventing end-stage organ failure. Tracked using the lacZ reporter transgene, stem cells engrafted into host heart. Beyond formation of cardiac tissue positive for Kir6.2, transplantation induced cell cycle activation and halved fibrotic zones, normalizing sarcomeric and gap junction organization within remuscularized hearts. Improved systemic function induced by stem cell therapy translated into increased stamina, absence of anasarca, and benefit to overall survivorship. Embryonic stem cells thus achieve functional repair in nonischemic genetic cardiomyopathy, expanding indications to the therapy of heritable heart failure. PMID:18669912

Highlights from the British Society for Heart Failure 20th Annual Autumn Meeting: three decades of heart failure.

PubMed

Abel, Alexandra AI

2018-05-16

The 20th Annual Autumn Meeting of the British Society for Heart Failure took place on the 23-24 November 2017 at the Queen Elizabeth II Conference Centre, London, UK. Over 800 delegates were in attendance: a multidisciplinary league of professionals who treat patients with heart failure, including specialist nurses, trainees, cardiologists, geriatricians, pharmacists and general practitioners. The theme of the conference was 'three decades of heart failure' and celebrated the success of modern heart failure management. This report highlights the 'three decades' session, the clinical trials update, and the main discussion points from heart failure question time.

Iron deficiency and anemia in heart failure.

PubMed

Çavuşoğlu, Yüksel; Altay, Hakan; Çetiner, Mustafa; Güvenç, Tolga Sinan; Temizhan, Ahmet; Ural, Dilek; Yeşilbursa, Dilek; Yıldırım, Nesligül; Yılmaz, Mehmet Birhan

2017-03-01

Heart failure is an important community health problem. Prevalence and incidence of heart failure have continued to rise over the years. Despite recent advances in heart failure therapy, prognosis is still poor, rehospitalization rate is very high, and quality of life is worse. Co-morbidities in heart failure have negative impact on clinical course of the disease, further impair prognosis, and add difficulties to treatment of clinical picture. Therefore, successful management of co-morbidities is strongly recommended in addition to conventional therapy for heart failure. One of the most common co-morbidities in heart failure is presence of iron deficiency and anemia. Current evidence suggests that iron deficiency and anemia are more prevalent in patients with heart failure and reduced ejection fraction, as well as those with heart failure and preserved ejection fraction. Moreover, iron deficiency and anemia are referred to as independent predictors for poor prognosis in heart failure. There is strong relationship between iron deficiency or anemia and severity of clinical status of heart failure. Over the last two decades, many clinical investigations have been conducted on clinical effectiveness of treatment of iron deficiency or anemia with oral iron, intravenous iron, and erythropoietin therapies. Studies with oral iron and erythropoietin therapies did not provide any clinical benefit and, in fact, these therapies have been shown to be associated with increase in adverse clinical outcomes. However, clinical trials in patients with iron deficiency in the presence or absence of anemia have demonstrated considerable clinical benefits of intravenous iron therapy, and based on these positive outcomes, iron deficiency has become target of therapy in management of heart failure. The present report assesses current approaches to iron deficiency and anemia in heart failure in light of recent evidence.

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 ...

Efficacy and Safety of Renal Sympathetic Denervation on Dogs with Pressure Overload-Induced Heart Failure.

PubMed

Chen, Pingan; Leng, Shuilong; Luo, Yishan; Li, Shaonan; Huang, Zicheng; Liu, Zhenxi; Liu, Zhen; Wang, Jie; Lei, Xiaoming

2017-02-01

In dogs with heart failure (HF) induced by overload pressure, the role of renal sympathetic denervation (RSD) on heart failure and in the renal artery is unclear. Therefore, we investigated the efficacy and safety of RSD in dogs with pressure overload-induced heart failure. Twenty mongrel dogs were divided into a sham-operated group, an HF group and an HF + RSD group. In the sham-operated group, the abdominal aorta was located but was not constricted, in the HF group, the abdominal aorta was constricted without RSD, and the HF+RSD group underwent RSD with constriction of the abdominal aorta after 10 weeks. Blood sampling assays, echocardiography, intravascular ultrasound (IVUS) measurement and histopathological examination were performed. Renal sympathetic denervation caused a significant reduction in the levels of noradrenaline (166.62±6.84 vs. 183.48±13.66 pg/ml, P<0.05), plasma renin activity (1.93±0.12 vs. 2.10±0.13 ng/mlh, P<0.05) and B-type natriuretic peptide (71.14±3.86 vs. 83.15±5.73 pg/ml, P<0.05) at eight weeks after RSD in the HF+RSD group. Compared with the HF group at eight weeks, the left ventricular internal dimension at end-diastole and end-systole were lower and the left ventricular ejection fraction was higher (all P<0.05) at eight weeks after RSD in the HF+RSD group. Intravenous ultrasound images showed no changes in the renal artery lumen, and intimal hyperplasia and vascular lumen stenosis were not observed after RSD. Renal sympathetic denervation could improve cardiac function in dogs with HF induced by pressure overload; RSD had no adverse influence on the renal artery. Copyright © 2016 Australian and New Zealand Society of Cardiac and Thoracic Surgeons (ANZSCTS) and the Cardiac Society of Australia and New Zealand (CSANZ). Published by Elsevier B.V. All rights reserved.

Role of heat shock transcription factor 1(HSF1)-upregulated macrophage in ameliorating pressure overload-induced heart failure in mice.

PubMed

Du, Peizhao; Chang, Yaowei; Dai, Fangjie; Wei, Chunyan; Zhang, Qi; Li, Jiming

2018-08-15

In order to explore the role of macrophages in HSF1-mediated alleviation of heart failure, mice model of pressure overload-induced heart failure was established using transverse aortic constriction (TAC). Changes in cardiac function and morphology were studied in TAC and SHAM groups using ultrasonic device, tissue staining, electron microscopy, real-time quantitative polymerase chain reaction (RT-QPCR), and Western blotting. We found that mice in the TAC group showed evidence of impaired cardiac function and aggravation of fibrosis on ultrasonic and histopathological examination when compared to those in the SHAM group. The expressions of HSF1, LC3II/LC3I, Becline-1 and HIF-1, as well as autophagosome formation in TAC group were greater than that in SHAM group. On sub-group analyses in the TAC group, improved cardiac function and alleviation of fibrosis was observed in the HSF1 TG subgroup as compared to that in the wild type subgroup. Expressions of LC3II/LC3I, Becline-1 and HIF-1, too showed an obvious increase; and increased autophagosome formation was observed on electron microscopy. Opposite results were observed in the HSF1 KO subgroup. These results collectively suggest that in the pressure overload heart failure model, HSF1 promoted formation of macrophages by inducing upregulation of HIF-1 expression, through which heart failure was ameliorated. Copyright © 2018 Elsevier B.V. All rights reserved.

Paroxysmal ventricular tachycardia and paroxysmal atrial fibrillation associated with subclinical hyperthyroidism, chronic renal failure and elevation of prostate-specific antigen during acute myocardial infarction.

PubMed

Patanè, Salvatore; Marte, Filippo

2010-02-04

Subclinical hyperthyroidism is an increasingly recognized entity that is defined as a normal serum free thyroxine and free triiodothyronine levels with a thyroid-stimulating hormone level suppressed below the normal range and usually undetectable. Paroxysmal atrial fibrillation is a frequent complication of acute myocardial infarction. It has been reported that subclinical hyperthyroidism is not associated with coronary heart disease or mortality from cardiovascular causes but it is sufficient to induce arrhythmias including an increase in atrial fibrillation rate. It has also been reported that increased factor X activity in patients with subclinical hyperthyroidism represents a potential hypercoagulable state. Moreover chronic renal failure presents an increased arrhythmic risk. Apparently spurious result has been reported in a work about mean serum prostate-specific antigen (PSA) concentration during acute myocardial infarction with mean serum PSA concentration significantly lower on day 2 than either day 1 or day 3 and it has been reported that these preliminary results could reflect several factors, such as antiinfarctual treatment, reduced physical activity or an acute-phase response. We present a case of paroxysmal ventricular tachycardia and paroxysmal atrial fibrillation associated with subclinical hyperthyroidism, chronic renal failure and elevation of serum PSA concentration in a 90-year-old Italian man during acute myocardial infarction. Also this case focuses attention on the importance of a correct evaluation of subclinical hyperthyroidism and of chronic renal failure. Moreover, our report also confirms previous findings and extends the evaluation of PSA during acute myocardial infarction. Copyright 2008 Elsevier Ireland Ltd. All rights reserved.

Your Heart Failure Healthcare Team

MedlinePlus

... Thromboembolism Aortic Aneurysm More Your Heart Failure Healthcare Team Updated:May 9,2017 Patients with heart failure ... good relationships with all the members of this team. Learn to talk to them openly and honestly ...

Insulin Signaling and Heart Failure

PubMed Central

Riehle, Christian; Abel, E. Dale

2016-01-01

Heart failure is associated with generalized insulin resistance. Moreover, insulin resistant states such as type 2 diabetes and obesity increases the risk of heart failure even after adjusting for traditional risk factors. Insulin resistance or type 2 diabetes alters the systemic and neurohumoral milieu leading to changes in metabolism and signaling pathways in the heart that may contribute to myocardial dysfunction. In addition, changes in insulin signaling within cardiomyocytes develop in the failing heart. The changes range from activation of proximal insulin signaling pathways that may contribute to adverse left ventricular remodeling and mitochondrial dysfunction to repression of distal elements of insulin signaling pathways such as forkhead (FOXO) transcriptional signaling or glucose transport which may also impair cardiac metabolism, structure and function. This article will review the complexities of insulin signaling within the myocardium and ways in which these pathways are altered in heart failure or in conditions associated with generalized insulin resistance. The implications of these changes for therapeutic approaches to treating or preventing heart failure will be discussed. PMID:27034277

Cheyne-Stokes respiration in patients with congestive heart failure: causes and consequences.

PubMed

Lorenzi-Filho, Geraldo; Genta, Pedro R; Figueiredo, Adelaide C; Inoue, Daniel

2005-08-01

Cheyne-Stokes respiration is a form of periodic breathing in which central apneas and hypopneas alternate with periods of hyperventilation, producing a waxing and waning pattern of tidal volume. This review focuses on the causes and consequences of Cheyne-Stokes respiration in patients with congestive heart failure, in whom the prevalence is strikingly high and ranges from 30% to 50%. Several factors have been implicated in the genesis of Cheyne-Stokes respiration, including low cardiac output and recurrent hypoxia. The key pathophysiological mechanism triggering Cheyne-Stokes respiration is hyperventilation and low arterial CO2 (PaCO2) that when below the apneic threshold triggers a central apnea. Hyperventilation is associated with pulmonary congestion, and Cheyne-Stokes respiration is more prone to occur during sleep, when the respiratory system is mainly dependent on chemical control. It is associated with recurrent dips in oxygen saturation and arousals from sleep, with oscillations in blood pressure and heart rate, sympathetic activation and increased risk of ventricular tachycardia. Cheyne-Stokes respiration is an independent marker of poor prognosis and may participate in a vicious cycle, further stressing the failing heart.

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

The pathophysiology of heart failure.

PubMed

Kemp, Clinton D; Conte, John V

2012-01-01

Heart failure is a clinical syndrome that results when the heart is unable to provide sufficient blood flow to meet metabolic requirements or accommodate systemic venous return. This common condition affects over 5 million people in the United States at a cost of $10-38 billion per year. Heart failure results from injury to the myocardium from a variety of causes including ischemic heart disease, hypertension, and diabetes. Less common etiologies include cardiomyopathies, valvular disease, myocarditis, infections, systemic toxins, and cardiotoxic drugs. As the heart fails, patients develop symptoms which include dyspnea from pulmonary congestion, and peripheral edema and ascites from impaired venous return. Constitutional symptoms such as nausea, lack of appetite, and fatigue are also common. There are several compensatory mechanisms that occur as the failing heart attempts to maintain adequate function. These include increasing cardiac output via the Frank-Starling mechanism, increasing ventricular volume and wall thickness through ventricular remodeling, and maintaining tissue perfusion with augmented mean arterial pressure through activation of neurohormonal systems. Although initially beneficial in the early stages of heart failure, all of these compensatory mechanisms eventually lead to a vicious cycle of worsening heart failure. Treatment strategies have been developed based upon the understanding of these compensatory mechanisms. Medical therapy includes diuresis, suppression of the overactive neurohormonal systems, and augmentation of contractility. Surgical options include ventricular resynchronization therapy, surgical ventricular remodeling, ventricular assist device implantation, and heart transplantation. Despite significant understanding of the underlying pathophysiological mechanisms in heart failure, this disease causes significant morbidity and carries a 50% 5-year mortality. Copyright © 2012 Elsevier Inc. All rights reserved.

A RAT MODEL OF HEART FAILURE INDUCED BY ISOPROTERENOL AND A HIGH SALT DIET

EPA Science Inventory

Rat models of heart failure (HF) show varied pathology and time to disease outcome, dependent on induction method. We found that subchronic (4wk) isoproterenol (ISO) infusion in Spontaneously Hypertensive Heart Failure (SHHF) rats caused cardiac injury with minimal hypertrophy. O...

Diuretics for heart failure.

PubMed

Faris, Rajaa F; Flather, Marcus; Purcell, Henry; Poole-Wilson, Philip A; Coats, Andrew J S

2012-02-15

Chronic heart failure is a major cause of morbidity and mortality worldwide. Diuretics are regarded as the first-line treatment for patients with congestive heart failure since they provide symptomatic relief. The effects of diuretics on disease progression and survival remain unclear. To assess the harms and benefits of diuretics for chronic heart failure Updated searches were run in the Cochrane Central Register of Controlled Trials in The Cochrane Library (CENTRAL Issue 1 of 4, 2011), MEDLINE (1966 to 22 February 2011), EMBASE (1980 to 2011 Week 07) and HERDIN database (1990 to February 2011). We hand searched pertinent journals and reference lists of papers were inspected. We also contacted manufacturers and researchers in the field. No language restrictions were applied. Double-blinded randomised controlled trials of diuretic therapy comparing one diuretic with placebo, or one diuretic with another active agent (e.g. ACE inhibitors, digoxin) in patients with chronic heart failure. Two authors independently abstracted the data and assessed the eligibility and methodological quality of each trial. Extracted data were analysed by determining the odds ratio for dichotomous data, and difference in means for continuous data, of the treated group compared with controls. The likelihood of heterogeneity of the study population was assessed by the Chi-square test. If there was no evidence of statistical heterogeneity and pooling of results was clinically appropriate, a combined estimate was obtained using the fixed-effects model. This update has not identified any new studies for inclusion. The review includes 14 trials (525 participants), 7 were placebo-controlled, and 7 compared diuretics against other agents such as ACE inhibitors or digoxin. We analysed the data for mortality and for worsening heart failure. Mortality data were available in 3 of the placebo-controlled trials (202 participants). Mortality was lower for participants treated with diuretics than for

Diuretics as pathogenetic treatment for heart failure

PubMed Central

Guglin, Maya

2011-01-01

Increased intracardiac filling pressure or congestion causes symptoms and leads to hospital admissions in patients with heart failure, regardless of their systolic function. A history of hospital admission, in turn, predicts further hospitalizations and morbidity, and a higher number of hospitalizations determine higher mortality. Congestion is therefore the driving force of the natural history of heart failure. Congestion is the syndrome shared by heart failure with preserved and reduced systolic function. These two conditions have almost identical morbidity, mortality, and survival because the outcomes are driven by congestion. A small difference in favor of heart failure with preserved systolic function comes from decreased ejection fraction and left ventricular remodeling which is only present in heart failure with decreased systolic function. The magnitude of this difference reflects the contribution of decreased systolic function and ventricular remodeling to the progression of heart failure. The only treatment available for congestion is fluid removal via diuretics, ultrafiltration, or dialysis. It is the only treatment that works equally well for heart failure with reduced and preserved systolic function because it affects congestion, the main pathogenetic feature of the disease. Diuretics are pathogenetic therapy for heart failure. PMID:21403798

Reversal of subcellular remodelling by losartan in heart failure due to myocardial infarction

PubMed Central

Babick, Andrea; Chapman, Donald; Zieroth, Shelley; Elimban, Vijayan; Dhalla, Naranjan S

2012-01-01

This study tested the reversal of subcellular remodelling in heart failure due to myocardial infarction (MI) upon treatment with losartan, an angiotensin II receptor antagonist. Twelve weeks after inducing MI, rats were treated with or without losartan (20 mg/kg; daily) for 8 weeks and assessed for cardiac function, cardiac remodelling, subcellular alterations and plasma catecholamines. Cardiac hypertrophy and lung congestion in 20 weeks MI-induced heart failure were associated with increases in plasma catecholamine levels. Haemodynamic examination revealed depressed cardiac function, whereas echocardiographic analysis showed impaired cardiac performance and marked increases in left ventricle wall thickness and chamber dilatation at 20 weeks of inducing MI. These changes in cardiac function, cardiac remodelling and plasma dopamine levels in heart failure were partially or fully reversed by losartan. Sarcoplasmic reticular (SR) Ca2+-pump activity and protein expression, protein and gene expression for phospholamban, as well as myofibrillar (MF) Ca2+-stimulated ATPase activity and α-myosin heavy chain mRNA levels were depressed, whereas β-myosin heavy chain expression was increased in failing hearts; these alterations were partially reversed by losartan. Although SR Ca2+-release activity and mRNA levels for SR Ca2+-pump were decreased in failing heart, these changes were not reversed upon losartan treatment; no changes in mRNA levels for SR Ca2+-release channels were observed in untreated or treated heart failure. These results suggest that the partial improvement of cardiac performance in heart failure due to MI by losartan treatment is associated with partial reversal of cardiac remodelling as well as partial recovery of SR and MF functions. PMID:22947202

Heart failure symptom relationships: a systematic review.

PubMed

Herr, Janet K; Salyer, Jeanne; Lyon, Debra E; Goodloe, Lauren; Schubert, Christine; Clement, Dolores G

2014-01-01

Heart failure is a prevalent chronic health condition in the United States. Individuals who have heart failure experience as many as 2 to 9 symptoms. The examination of relationships among heart failure symptoms may benefit patients and clinicians who are charged with managing heart failure symptoms. The purpose of this systematic review was to summarize what is known about relationships among heart failure symptoms, a precursor to the identification of heart failure symptom clusters, as well as to examine studies specifically addressing symptom clusters described in this population. The Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines were followed in the conduct of this systematic review. PubMed, PsychINFO, Cumulative Index of Nursing and Allied Health Literature, and the Cochrane Database were searched using the search term heart failure in combination with a pair of symptoms. Of a total of 1316 studies identified from database searches, 34 were included in this systematic review. More than 1 investigator found a moderate level of correlation between depression and fatigue, depression and anxiety, depression and sleep, depression and pain, anxiety and fatigue, and dyspnea and fatigue. The findings of this systematic review provide support for the presence of heart failure symptom clusters. Depression was related to several of the symptoms, providing an indication to clinicians that individuals with heart failure who experience depression may have other concurrent symptoms. Some symptom relationships such as the relationships between fatigue and anxiety or sleep or pain were dependent on the symptom characteristics studied. Symptom prevalence in the sample and restricted sampling may influence the robustness of the symptom relationships. These findings suggest that studies defining the phenotype of individual heart failure symptoms may be a beneficial step in the study of heart failure symptom clusters.

Association of Smoking, Sleep Apnea, and Plasma Alkalosis With Nocturnal Ventricular Arrhythmias in Men With Systolic Heart Failure

PubMed Central

Shukla, Rakesh; Wexler, Laura

2012-01-01

Background: Excess sudden death due to ventricular tachyarrhythmias remains a major mode of mortality in patients with systolic heart failure. The aim of this study was to determine the association of nocturnal ventricular arrhythmias in patients with low ejection fraction heart failure. We incorporated a large number of known pathophysiologic triggers to identify potential targets for therapy to reduce the persistently high incidence of sudden death in this population despite contemporary treatment. Methods: Eighty-six ambulatory male patients with stable low (≤ 45%) ejection fraction heart failure underwent full-night attendant polysomnography and simultaneous Holter recordings. Patients were divided into groups according to the presence or absence of couplets (paired premature ventricular excitations) and ventricular tachycardia (VT) (at least three consecutive premature ventricular excitations) during sleep. Results: In multiple regression analysis, four variables (current smoking status, increased number of arousals, plasma alkalinity, and old age) were associated with VT and two variables (apnea-hypopnea index and low right ventricular ejection fraction) were associated with couplets during sleep. Conclusions: We speculate that cessation of smoking, effective treatment of sleep apnea, and plasma alkalosis could collectively decrease the incidence of nocturnal ventricular tachyarrhythmias and the consequent risk of sudden death, which remains high despite the use of β blockades. PMID:22172636

Decompensated Heart Failure in Pregnancy

PubMed Central

Anthony, John

2016-01-01

Heart disease is a common cause of morbidity and mortality during pregnancy. Symptoms and signs of heart failure in a pregnant woman are an indication for urgent assessment to establish a diagnosis and appropriate management. This is best accomplished through a multidisciplinary approach in which both cardiologists and obstetricians need to participate in order to provide expert counselling and care in pursuit of safe motherhood. Congenital heart disease, although common, once corrected is an unusual source of complications, which are more likely to develop as a consequence of ventricular failure, pulmonary hypertension and aortic arch disease. Rheumatic valvular heart disease is a challenge because of the need for anticoagulation during pregnancy and the risk of sepsis associated with childbirth. This review outlines a contemporary approach to heart failure presenting during pregnancy. PMID:28785449

Heart Failure Virtual Consultation: bridging the gap of heart failure care in the community - A mixed-methods evaluation.

PubMed

Gallagher, Joseph; James, Stephanie; Keane, Ciara; Fitzgerald, Annie; Travers, Bronagh; Quigley, Etain; Hecht, Christina; Zhou, Shuaiwei; Watson, Chris; Ledwidge, Mark; McDonald, Kenneth

2017-08-01

We undertook a mixed-methods evaluation of a Web-based conferencing service (virtual consult) between general practitioners (GPs) and cardiologists in managing patients with heart failure in the community to determine its effect on use of specialist heart failure services and acceptability to GPs. All cases from June 2015 to October 2016 were recorded using a standardized recording template, which recorded patient demographics, medical history, medications, and outcome of the virtual consult for each case. Quantitative surveys and qualitative interviewing of 17 participating GPs were also undertaken. During this time, 142 cases were discussed-68 relating to a new diagnosis of heart failure, 53 relating to emerging deterioration in a known heart failure patient, and 21 relating to therapeutic issues. Only 17% required review in outpatient department following the virtual consultation. GPs reported increased confidence in heart failure management, a broadening of their knowledge base, and a perception of overall better patient outcomes. These data from an initial experience with Heart Failure Virtual Consultation present a very positive impact of this strategy on the provision of heart failure care in the community and acceptability to users. Further research on the implementation and expansion of this strategy is warranted. © 2017 The Authors. ESC Heart Failure published by John Wiley & Sons Ltd on behalf of the European Society of Cardiology.

Embryonic stem cell therapy of heart failure in genetic cardiomyopathy.

PubMed

Yamada, Satsuki; Nelson, Timothy J; Crespo-Diaz, Ruben J; Perez-Terzic, Carmen; Liu, Xiao-Ke; Miki, Takashi; Seino, Susumu; Behfar, Atta; Terzic, Andre

2008-10-01

Pathogenic causes underlying nonischemic cardiomyopathies are increasingly being resolved, yet repair therapies for these commonly heritable forms of heart failure are lacking. A case in point is human dilated cardiomyopathy 10 (CMD10; Online Mendelian Inheritance in Man #608569), a progressive organ dysfunction syndrome refractory to conventional therapies and linked to mutations in cardiac ATP-sensitive K(+) (K(ATP)) channel subunits. Embryonic stem cell therapy demonstrates benefit in ischemic heart disease, but the reparative capacity of this allogeneic regenerative cell source has not been tested in inherited cardiomyopathy. Here, in a Kir6.2-knockout model lacking functional K(ATP) channels, we recapitulated under the imposed stress of pressure overload the gene-environment substrate of CMD10. Salient features of the human malignant heart failure phenotype were reproduced, including compromised contractility, ventricular dilatation, and poor survival. Embryonic stem cells were delivered through the epicardial route into the left ventricular wall of cardiomyopathic stressed Kir6.2-null mutants. At 1 month of therapy, transplantation of 200,000 cells per heart achieved teratoma-free reversal of systolic dysfunction and electrical synchronization and halted maladaptive remodeling, thereby preventing end-stage organ failure. Tracked using the lacZ reporter transgene, stem cells engrafted into host heart. Beyond formation of cardiac tissue positive for Kir6.2, transplantation induced cell cycle activation and halved fibrotic zones, normalizing sarcomeric and gap junction organization within remuscularized hearts. Improved systemic function induced by stem cell therapy translated into increased stamina, absence of anasarca, and benefit to overall survivorship. Embryonic stem cells thus achieve functional repair in nonischemic genetic cardiomyopathy, expanding indications to the therapy of heritable heart failure. Disclosure of potential conflicts of interest is

Gender differences in patients with heart failure.

PubMed

Strömberg, Anna; Mårtensson, Jan

2003-04-01

The aim of this literature review was to review and discuss the differences between men and women with heart failure with regard to epidemiology, aetiology, diagnostics, prognosis, pharmacological and non-pharmacological treatment, and the impact of heart failure on psychosocial factors and healthcare utilisation. Two primary health care resources, MEDLINE and CINAHL, were selected to review the current literature. In MEDLINE, 234 abstracts dealing with heart failure and gender/sex were found and in CINAHL, 20 abstracts. Men have a higher incidence of heart failure, but the overall prevalence rate is similar in both sexes, since women survive longer after the onset of heart failure. Women tend to be older when diagnosed with heart failure and more often have diastolic dysfunction than men. The extent of sex differences in treatment, hospital cost and quality of care can partly be explained by age differences. The life situations for men and women with heart failure are different. Physical and social restrictions affecting daily life activities are experienced as most bothersome for men, whereas restrictions affecting the possibility to support family and friends are most difficult to accept for women. Women with heart failure ascribe more positive meanings to their illness. Despite this, women seem to experience a lower overall quality of life than men. The known gender differences in patients with heart failure need to be highlighted in guidelines as well as implemented in standard care.

Animal model of neuropathic tachycardia syndrome

NASA Technical Reports Server (NTRS)

Carson, R. P.; Appalsamy, M.; Diedrich, A.; Davis, T. L.; Robertson, D.

2001-01-01

Clinically relevant autonomic dysfunction can result from either complete or partial loss of sympathetic outflow to effector organs. Reported animal models of autonomic neuropathy have aimed to achieve complete lesions of sympathetic nerves, but incomplete lesions might be more relevant to certain clinical entities. We hypothesized that loss of sympathetic innervation would result in a predicted decrease in arterial pressure and a compensatory increase in heart rate. Increased heart rate due to loss of sympathetic innervation is seemingly paradoxical, but it provides a mechanistic explanation for clinical autonomic syndromes such as neuropathic postural tachycardia syndrome. Partially dysautonomic animals were generated by selectively lesioning postganglionic sympathetic neurons with 150 mg/kg 6-hydroxydopamine hydrobromide in male Sprague-Dawley rats. Blood pressure and heart rate were monitored using radiotelemetry. Systolic blood pressure decreased within hours postlesion (Delta>20 mm Hg). Within 4 days postlesion, heart rate rose and remained elevated above control levels. The severity of the lesion was determined functionally and pharmacologically by spectral analysis and responsiveness to tyramine. Low-frequency spectral power of systolic blood pressure was reduced postlesion and correlated with the diminished tyramine responsiveness (r=0.9572, P=0.0053). The tachycardia was abolished by treatment with the beta-antagonist propranolol, demonstrating that it was mediated by catecholamines acting on cardiac beta-receptors. Partial lesions of the autonomic nervous system have been hypothesized to underlie many disorders, including neuropathic postural tachycardia syndrome. This animal model may help us better understand the pathophysiology of autonomic dysfunction and lead to development of therapeutic interventions.

Malnutrition and Cachexia in Heart Failure.

PubMed

Rahman, Adam; Jafry, Syed; Jeejeebhoy, Khursheed; Nagpal, A Dave; Pisani, Barbara; Agarwala, Ravi

2016-05-01

Heart failure is a growing public health concern. Advanced heart failure is frequently associated with severe muscle wasting, termed cardiac cachexia This process is driven by systemic inflammation and tumor necrosis factor in a manner common to other forms of disease-related wasting seen with cancer or human immunodeficiency virus. A variable degree of malnutrition is often superimposed from poor nutrient intake. Cardiac cachexia significantly decreases quality of life and survival in patients with heart failure. This review outlines the evaluation of nutrition status in heart failure, explores the pathophysiology of cardiac cachexia, and discusses therapeutic interventions targeting wasting in these patients. © 2015 American Society for Parenteral and Enteral Nutrition.

Heart Failure Questions to Ask Your Doctor

MedlinePlus

... Peripheral Artery Disease Venous Thromboembolism Aortic Aneurysm More Heart Failure Questions to Ask Your Doctor Updated:May 9, ... you? This content was last reviewed May 2017. Heart Failure • Home • About Heart Failure • Causes and Risks for ...

Cardiac Ablation of Rheb1 Induces Impaired Heart Growth, Endoplasmic Reticulum-Associated Apoptosis and Heart Failure in Infant Mice

PubMed Central

Cao, Yunshan; Tao, Lichan; Shen, Shutong; Xiao, Junjie; Wu, Hang; Li, Beibei; Wu, Xiangqi; Luo, Wen; Xiao, Qi; Hu, Xiaoshan; Liu, Hailang; Nie, Junwei; Lu, Shuangshuang; Yuan, Baiyin; Han, Zhonglin; Xiao, Bo; Yang, Zhongzhou; Li, Xinli

2013-01-01

Ras homologue enriched in brain 1 (Rheb1) plays an important role in a variety of cellular processes. In this study, we investigate the role of Rheb1 in the post-natal heart. We found that deletion of the gene responsible for production of Rheb1 from cardiomyocytes of post-natal mice resulted in malignant arrhythmias, heart failure, and premature death of these mice. In addition, heart growth impairment, aberrant metabolism relative gene expression, and increased cardiomyocyte apoptosis were observed in Rheb1-knockout mice prior to the development of heart failure and arrhythmias. Also, protein kinase B (PKB/Akt) signaling was enhanced in Rheb1-knockout mice, and removal of phosphatase and tensin homolog (Pten) significantly prolonged the survival of Rheb1-knockouts. Furthermore, signaling via the mammalian target of rapamycin complex 1 (mTORC1) was abolished and C/EBP homologous protein (CHOP) and phosphorylation levels of c-Jun N-terminal kinase (JNK) were increased in Rheb1 mutant mice. In conclusion, this study demonstrates that Rheb1 is important for maintaining cardiac function in post-natal mice via regulation of mTORC1 activity and stress on the endoplasmic reticulum. Moreover, activation of Akt signaling helps to improve the survival of mice with advanced heart failure. Thus, this study provides direct evidence that Rheb1 performs multiple important functions in the heart of the post-natal mouse. Enhancing Akt activity improves the survival of infant mice with advanced heart failure. PMID:24351823

[Acute and chronic heart failure].

PubMed

Kresoja, K-P; Schmidt, G; Kherad, B; Krackhardt, F; Spillmann, F; Tschöpe, C

2017-11-01

The initial therapy of chronic heart failure is still based on diuretics, angiotensin-converting enzyme (ACE) inhibitors, beta-blockers and in specific cases mineralocorticoid receptor antagonists. The new European Society of Cardiology (ESC) guidelines published in 2016 introduced angiotensin-receptor-neprilysin inhibitors, such as sacubitril/valsartan (LCZ 696) as new therapeutic agents in patients with chronic and progressive heart failure. New subgroup analyses for LCZ 696 have been published showing a beneficial effect in the context of various comorbidities, such as renal insufficiency, diabetes and hypotension. Furthermore, new data are available on intravenous iron substitution in chronic heart failure and on the indications for implantable converter defibrillators, cardiac resynchronization therapy and other cardiac devices. Medicinal therapy of acute heart failure is still limited. For patients who cannot be treated with medicinal therapy, mechanical circulatory support, such as extracorporeal membrane oxygenation (ECMO) should be recommended.

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

Sodium Accumulation in SERCA Knockout-Induced Heart Failure

PubMed Central

Li, Liren; Louch, William E.; Niederer, Steven A.; Aronsen, Jan M.; Christensen, Geir; Sejersted, Ole M.; Smith, Nicolas P.

2012-01-01

In cardiomyocytes, a major decrease in the level of sarco/endoplasmic reticulum Ca2+ ATPase (SERCA) can severely impair systolic and diastolic functions. In mice with cardiomyocyte-specific conditional excision of the Serca2 gene (SERCA2 KO), end-stage heart failure developed between four and seven weeks after gene deletion combined with [Na+]i elevation and intracellular acidosis. In this study, to investigate the underpinning changes in Ca2+ dynamics and metabolic homeostasis, we developed data-driven mathematical models of Ca2+ dynamics in the ventricular myocytes of the control, four-week, and seven-week SERCA2 knockout (KO) mice. The seven-week KO model showed that elevated [Na+]i was due to increased Na+ influxes through the Na+/Ca2+ exchanger (NCX) and the Na+/H+ exchanger, with the latter exacerbated by intracellular acidosis. Furthermore, NCX upregulation in the seven-week KO model resulted in increased ATP consumption for ion transport. Na+ accumulation in the SERCA KO due to NCX upregulation and intracellular acidosis potentially play a role in the development of heart failure, by initiating a reinforcing cycle involving: a mismatch between ATP demand and supply; an increasingly compromised metabolism; a decreased pHi; and, finally, an even greater [Na+]i elevation. PMID:22824267

Construct validity of the Heart Failure Screening Tool (Heart-FaST) to identify heart failure patients at risk of poor self-care: Rasch analysis.

PubMed

Reynolds, Nicholas A; Ski, Chantal F; McEvedy, Samantha M; Thompson, David R; Cameron, Jan

2018-02-14

The aim of this study was to psychometrically evaluate the Heart Failure Screening Tool (Heart-FaST) via: (1) examination of internal construct validity; (2) testing of scale function in accordance with design; and (3) recommendation for change/s, if items are not well adjusted, to improve psychometric credential. Self-care is vital to the management of heart failure. The Heart-FaST may provide a prospective assessment of risk, regarding the likelihood that patients with heart failure will engage in self-care. Psychometric validation of the Heart-FaST using Rasch analysis. The Heart-FaST was administered to 135 patients (median age = 68, IQR = 59-78 years; 105 males) enrolled in a multidisciplinary heart failure management program. The Heart-FaST is a nurse-administered tool for screening patients with HF at risk of poor self-care. A Rasch analysis of responses was conducted which tested data against Rasch model expectations, including whether items serve as unbiased, non-redundant indicators of risk and measure a single construct and that rating scales operate as intended. The results showed that data met Rasch model expectations after rescoring or deleting items due to poor discrimination, disordered thresholds, differential item functioning, or response dependence. There was no evidence of multidimensionality which supports the use of total scores from Heart-FaST as indicators of risk. Aggregate scores from this modified screening tool rank heart failure patients according to their "risk of poor self-care" demonstrating that the Heart-FaST items constitute a meaningful scale to identify heart failure patients at risk of poor engagement in heart failure self-care. © 2018 John Wiley & Sons Ltd.

Ryanodine receptor phosphorylation by calcium/calmodulin-dependent protein kinase II promotes life-threatening ventricular arrhythmias in mice with heart failure.

PubMed

van Oort, Ralph J; McCauley, Mark D; Dixit, Sayali S; Pereira, Laetitia; Yang, Yi; Respress, Jonathan L; Wang, Qiongling; De Almeida, Angela C; Skapura, Darlene G; Anderson, Mark E; Bers, Donald M; Wehrens, Xander H T

2010-12-21

approximately half of patients with heart failure die suddenly as a result of ventricular arrhythmias. Although abnormal Ca(2+) release from the sarcoplasmic reticulum through ryanodine receptors (RyR2) has been linked to arrhythmogenesis, the molecular mechanisms triggering release of arrhythmogenic Ca(2+) remain unknown. We tested the hypothesis that increased RyR2 phosphorylation by Ca(2+)/calmodulin-dependent protein kinase II is both necessary and sufficient to promote lethal ventricular arrhythmias. mice in which the S2814 Ca(2+)/calmodulin-dependent protein kinase II site on RyR2 is constitutively activated (S2814D) develop pathological sarcoplasmic reticulum Ca(2+) release events, resulting in reduced sarcoplasmic reticulum Ca(2+) load on confocal microscopy. These Ca(2+) release events are associated with increased RyR2 open probability in lipid bilayer preparations. At baseline, young S2814D mice have structurally and functionally normal hearts without arrhythmias; however, they develop sustained ventricular tachycardia and sudden cardiac death on catecholaminergic provocation by caffeine/epinephrine or programmed electric stimulation. Young S2814D mice have a significant predisposition to sudden arrhythmogenic death after transverse aortic constriction surgery. Finally, genetic ablation of the Ca(2+)/calmodulin-dependent protein kinase II site on RyR2 (S2814A) protects mutant mice from pacing-induced arrhythmias versus wild-type mice after transverse aortic constriction surgery. our results suggest that Ca(2+)/calmodulin-dependent protein kinase II phosphorylation of RyR2 Ca(2+) release channels at S2814 plays an important role in arrhythmogenesis and sudden cardiac death in mice with heart failure.

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.

Sleep in heart failure.

PubMed

Naughton, Matthew T; Lorenzi-Filho, Geraldo

2009-01-01

Sleep plays a large role in patients with heart failure. In normal subjects, sleep is usually in a supine position with reduced sympathetic drive, elevated vagal tone and as such a relatively lower cardiac output and minute ventilation, allowing for recuperation. Patients with heart failure may not experience the same degree of autonomic activity change and the supine position may place a large strain on the pulmonary system. More than half of all heart failure patients have one of two types of sleep apnea: either obstructive or central sleep apnea. Some patients have both types. Obstructive sleep apnea is likely to be a cause of heart failure due to large negative intrathoracic pressures, apnea related hypoxemia and hypercapnia, terminated by an arousal and surge in systemic blood pressure associated with endothelial damage and resultant premature atherosclerosis. Reversal of obstructive sleep apnea improves blood pressure, systolic contraction and autonomic dysfunction however mortality studies are lacking. Central sleep apnea with Cheyne Stokes pattern of respiration (CSA-CSR) occurs as a result of increased central controller (brainstem driving ventilation) and plant (ventilation driving CO2) gain in the setting of a delayed feed back (i.e., low cardiac output). It is thought this type of apnea is a result of moderately to severely impaired cardiac function and is possibly indicative of high mortality. Treatment of CSA-CSR is best undertaken by treating the underlying cardiac condition which may include with medications, pacemakers, transplantation or continuous positive airway pressure (CPAP). In such patients CPAP exerts unique effects to assist cardiac function and reduce pulmonary edema. Whether CPAP improves survival in this heart failure population remains to be determined.

Management protocols for chronic heart failure in India.

PubMed

Mishra, S; Mohan, J C; Nair, Tiny; Chopra, V K; Harikrishnan, S; Guha, S; Ramakrishnan, S; Ray, S; Sethi, R; Samal, U C; Sarat Chandra, K; Hiremath, M S; Banerjee, A K; Kumar, S; Das, M K; Deb, P K; Bahl, V K

Heart failure is a common clinical syndrome and a global health priority. The burden of heart failure is increasing at an alarming rate worldwide as well as in India. Heart failure not only increases the risk of mortality, morbidity and worsens the patient's quality of life, but also puts a huge burden on the overall healthcare system. The management of heart failure has evolved over the years with the advent of new drugs and devices. This document has been developed with an objective to provide standard management guidance and simple heart failure algorithms to aid Indian clinicians in their daily practice. It would also inform the clinicians on the latest evidence in heart failure and provide guidance to recognize and diagnose chronic heart failure early and optimize management. Copyright © 2017. Published by Elsevier B.V.

Differentiation of ventricular and supraventricular tachycardias based on the analysis of the first postpacing interval after sequential anti-tachycardia pacing in implantable cardioverter-defibrillator patients.

PubMed

Arenal, Angel; Ortiz, Mercedes; Peinado, Rafael; Merino, Jose L; Quesada, Aurelio; Atienza, Felipe; Alberola, Arcadio García; Ormaetxe, Jose; Castellanos, Eduardo; Rodriguez, Juan C; Pérez, Nicasio; García, Javier; Boluda, Luis; del Prado, Mario; Artés, Antonio

2007-03-01

Current discrimination algorithms do not completely avoid inappropriate tachycardia detection. This study analyzes the discrimination capability of the changes of the first postpacing interval (FPPI) after successive bursts of anti-tachycardia pacing (ATP) trains in implantable cardioverter-defibrillator (ICD)-recorded tachycardias. We included 50 ICD patients in this prospective study. We hypothesized that the FPPI variability (FPPIV) when comparing bursts with different numbers of beats would be shorter in ventricular tachycardias (VTs) compared with supraventricular tachycardias (SVTs). The ATP (5-10 pulses, 91% of tachycardia cycle length) was programmed for tachycardias >240 ms. Anti-tachycardia pacing was delivered during 37 sinus tachycardias (STs) in an exercise test, 96 induced VTs in an electrophysiological study, and 198 spontaneous episodes (144 VTs and 54 SVTs). The FPPI remained stable after all ATP bursts in VT but changed continuously in SVT; when comparing bursts of 5 and 10 pulses, the FPPIV was shorter in VT (34 +/- 65 vs.138 +/- 69, P<.0001, in all T and 12 +/- 20 vs. 138 +/- 69, P<.0001, in T>or=320 ms) than in SVT. In T>or=320 ms an FPPIVtachycardia pacing terminated 66% of induced VTs, 60% of spontaneous VTs, and 20% of spontaneous SVTs and induced no VT during spontaneous or exercise induced SVT. Five induced and two spontaneous VT episodes were accelerated. Analysis of FPPIV after ATP discriminates ICD-detected T. Successive bursts (of ATP) trains at 91% of tachycardia cycle length are safe, despite being delivered before rhythm classification.

Electrophysiological actions of somatostatin on the atrioventricular junction in sinus rhythm and reentry tachycardia.

PubMed

Webb, S C; Krikler, D M; Hendry, W G; Adrian, T E; Bloom, S R

1986-09-01

Because somatostatin, a neuroregulatory peptide, is found in abundance in the atria and atrioventricular node, its electrophysiological and antiarrhythmic properties were compared with those of verapamil in ten patients with paroxysmal atrioventricular tachycardia. During sinus rhythm, intravenous somatostatin slowed the heart rate whereas verapamil increased it. Though both agents prolonged atrioventricular conduction time and refractoriness, verapamil was more potent. They were equally effective at terminating reentry atrioventricular tachycardia, restoring sinus rhythm in six of seven patients. Whereas verapamil consistently blocked conduction in the atrioventricular node, somatostatin usually induced ventricular extrasystoles at the time of conversion. Somatostatin may have physiological importance in the neurohumoral control of cardiac impulse formation and conduction.

Effect of novel mucoadhesive buccal patches of carvedilol on isoprenaline-induced tachycardia

PubMed Central

Verma, Navneet; Chattopadhyay, Pronobesh

2014-01-01

The main aim of the study was designed to develop bioadhesive buccal patches of carvedilol (CR) and evaluate for isoprenaline-induced tachycardia. Buccal patches of carvedilol were prepared by using chitosan (CH), sodium salt of carboxy methyl cellulose (NaCMC), and polyvinyl alcohol (PVA) as mucoadhesive polymers. The solvent evaporation method was used for the preparation of buccal patches. The patches were evaluated for their physical characteristics like patch thickness, weight variation, content uniformity, folding endurance, surface pH, residence time, in vitro drug release, and in vivo pharmacodynamic study. The swelling index of the patches was found to be proportional to the polymer concentration, whereas surface pH of all the formulated bioadhesive patches was found to lie between neutral ranges. In-vitro release study shows that 94.75% drug was release in 8 hours from the patch, which containing 2% w/v chitosan. The folding endurance result shows good elasticity in all the patches. Application of buccal patches on buccal mucosa of rabbit shows a significant result in % inhibition of isoprenaline-induced tachycardia. Prepared buccal patches of chitosan, NaCMC, and PVA containing Carvedilol meet the ideal requirement for the delivery of cardiovascular drugs and inhibit the isoprenaline tachycardia. PMID:24959419

Effect of novel mucoadhesive buccal patches of carvedilol on isoprenaline-induced tachycardia.

PubMed

Verma, Navneet; Chattopadhyay, Pronobesh

2014-04-01

The main aim of the study was designed to develop bioadhesive buccal patches of carvedilol (CR) and evaluate for isoprenaline-induced tachycardia. Buccal patches of carvedilol were prepared by using chitosan (CH), sodium salt of carboxy methyl cellulose (NaCMC), and polyvinyl alcohol (PVA) as mucoadhesive polymers. The solvent evaporation method was used for the preparation of buccal patches. The patches were evaluated for their physical characteristics like patch thickness, weight variation, content uniformity, folding endurance, surface pH, residence time, in vitro drug release, and in vivo pharmacodynamic study. The swelling index of the patches was found to be proportional to the polymer concentration, whereas surface pH of all the formulated bioadhesive patches was found to lie between neutral ranges. In-vitro release study shows that 94.75% drug was release in 8 hours from the patch, which containing 2% w/v chitosan. The folding endurance result shows good elasticity in all the patches. Application of buccal patches on buccal mucosa of rabbit shows a significant result in % inhibition of isoprenaline-induced tachycardia. Prepared buccal patches of chitosan, NaCMC, and PVA containing Carvedilol meet the ideal requirement for the delivery of cardiovascular drugs and inhibit the isoprenaline tachycardia.

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

Renal sympathetic denervation alleviates myocardial fibrosis following isoproterenol-induced heart failure.

PubMed

Wang, Neng; Zheng, Xiaoxin; Qian, Jin; Yao, Wei; Bai, Lu; Hou, Guo; Qiu, Xuan; Li, Xiaoyan; Jiang, Xuejun

2017-10-01

The aim of the present study was to determine if renal sympathetic denervation (RSD) may alleviate isoproterenol-induced left ventricle remodeling, and to identify the underlying mechanism. A total of 70 rats were randomly divided into control (n=15), sham operation (n=15), heart failure (HF) with sham operation (HF + sham; n=20) and HF with treatment (HF + RSD; n=20) groups. The HF model was established by subcutaneous injection of isoproterenol; six weeks later, 1eft ventricular internal diameter at end‑systole (LVIDs), left ventricular systolic posterior wall thickness (LVPWs), 1eft ventricular ejection fraction (LVEF) and left ventricular fractional shortening (LVFS) were measured. Plasma norepinephrine (NE), angiotensin II (Ang II) and aldosterone (ALD) levels were measured by ELISA. Myocardial collagen volume fraction (CVF) was determined by Masson's staining. Reverse transcription‑quantitative polymerase chain reaction was used to determine the mRNA expression levels of ventricular transforming growth factor‑β (TGF‑β), connective tissue growth factor (CTGF) and microRNAs (miRs), including miR‑29b, miR‑30c and miR‑133a. The results demonstrated that LVIDs and LVPWs in the HF + RSD group were significantly decreased compared with the HF + sham group. By contrast, LVFS and LVEF in the HF + RSD group were significantly increased compared with the HF + sham group. RSD significantly reduced the levels of plasma NE, Ang II and ALD. CVF in the HF + RSD group was reduced by 38.1% compared with the HF + sham group. Expression levels of TGF‑β and CTGF were decreased, whereas those of miR‑29b, miR‑30c and miR‑133a were increased, in the HF + RSD group compared with the HF + sham group. These results indicated that RSD alleviates isoproterenol‑induced left ventricle remodeling potentially via downregulation of TGF‑β/CTGF and upregulation of miR‑29b, miR‑30c and miR‑133a. RSD may therefore be an effective non‑drug therapy for the

Renal sympathetic denervation alleviates myocardial fibrosis following isoproterenol-induced heart failure

PubMed Central

Wang, Neng; Zheng, Xiaoxin; Qian, Jin; Yao, Wei; Bai, Lu; Hou, Guo; Qiu, Xuan; Li, Xiaoyan; Jiang, Xuejun

2017-01-01

The aim of the present study was to determine if renal sympathetic denervation (RSD) may alleviate isoproterenol-induced left ventricle remodeling, and to identify the underlying mechanism. A total of 70 rats were randomly divided into control (n=15), sham operation (n=15), heart failure (HF) with sham operation (HF + sham; n=20) and HF with treatment (HF + RSD; n=20) groups. The HF model was established by subcutaneous injection of isoproterenol; six weeks later, 1eft ventricular internal diameter at end-systole (LVIDs), left ventricular systolic posterior wall thickness (LVPWs), 1eft ventricular ejection fraction (LVEF) and left ventricular fractional shortening (LVFS) were measured. Plasma norepinephrine (NE), angiotensin II (Ang II) and aldosterone (ALD) levels were measured by ELISA. Myocardial collagen volume fraction (CVF) was determined by Masson's staining. Reverse transcription-quantitative polymerase chain reaction was used to determine the mRNA expression levels of ventricular transforming growth factor-β (TGF-β), connective tissue growth factor (CTGF) and microRNAs (miRs), including miR-29b, miR-30c and miR-133a. The results demonstrated that LVIDs and LVPWs in the HF + RSD group were significantly decreased compared with the HF + sham group. By contrast, LVFS and LVEF in the HF + RSD group were significantly increased compared with the HF + sham group. RSD significantly reduced the levels of plasma NE, Ang II and ALD. CVF in the HF + RSD group was reduced by 38.1% compared with the HF + sham group. Expression levels of TGF-β and CTGF were decreased, whereas those of miR-29b, miR-30c and miR-133a were increased, in the HF + RSD group compared with the HF + sham group. These results indicated that RSD alleviates isoproterenol-induced left ventricle remodeling potentially via downregulation of TGF-β/CTGF and upregulation of miR-29b, miR-30c and miR-133a. RSD may therefore be an effective non-drug therapy for the treatment of heart failure. PMID

[Management of heart failure in cardiology and primary care (MICCAP) program: Improving the management of patients with heart failure].

PubMed

Barrios, V; Escobar, C; Pallares, V; Egocheaga, M I; Lobos, J M; Bover, R; Gómez Doblas, J J; Cosín, J

2018-03-26

Despite current treatments, morbidity and mortality of patients with heart failure remain high. The late diagnosis of heart failure, the insufficient heart failure treatment (i.e. not using the appropriate drugs, prescribing lower doses of drugs than recommended, etc.), and a poor coordination between different health care levels, may explain, at least in part, these figures. The Management of Heart Failure in Cardiology and Primary Care (MICCAP) program has been developed with the aim of optimising the integrated management of patients with heart failure between Primary Care and Cardiology, through the improvement of coordination between both health care levels. This includes continuous medical education to reinforce the diagnostic and therapeutic skills of general practitioners in the field of heart failure. The rationale and objectives of the MICCAP program are summarised in this article. Copyright © 2018 Sociedad Española de Médicos de Atención Primaria (SEMERGEN). Publicado por Elsevier España, S.L.U. All rights reserved.

Incessant atrial tachycardias in a dog with tricuspid dysplasia. Clinical management and electrophysiology.

PubMed

de Madron, E; Kadish, A; Spear, J F; Knight, D H

1987-01-01

In a dog, tricuspid regurgitation due to congenital tricuspid dysplasia resulted in extreme right heart enlargement and right heart failure. Incessant supraventricular tachycardias were present, requiring the intravenous administration of verapamil to reduce the ventricular rate. Oral therapy using a combination of verapamil and quinidine was partially effective in controlling the ventricular rate during the following week. At that time, electrophysiologic studies were performed. They revealed that a succession of several atrial tachycardias with different cycle lengths, including one episode of atrial flutter, was present. Atrial activity was spanning the majority of the cycle length in all these arrhythmias. Epicardial mapping was performed during the atrial flutter. This enabled the detection of a depolarization wave-front traveling counterclockwise from the dorsolateral right atrium toward the right appendage, following the tricuspid valve annulus. No areas of abnormal conduction were detected. Because programmed electric stimulation maneuvers could not be performed, definitive conclusions about the mechanism of the arrhythmia could not be drawn. The two most likely possibilities were circus movement using part of the dilated tricuspid valve annulus as an anatomic barrier or a leading circle type of re-entry.

'Hearts and minds': association, causation and implication of cognitive impairment in heart failure.

PubMed

Cannon, Jane A; McMurray, John Jv; Quinn, Terry J

2015-01-01

The clinical syndrome of heart failure is one of the leading causes of hospitalisation and mortality in older adults. An association between cognitive impairment and heart failure is well described but our understanding of the relationship between the two conditions remains limited. In this review we provide a synthesis of available evidence, focussing on epidemiology, the potential pathogenesis, and treatment implications of cognitive decline in heart failure. Most evidence available relates to heart failure with reduced ejection fraction and the syndromes of chronic cognitive decline or dementia. These conditions are only part of a complex heart failure-cognition paradigm. Associations between cognition and heart failure with preserved ejection fraction and between acute delirium and heart failure also seem evident and where data are available we will discuss these syndromes. Many questions remain unanswered regarding heart failure and cognition. Much of the observational evidence on the association is confounded by study design, comorbidity and insensitive cognitive assessment tools. If a causal link exists, there are several potential pathophysiological explanations. Plausible underlying mechanisms relating to cerebral hypoperfusion or occult cerebrovascular disease have been described and it seems likely that these may coexist and exert synergistic effects. Despite the prevalence of the two conditions, when cognitive impairment coexists with heart failure there is no specific guidance on treatment. Institution of evidence-based heart failure therapies that reduce mortality and hospitalisations seems intuitive and there is no signal that these interventions have an adverse effect on cognition. However, cognitive impairment will present a further barrier to the often complex medication self-management that is required in contemporary heart failure treatment.

Acute Heart Failure Triggered by Coronary Spasm With Transient Left Ventricular Dysfunction.

PubMed

Adachi, Yusuke; Sakakura, Kenichi; Ibe, Tatsuro; Yoshida, Nanae; Wada, Hiroshi; Fujita, Hideo; Momomura, Shin-Ichi

2017-04-06

Coronary spasm is abnormal contraction of an epicardial coronary artery resulting in myocardial ischemia. Coronary spasm induces not only depressed myocardial contractility, but also incomplete myocardial relaxation, which leads to elevated ventricular filling pressure. We herein report the case of a 55-year-old woman who had repeated acute heart failure caused by coronary spasm. Acetylcholine provocation test with simultaneous right heart catheterization was useful for the diagnosis of elevated ventricular filling pressure as well as coronary artery spasm. We should add coronary spasm to a differential diagnosis for repeated acute heart failure.

Liver congestion in heart failure contributes to inappropriately increased serum hepcidin despite anemia.

PubMed

Ohno, Yukako; Hanawa, Haruo; Jiao, Shuang; Hayashi, Yuka; Yoshida, Kaori; Suzuki, Tomoyasu; Kashimura, Takeshi; Obata, Hiroaki; Tanaka, Komei; Watanabe, Tohru; Minamino, Tohru

2015-01-01

Hepcidin is a key regulator of mammalian iron metabolism and mainly produced by the liver. Hepcidin excess causes iron deficiency and anemia by inhibiting iron absorption from the intestine and iron release from macrophage stores. Anemia is frequently complicated with heart failure. In heart failure patients, the most frequent histologic appearance of liver is congestion. However, it remains unclear whether liver congestion associated with heart failure influences hepcidin production, thereby contributing to anemia and functional iron deficiency. In this study, we investigated this relationship in clinical and basic studies. In clinical studies of consecutive heart failure patients (n = 320), anemia was a common comorbidity (41%). In heart failure patients without active infection and ongoing cancer (n = 30), log-serum hepcidin concentration of patients with liver congestion was higher than those without liver congestion (p = 0.0316). Moreover, in heart failure patients with liver congestion (n = 19), the anemia was associated with the higher serum hepcidin concentrations, which is a type of anemia characterized by induction of hepcidin. Subsequently, we produced a rat model of heart failure with liver congestion by injecting monocrotaline that causes pulmonary hypertension. The monocrotaline-treated rats displayed liver congestion with increase of hepcidin expression at 4 weeks after monocrotaline injection, followed by anemia and functional iron deficiency observed at 5 weeks. We conclude that liver congestion induces hepcidin production, which may result in anemia and functional iron deficiency in some patients with heart failure.

Combined atorvastatin and coenzyme Q10 improve the left ventricular function in isoproterenol-induced heart failure in rat.

PubMed

Garjani, Alireza; Andalib, Sina; Biabani, Sajjad; Soraya, Hamid; Doustar, Yousef; Garjani, Afagh; Maleki-Dizaji, Nasrin

2011-09-01

The effect of atorvastatin on cardiac remodeling, function, and homodynamic parameters in isoproterenol-induced heart failure was evaluated in the present study. A subcutaneous injection of isoproterenol (5mg/kg/day) for 10 days was used for the induction of heart failure. Isoproterenol administration produced intensive myocardial necrosis and fibrosis with a significant decrease in the arterial pressure indices, heart rate, contractility (LVdP/dt(max)) and relaxation (LVdP/dt(min)), but an increase in the left ventricular end-diastolic pressure. Rats were randomly assigned to control, treatment with only atorvastatin, and treatment with atorvastatin plus coenzyme Q10. Histopathological analysis showed a marked attenuation of myocyte necrosis and interstitial fibrosis in all atorvastatin treated groups (P<0.001). A low dose of atorvastatin (5mg/kg/day) significantly improved the left ventricular systolic pressure, contractility and relaxation (P<0.01). On the contrary, a high dose of atorvastatin (20mg/kg/day) worsened the isoproterenol-induced left ventricular dysfunction by a further reduction of LVdP/dt(max) from +2780 ± 94 to +1588 ± 248 (mmHg/s; P<0.01) and LVdP/dt(min) from -2007 ± 190 to -2939 ± 291 (mmHg/s; P<0.05). Co-administration of coenzyme Q10 with atorvastatin reversed the hemodynamic depression and the left ventricular dysfunction to a high level (P<0.001). There was a lower level of LVEDPs in the atorvastatin+coenzyme Q10 treated groups (3 ± 1 and 4 ± 1.4 versus 8 ± 3.5 and 14 ± 3.6 mmHg, respectively), thereby suggesting improvement in the myocardial stiffness by the combined coenzyme Q10 and atorvastatin treatment. The atorvastatin therapy attenuated myocardial necrosis and fibrosis in isoproterenol-induced heart failure. However, a high dose of the drug considerably worsened the left ventricular dysfunction and hemodynamic depression, which was reversed by coenzyme Q10 co-administration. Copyright © 2011 Elsevier B.V. All rights

Glycosylated Chromogranin A: Potential Role in the Pathogenesis of Heart Failure.

PubMed

Ottesen, Anett H; Christensen, Geir; Omland, Torbjørn; Røsjø, Helge

2017-12-01

Endocrine and paracrine factors influence the cardiovascular system and the heart by a number of different mechanisms. The chromogranin-secretogranin (granin) proteins seem to represent a new family of proteins that exerts both direct and indirect effects on cardiac and vascular functions. The granin proteins are produced in multiple tissues, including cardiac cells, and circulating granin protein concentrations provide incremental prognostic information to established risk indices in patients with myocardial dysfunction. In this review, we provide recent data for the granin proteins in relation with cardiovascular disease, and with a special focus on chromogranin A and heart failure. Chromogranin A is the most studied member of the granin protein family, and shorter, functionally active peptide fragments of chromogranin A exert protective effects on myocardial cell death, ischemia-reperfusion injury, and cardiomyocyte Ca 2+ handling. Granin peptides have also been found to induce angiogenesis and vasculogenesis. Protein glycosylation is an important post-translational regulatory mechanism, and we recently found chromogranin A molecules to be hyperglycosylated in the failing myocardium. Chromogranin A hyperglycosylation impaired processing of full-length chromogranin A molecules into physiologically active chromogranin A peptides, and patients with acute heart failure and low rate of chromogranin A processing had increased mortality compared to other acute heart failure patients. Other studies have also demonstrated that circulating granin protein concentrations increase in parallel with heart failure disease stage. The granin protein family seems to influence heart failure pathophysiology, and chromogranin A hyperglycosylation could directly be implicated in heart failure disease progression.

Biomarker Guided Therapy in Chronic Heart Failure

PubMed Central

Bektas, Sema

2015-01-01

This review article addresses the question of whether biomarker-guided therapy is ready for clinical implementation in chronic heart failure. The most well-known biomarkers in heart failure are natriuretic peptides, namely B-type natriuretic peptide (BNP) and N-terminal pro-BNP. They are well-established in the diagnostic process of acute heart failure and prediction of disease prognosis. They may also be helpful in screening patients at risk of developing heart failure. Although studied by 11 small- to medium-scale trials resulting in several positive meta-analyses, it is less well-established whether natriuretic peptides are also helpful for guiding chronic heart failure therapy. This uncertainty is expressed by differences in European and American guideline recommendations. In addition to reviewing the evidence surrounding the use of natriuretic peptides to guide chronic heart failure therapy, this article gives an overview of the shortcomings of the trials, how the results may be interpreted and the future directions necessary to fill the current gaps in knowledge. Therapy guidance in chronic heart failure using other biomarkers has not been prospectively tested to date. Emerging biomarkers, such as galectin-3 and soluble ST2, might be useful in this regard, as suggested by several post-hoc analyses. PMID:28785440

2013 update on congenital heart disease, clinical cardiology, heart failure, and heart transplant.

PubMed

Subirana, M Teresa; Barón-Esquivias, Gonzalo; Manito, Nicolás; Oliver, José M; Ripoll, Tomás; Lambert, Jose Luis; Zunzunegui, José L; Bover, Ramon; García-Pinilla, José Manuel

2014-03-01

This article presents the most relevant developments in 2013 in 3 key areas of cardiology: congenital heart disease, clinical cardiology, and heart failure and transplant. Within the area of congenital heart disease, we reviewed contributions related to sudden death in adult congenital heart disease, the importance of specific echocardiographic parameters in assessing the systemic right ventricle, problems in patients with repaired tetralogy of Fallot and indication for pulmonary valve replacement, and confirmation of the role of specific factors in the selection of candidates for Fontan surgery. The most recent publications in clinical cardiology include a study by a European working group on correct diagnostic work-up in cardiomyopathies, studies on the cost-effectiveness of percutaneous aortic valve implantation, a consensus document on the management of type B aortic dissection, and guidelines on aortic valve and ascending aortic disease. The most noteworthy developments in heart failure and transplantation include new American guidelines on heart failure, therapeutic advances in acute heart failure (serelaxin), the management of comorbidities such as iron deficiency, risk assessment using new biomarkers, and advances in ventricular assist devices. Copyright © 2013 Sociedad Española de Cardiología. Published by Elsevier Espana. All rights reserved.

Right heart dysfunction and failure in heart failure with preserved ejection fraction: mechanisms and management. Position statement on behalf of the Heart Failure Association of the European Society of Cardiology.

PubMed

Gorter, Thomas M; van Veldhuisen, Dirk J; Bauersachs, Johann; Borlaug, Barry A; Celutkiene, Jelena; Coats, Andrew J S; Crespo-Leiro, Marisa G; Guazzi, Marco; Harjola, Veli-Pekka; Heymans, Stephane; Hill, Loreena; Lainscak, Mitja; Lam, Carolyn S P; Lund, Lars H; Lyon, Alexander R; Mebazaa, Alexandre; Mueller, Christian; Paulus, Walter J; Pieske, Burkert; Piepoli, Massimo F; Ruschitzka, Frank; Rutten, Frans H; Seferovic, Petar M; Solomon, Scott D; Shah, Sanjiv J; Triposkiadis, Filippos; Wachter, Rolf; Tschöpe, Carsten; de Boer, Rudolf A

2018-01-01

There is an unmet need for effective treatment strategies to reduce morbidity and mortality in patients with heart failure with preserved ejection fraction (HFpEF). Until recently, attention in patients with HFpEF was almost exclusively focused on the left side. However, it is now increasingly recognized that right heart dysfunction is common and contributes importantly to poor prognosis in HFpEF. More insights into the development of right heart dysfunction in HFpEF may aid to our knowledge about this complex disease and may eventually lead to better treatments to improve outcomes in these patients. In this position paper from the Heart Failure Association of the European Society of Cardiology, the Committee on Heart Failure with Preserved Ejection Fraction reviews the prevalence, diagnosis, and pathophysiology of right heart dysfunction and failure in patients with HFpEF. Finally, potential treatment strategies, important knowledge gaps and future directions regarding the right side in HFpEF are discussed. © 2017 The Authors. European Journal of Heart Failure © 2017 European Society of Cardiology.

SPECT and PET in ischemic heart failure.

PubMed

Angelidis, George; Giamouzis, Gregory; Karagiannis, Georgios; Butler, Javed; Tsougos, Ioannis; Valotassiou, Varvara; Giannakoulas, George; Dimakopoulos, Nikolaos; Xanthopoulos, Andrew; Skoularigis, John; Triposkiadis, Filippos; Georgoulias, Panagiotis

2017-03-01

Heart failure is a common clinical syndrome associated with significant morbidity and mortality worldwide. Ischemic heart disease is the leading cause of heart failure, at least in the industrialized countries. Proper diagnosis of the syndrome and management of patients with heart failure require anatomical and functional information obtained through various imaging modalities. Nuclear cardiology techniques play a main role in the evaluation of heart failure. Myocardial single photon emission computed tomography (SPECT) with thallium-201 or technetium-99 m labelled tracers offer valuable data regarding ventricular function, myocardial perfusion, viability, and intraventricular synchronism. Moreover, positron emission tomography (PET) permits accurate evaluation of myocardial perfusion, metabolism, and viability, providing high-quality images and the ability of quantitative analysis. As these imaging techniques assess different parameters of cardiac structure and function, variations of sensitivity and specificity have been reported among them. In addition, the role of SPECT and PET guided therapy remains controversial. In this comprehensive review, we address these controversies and report the advances in patient's investigation with SPECT and PET in ischemic heart failure. Furthermore, we present the innovations in technology that are expected to strengthen the role of nuclear cardiology modalities in the investigation of heart failure.

Advances in gene therapy for heart failure.

PubMed

Fish, Kenneth M; Ishikawa, Kiyotake

2015-04-01

Chronic heart failure is expected to increase its social and economic burden as a consequence of improved survival in patients with acute cardiac events. Cardiac gene therapy holds significant promise in heart failure treatment for patients with currently very limited or no treatment options. The introduction of adeno-associated virus (AAV) gene vector changed the paradigm of cardiac gene therapy, and now it is the primary vector of choice for chronic heart failure gene therapy in clinical and preclinical studies. Recently, there has been significant progress towards clinical translation in this field spearheaded by AAV-1 mediated sarcoplasmic reticulum Ca2+ ATPase (SERCA2a) gene therapy targeting chronic advanced heart failure patients. Meanwhile, several independent laboratories are reporting successful gene therapy approaches in clinically relevant large animal models of heart failure and some of these approaches are expected to enter clinical trials in the near future. This review will focus on gene therapy approaches targeting heart failure that is in clinical trials and those close to its initial clinical trial application.

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. © 2014 Published by International Society for the Heart and Lung Transplantation on behalf of International Society for Heart and Lung Transplantation.

Data and Statistics: Heart Failure

MedlinePlus

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The effects of heart rate control in chronic heart failure with reduced ejection fraction.

PubMed

Grande, Dario; Iacoviello, Massimo; Aspromonte, Nadia

2018-07-01

Elevated heart rate has been associated with worse prognosis both in the general population and in patients with heart failure. Heart rate is finely modulated by neurohormonal signals and it reflects the balance between the sympathetic and the parasympathetic limbs of the autonomic nervous system. For this reason, elevated heart rate in heart failure has been considered an epiphenomenon of the sympathetic hyperactivation during heart failure. However, experimental and clinical evidence suggests that high heart rate could have a direct pathogenetic role. Consequently, heart rate might act as a pathophysiological mediator of heart failure as well as a marker of adverse outcome. This hypothesis has been supported by the observation that the positive effect of beta-blockade could be linked to the degree of heart rate reduction. In addition, the selective heart rate control with ivabradine has recently been demonstrated to be beneficial in patients with heart failure and left ventricular systolic dysfunction. The objective of this review is to examine the pathophysiological implications of elevated heart rate in chronic heart failure and explore the mechanisms underlying the effects of pharmacological heart rate control.

Left septal atrial tachycardia after open-heart surgery: relevance to surgical approach, anatomical and electrophysiological characteristics associated with catheter ablation, and procedural outcomes.

PubMed

Adachi, Toru; Yoshida, Kentaro; Takeyasu, Noriyuki; Masuda, Keita; Sekiguchi, Yukio; Sato, Akira; Tada, Hiroshi; Nogami, Akihiko; Aonuma, Kazutaka

2015-02-01

Septal atrial tachycardia (AT) can occur in patients without structural heart disease and in patients with previous catheter ablation of atrial fibrillation. We aimed to assess septal AT that occurs after open-heart surgery. This study comprised 20 consecutive patients undergoing catheter ablation of macroreentrant AT after open-heart surgery. Relevance to surgical approach, mechanisms, anatomic and electrophysiological characteristics, and outcomes were assessed. Septal AT was identified in 7 patients who had all undergone mitral valve surgery. All septal ATs were localized in the left atrial septum, whereas 10 of 13 nonseptal ATs originated from the right atrium. Patients with left septal AT had a thicker fossa ovalis (median, 4.0; 25th-75th percentile, 3.6-4.2 versus 2.3; 1.6-2.6 mm; P=0.006) and broader area of low voltage (<0.3 mV) in the septum than patients with nonseptal AT (82; 76-89 versus 31; 28%-36%; P=0.02). Repeated gradual prolongations of the tachycardia cycle length without change of the septal circuit were observed in all patients with septal AT (70; 63-100 versus 15; 10-40 ms; P=0.0008). Although ablation terminated all ATs, recurrence of targeted ATs was more frequent in patients with left septal AT during 30-month follow-up (71 versus 0%; P=0.001). Left septal AT after open-heart surgery was characterized by a thicker septum, more scar burden in the septum, and repeated prolongations of the tachycardia cycle length during ablation. Such an arrhythmogenic substrate may interfere with transmural lesion formation by ablation and may account for higher likelihood of recurrence of left septal AT. © 2014 American Heart Association, Inc.

The Loss of GSTM1 Associates with Kidney Failure and Heart Failure.

PubMed

Tin, Adrienne; Scharpf, Robert; Estrella, Michelle M; Yu, Bing; Grove, Megan L; Chang, Patricia P; Matsushita, Kunihiro; Köttgen, Anna; Arking, Dan E; Boerwinkle, Eric; Le, Thu H; Coresh, Josef; Grams, Morgan E

2017-11-01

Glutathione S-transferase mu 1 ( GSTM1) encodes an enzyme that catalyzes the conjugation of electrophilic compounds with glutathione to facilitate their degradation or excretion. The loss of one or both copies of GSTM1 is common in many populations and has been associated with CKD progression. With the hypothesis that the loss of GSTM1 is also associated with incident kidney failure and heart failure, we estimated GSTM1 copy number using exome sequencing reads in the Atherosclerosis Risk in Communities (ARIC) Study, a community-based prospective cohort of white and black participants. Overall, 51.2% and 39.8% of white participants and 25.6% and 48.5% of black participants had zero or one copy of GSTM1 , respectively. Over a median follow-up of 24.6 years, 256 kidney failure events occurred in 5715 participants without prevalent kidney failure, and 1028 heart failure events occurred in 5368 participants without prevalent heart failure. In analysis adjusted for demographics, diabetes, and hypertension, having zero or one copy of GSTM1 associated with higher risk of kidney failure and heart failure (adjusted hazard ratio [95% confidence interval] for zero or one versus two copies of GSTM1 : kidney failure, 1.66 [1.27 to 2.17]; heart failure, 1.16 [1.04 to 1.29]). Risk did not differ significantly between participants with zero and one copy of GSTM1 ( P >0.10). In summary, the loss of GSTM1 was significantly associated with incident kidney and heart failure, independent of traditional risk factors. These results suggest GSTM1 function is a potential treatment target for the prevention of kidney and heart failure. Copyright © 2017 by the American Society of Nephrology.

Depressed heart rate variability as an independent predictor of death in chronic congestive heart failure secondary to ischemic or idiopathic dilated cardiomyopathy.

PubMed

Ponikowski, P; Anker, S D; Chua, T P; Szelemej, R; Piepoli, M; Adamopoulos, S; Webb-Peploe, K; Harrington, D; Banasiak, W; Wrabec, K; Coats, A J

1997-06-15

After acute myocardial infarction, depressed heart rate variability (HRV) has been proven to be a powerful independent predictor of a poor outcome. Although patients with chronic congestive heart failure (CHF) have also markedly impaired HRV, the prognostic value of HRV analysis in these patients remains unknown. The aim of this study was to investigate whether HRV parameters could predict survival in 102 consecutive patients with moderate to severe CHF (90 men, mean age 58 years, New York Heart Association [NYHA] class II to IV, CHF due to idiopathic dilated cardiomyopathy in 24 patients and ischemic heart disease in 78 patients, ejection fraction [EF], 26%; peak oxygen consumption, 16.9 ml/kg/min) after exclusion of patients in atrial fibrilation with diabetes or with chronic renal failure. In the prognostic analysis (Cox proportional-hazards model, Kaplan-Meier survival analysis), the following factors were investigated: age, CHF etiology, NYHA class, EF, peak oxygen consumption, presence of ventricular tachycardia on Holter monitoring, and HRV measures derived from 24-hour electrocardiography monitoring, calculated in the time (standard deviation of all normal RR intervals [SDNN], standard deviation of 5-minute RR intervals [SDANN], mean of all 5-minute standard deviations of RR intervals [SD], root-mean-square of difference of successive RR intervals [rMSSD], and percentage of adjacent RR intervals >50 ms different [pNN50]) and frequency domain (total power [TP], power within low-frequency band [LF], and power within high-frequency band [HF]). During follow-up of 584 +/- 405 days (365 days in all who survived), 19 patients (19%) died (mean time to death: 307 +/- 315 days, range 3 to 989). Cox's univariate analysis identified the following factors to be predictors of death: NYHA (p = 0.003), peak oxygen consumption (p = 0.01), EF (p = 0.02), ventricular tachycardia on Holter monitoring (p = 0.05), and among HRV measures: SDNN (p = 0.004), SDANN (p = 0.003), SD

A Matched Cohort Study of Patients With End-Stage Heart Failure from Anthracycline-Induced Cardiomyopathy Requiring Advanced Cardiac Support.

PubMed

Thomas, Garry R; McDonald, Michael A; Day, Jennifer; Ross, Heather J; Delgado, Diego H; Billia, Filio; Butany, Jagdish W; Rao, Vivek; Amir, Eitan; Bedard, Philippe L; Thavendiranathan, Paaladinesh

2016-11-15

Anthracycline-induced cardiomyopathy (AIC) may progress to end-stage heart failure requiring mechanical circulatory support or orthotopic heart transplantation (OHT). Previous studies have described important clinical differences between AIC and nonischemic cardiomyopathy (NIC) cohorts requiring these advanced interventions. Therefore, we sought to extend this literature by comparing echocardiographic parameters, treatment strategies, and the prognosis between matched patients from these cohorts. This is a retrospective matched cohort study. All patients who received a ventricular assist device or OHT at a large Canadian center were reviewed (n = 421; 1988 to 2015) and subjects with clinical and pathologic evidence of AIC were included (n = 17, 4.0%). A comparison cohort with idiopathic NIC from the same database, matched 3:1 for age, gender, ethnicity, and year of heart failure onset was selected. The Mann-Whitney rank-sum and Fisher's exact tests were used for comparisons. Patients with AIC were predominantly women (70.6%) with heart failure diagnosed at age 40.2 ± 15.8 and 8.3 ± 8.9 years after anthracycline treatment. Compared with NIC, no differences were seen in co-morbidities, echocardiographic measures, the proportion of patients receiving a defibrillator, ventricular assist device, or OHT, the incidence of graft failure, and all-cause mortality. In contrast to other studies, AIC was not associated with a higher incidence of right ventricular dysfunction. A greater proportion of patients with AIC developed cancer (recurrence or new primary) post-OHT (21.4% vs 2.3%, p = 0.042). In conclusion, we demonstrate that when matched cohorts of patients with end-stage heart failure secondary to AIC and idiopathic NIC are compared, they are similar with respect to co-morbidities, degree of ventricular dysfunction, and advanced therapeutics used. The prognosis with OHT is also similar. Copyright © 2016 Elsevier Inc. All rights reserved.

Biofeedback in the treatment of heart failure.

PubMed

McKee, Michael G; Moravec, Christine S

2010-07-01

Biofeedback training can be used to reduce activation of the sympathetic nervous system (SNS) and increase activation of the parasympathetic nervous system (PNS). It is well established that hyperactivation of the SNS contributes to disease progression in chronic heart failure. It has been postulated that underactivation of the PNS may also play a role in heart failure pathophysiology. In addition to autonomic imbalance, a chronic inflammatory process is now recognized as being involved in heart failure progression, and recent work has established that activation of the inflammatory process may be attenuated by vagal nerve stimulation. By interfering with both autonomic imbalance and the inflammatory process, biofeedback-assisted stress management may be an effective treatment for patients with heart failure by improving clinical status and quality of life. Recent studies have suggested that biofeedback and stress management have a positive impact in patients with chronic heart failure, and patients with higher perceived control over their disease have been shown to have better quality of life. Our ongoing study of biofeedback-assisted stress management in the treatment of end-stage heart failure will also examine biologic end points in treated patients at the time of heart transplant, in order to assess the effects of biofeedback training on the cellular and molecular components of the failing heart. We hypothesize that the effects of biofeedback training will extend to remodeling the failing human heart, in addition to improving quality of life.

[Comorbidities of heart failure: sleep apnea].

PubMed

Woehrle, H; Oldenburg, O; Stadler, S; Arzt, M

2018-05-01

Since sleep apnea often occurs in heart failure, physicians regularly need to decide whether further diagnostic procedures and/or treatment are required. Which types of sleep apnea occur in heart failure patients? When is treatment needed? Which treatments and treatment goals are appropriate? Clinical trials and guidelines as well as their implementation in clinical practice are discussed. At least 40% of patients with heart failure, both with reduced and preserved left ventricular ejection fraction (HFrEF and HFpEF, respectively), suffer from relevant sleep apnea. In heart failure patients both obstructive and central sleep apnea are associated with increased mortality. In HFrEF as well as in HFpEF patients with obstructive sleep apnea, treatment with continuous positive airway pressure (CPAP) achieves symptomatic and functional improvements. In patients with HFpEF, positive airway pressure treatment of central sleep apnea may be beneficial. In patients with HFrEF and left ventricular ejection fraction ≤45%, adaptive servoventilation is contraindicated. Sleep apnea is highly prevalent in heart failure patients and its treatment in specific patient groups can improve symptoms and functional outcomes. Thus, testing for sleep apnea is recommended.

Geographic differences in heart failure trials.

PubMed

Ferreira, João Pedro; Girerd, Nicolas; Rossignol, Patrick; Zannad, Faiez

2015-09-01

Randomized controlled trials (RCTs) are essential to develop advances in heart failure (HF). The need for increasing numbers of patients (without substantial cost increase) and generalization of results led to the disappearance of international boundaries in large RCTs. The significant geographic differences in patients' characteristics, outcomes, and, most importantly, treatment effect observed in HF trials have recently been highlighted. Whether the observed regional discrepancies in HF trials are due to trial-specific issues, patient heterogeneity, structural differences in countries, or a complex interaction between factors are the questions we propose to debate in this review. To do so, we will analyse and review data from HF trials conducted in different world regions, from heart failure with preserved ejection fraction (HF-PEF), heart failure with reduced ejection fraction (HF-REF), and acute heart failure (AHF). Finally, we will suggest objective and actionable measures in order to mitigate regional discrepancies in future trials, particularly in HF-PEF where prognostic modifying treatments are urgently needed and in which trials are more prone to selection bias, due to a larger patient heterogeneity. © 2015 The Authors European Journal of Heart Failure © 2015 European Society of Cardiology.

Telerehabilitation for patients with heart failure.

PubMed

Tousignant, Michel; Mampuya, Warner Mbuila

2015-02-01

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.

Implantable Hemodynamic Monitoring for Heart Failure Patients.

PubMed

Abraham, William T; Perl, Leor

2017-07-18

Rates of heart failure hospitalization remain unacceptably high. Such hospitalizations are associated with substantial patient, caregiver, and economic costs. Randomized controlled trials of noninvasive telemedical systems have failed to demonstrate reduced rates of hospitalization. The failure of these technologies may be due to the limitations of the signals measured. Intracardiac and pulmonary artery pressure-guided management has become a focus of hospitalization reduction in heart failure. Early studies using implantable hemodynamic monitors demonstrated the potential of pressure-based heart failure management, whereas subsequent studies confirmed the clinical utility of this approach. One large pivotal trial proved the safety and efficacy of pulmonary artery pressure-guided heart failure management, showing a marked reduction in heart failure hospitalizations in patients randomized to active pressure-guided management. "Next-generation" implantable hemodynamic monitors are in development, and novel approaches for the use of this data promise to expand the use of pressure-guided heart failure management. Copyright © 2017 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.

Ventricular Tachycardia or not? An Unexpected Reason of Wide QRS Complex Tachycardia in a Young Healthy Man: Sodium Bicarbonate.

PubMed

Eyuboglu, Mehmet

2016-10-01

Ventricular tachycardia (VT) is life-threatening subgroup of wide QRS complex tachycardia (WCT). VT is usually associated with structural heart diseases, but it can occur in the absence of any cardiovascular diseases. Adverse cardiac effect of sodium bicarbonate in healthy subjects is not well described. A 30-year-old healthy man with excessive intake of sodium bicarbonate-related VT is presented. He was using sodium bicarbonate during last 2 months to lose weight. He has no risk factors and any cardiovascular or systemic diseases. After intravenous administration of amiodarone, tachycardia ended and his rhythm converted to sinus rhythm with normal electrocardiogram. Patient is asymptomatic, and no VT was observed without any medications at 1 year of follow-up.

Focal Atrial Tachycardia Arising from the Inferior Vena Cava

PubMed Central

Lim, Yeong-Min; Uhm, Jae-Sun

2017-01-01

The inferior vena cava (IVC) is a rare site of focal atrial tachycardia (AT). Here, we report a 20-year-old woman who underwent catheter ablation for anti-arrhythmic drug-resistant AT originating from the IVC. She had undergone open-heart surgery for patch closure of an atrial septal defect 17 years previously and permanent pacemaker implantation for sinus node dysfunction 6 years previously. The AT focus was at the anterolateral aspect of the IVC-right atrial junction, and it was successfully ablated under three-dimensional electroanatomical-mapping guidance. We suspect that the mechanism of this tachycardia was associated with previous IVC cannulation for open-heart surgery. PMID:28541006

Pathophysiological relationships between heart failure and depression and anxiety.

PubMed

Chapa, Deborah W; Akintade, Bimbola; Son, Heesook; Woltz, Patricia; Hunt, Dennis; Friedmann, Erika; Hartung, Mary Kay; Thomas, Sue Ann

2014-04-01

Depression and anxiety are common comorbid conditions in patients with heart failure. Patients with heart failure and depression have increased mortality. The association of anxiety with increased mortality in patients with heart failure is not established. The purpose of this article is to illustrate the similarities of the underlying pathophysiology of heart failure, depression, and anxiety by using the Biopsychosocial Holistic Model of Cardiovascular Health. Depression and anxiety affect biological processes of cardiovascular function in patients with heart failure by altering neurohormonal function via activation of the hypothalamic-pituitary-adrenal axis, autonomic dysregulation, and activation of cytokine cascades and platelets. Patients with heart failure and depression or anxiety may exhibit a continued cycle of heart failure progression, increased depression, and increased anxiety. Understanding the underlying pathophysiological relationships in patients with heart failure who experience comorbid depression and/or anxiety is critical in order to implement appropriate treatments, educate patients and caregivers, and educate other health professionals.

Electrophysiological actions of somatostatin on the atrioventricular junction in sinus rhythm and reentry tachycardia.

PubMed Central

Webb, S C; Krikler, D M; Hendry, W G; Adrian, T E; Bloom, S R

1986-01-01

Because somatostatin, a neuroregulatory peptide, is found in abundance in the atria and atrioventricular node, its electrophysiological and antiarrhythmic properties were compared with those of verapamil in ten patients with paroxysmal atrioventricular tachycardia. During sinus rhythm, intravenous somatostatin slowed the heart rate whereas verapamil increased it. Though both agents prolonged atrioventricular conduction time and refractoriness, verapamil was more potent. They were equally effective at terminating reentry atrioventricular tachycardia, restoring sinus rhythm in six of seven patients. Whereas verapamil consistently blocked conduction in the atrioventricular node, somatostatin usually induced ventricular extrasystoles at the time of conversion. Somatostatin may have physiological importance in the neurohumoral control of cardiac impulse formation and conduction. PMID:2875723

Malignant vagotonia due to selective baroreflex failure

NASA Technical Reports Server (NTRS)

Jordan, J.; Shannon, J. R.; Black, B. K.; Costa, F.; Ertl, A. C.; Furlan, R.; Biaggioni, I.; Robertson, D.

1997-01-01

Baroreflex failure is characterized by dramatic fluctuations of sympathetic activity and paroxysms of hypertension and tachycardia. In contrast, unopposed parasympathetic activity has not been described in patients with baroreflex failure because of concurrent parasympathetic denervation of the heart. We describe the unusual case of a patient with baroreflex failure in a setting of preserved parasympathetic control of HR manifesting episodes of severe bradycardia and asystole. Thus, parasympathetic control of the HR may be intact in occasional patients with baroreflex failure. Patients with this selective baroreflex failure require a unique therapeutic strategy for the control of disease manifestations.

Heart failure caused by toxoplasmosis in a fennec fox (Fennecus zerda).

PubMed

Kottwitz, Jack J; Preziosi, Diane E; Miller, Margaret A; Ramos-Vara, Jose A; Maggs, David J; Bonagura, John D

2004-01-01

A male fennec fox (Fennecus zerda) kit was examined for lethargy, inappetence, and weight loss. Clinical findings included respiratory distress, a gallop rhythm, and retinochoroiditis. Radiography indicated pleural effusion and cardiomegaly. Echocardiographic findings included left ventricular dilatation, low left ventricular ejection fraction, and atrioventricular valvular regurgitation. Necropsy findings were compatible with a diagnosis of congestive heart failure caused by myocarditis. Histopathology showed a disseminated infection with Toxoplasma gondii causing myocarditis, skeletal polymyositis, gastrointestinal myositis, and panuveitis. Toxoplasma-induced myocarditis should be included in the differential diagnosis of heart failure and retinochoroiditis in the fennec fox.

A palliative approach for heart failure end-of-life care

PubMed Central

Maciver, Jane; Ross, Heather J.

2018-01-01

Purpose of review The current review discusses the integration of guideline and evidence-based palliative care into heart failure end-of-life (EOL) care. Recent findings North American and European heart failure societies recommend the integration of palliative care into heart failure programs. Advance care planning, shared decision-making, routine measurement of symptoms and quality of life and specialist palliative care at heart failure EOL are identified as key components to an effective heart failure palliative care program. There is limited evidence to support the effectiveness of the individual elements. However, results from the palliative care in heart failure trial suggest an integrated heart failure palliative care program can significantly improve quality of life for heart failure patients at EOL. Summary Integration of a palliative approach to heart failure EOL care helps to ensure patients receive the care that is congruent with their values, wishes and preferences. Specialist palliative care referrals are limited to those who are truly at heart failure EOL. PMID:29135524

Predictors of incident heart failure in patients after an acute coronary syndrome: The LIPID heart failure risk-prediction model.

PubMed

Driscoll, Andrea; Barnes, Elizabeth H; Blankenberg, Stefan; Colquhoun, David M; Hunt, David; Nestel, Paul J; Stewart, Ralph A; West, Malcolm J; White, Harvey D; Simes, John; Tonkin, Andrew

2017-12-01

Coronary heart disease is a major cause of heart failure. Availability of risk-prediction models that include both clinical parameters and biomarkers is limited. We aimed to develop such a model for prediction of incident heart failure. A multivariable risk-factor model was developed for prediction of first occurrence of heart failure death or hospitalization. A simplified risk score was derived that enabled subjects to be grouped into categories of 5-year risk varying from <5% to >20%. Among 7101 patients from the LIPID study (84% male), with median age 61years (interquartile range 55-67years), 558 (8%) died or were hospitalized because of heart failure. Older age, history of claudication or diabetes mellitus, body mass index>30kg/m 2 , LDL-cholesterol >2.5mmol/L, heart rate>70 beats/min, white blood cell count, and the nature of the qualifying acute coronary syndrome (myocardial infarction or unstable angina) were associated with an increase in heart failure events. Coronary revascularization was associated with a lower event rate. Incident heart failure increased with higher concentrations of B-type natriuretic peptide >50ng/L, cystatin C>0.93nmol/L, D-dimer >273nmol/L, high-sensitivity C-reactive protein >4.8nmol/L, and sensitive troponin I>0.018μg/L. Addition of biomarkers to the clinical risk model improved the model's C statistic from 0.73 to 0.77. The net reclassification improvement incorporating biomarkers into the clinical model using categories of 5-year risk was 23%. Adding a multibiomarker panel to conventional parameters markedly improved discrimination and risk classification for future heart failure events. Copyright © 2017 Elsevier Ireland Ltd. All rights reserved.

Postural tachycardia syndrome: time frequency mapping

NASA Technical Reports Server (NTRS)

Novak, V.; Novak, P.; Opfer-Gehrking, T. L.; Low, P. A.

1996-01-01

Orthostatic tachycardia is common but its specificity remains uncertain. Our preliminary work suggested that using autonomic function testing in conjunction with time-frequency mapping (TFM), it might be possible to characterize a subset of the postural tachycardia syndrome (POTS), that is due to a restricted autonomic neuropathy. We describe 20 patients (17 women and 3 men, aged 14-43 years) with florid POTS and 20 controls (14 women and 6 men, aged 20-41 years). Autonomic failure was quantified by its distribution (cardiovagal, adrenergic and sudomotor) and severity, a symptom profile was generated, and spectral indices, based on modified Wigner distribution during rest and head-up tilt (80 degrees) were evaluated. During tilt-up POTS patients differed from controls by an excessive heart rate (> 130 bpm) (P < 0.001), and higher diastolic pressure (P < 0.01). During rest, cardiovagal oscillations (at respiratory frequencies [RF]) and slow rhythms at nonrespiratory frequencies (NONRF) (from 0.01 to 0.07 Hz) in R-R intervals (RRI) (P < 0.01) were reduced. Both RF and NONRF rhythms in RRI were further blunted with tilt-up (P < 0.001). Slow adrenergic vasomotor rhythms in blood pressure (BP) (approximately 0.07 Hz) surged with tilt-up and returned to normal levels afterwards. The index of sympatho-vagal balance (NONRF-Systolic BP (SBP)/RF-RRI) was dramatically increased in POTS (P < 0.001). Distal postganglionic sudomotor failure was observed, and impairment of the BP responses to the Valsalva maneuver (phase II) suggested peripheral adrenergic dysfunction. Persistent orthostatic dizziness, tiredness, gastrointestinal symptoms and palpitations were common in POTS patients. It is possible to identify a subset of POTS patients who have a length-dependent autonomic neuropathy, affecting the peripheral adrenergic and cardiovagal fibers, with relative preservation of cardiac adrenergic fibers.

Sleep apnoea in heart failure.

PubMed

Schulz, R; Blau, A; Börgel, J; Duchna, H W; Fietze, I; Koper, I; Prenzel, R; Schädlich, S; Schmitt, J; Tasci, S; Andreas, S

2007-06-01

Studies from the USA have reported that sleep apnoea is common in congestive heart failure (CHF), with Cheyne-Stokes respiration (CSR) being the most frequent type of sleep-disordered breathing (SDB) in these patients. Within the present study, the authors sought to assess the prevalence and type of SDB among CHF patients in Germany. A total of 203 CHF patients participated in this prospective multicentre study. All patients were stable in New York Heart Association classes II and III and had a left ventricular ejection fraction (LVEF)<40%. The patients were investigated by polygraphy and all data were centrally analysed. Patient enrolment was irrespective of sleep-related symptoms. The majority of patients were male with a mean age of 65 yrs and hospitalised. Of the 203 patients, 145 (71%) had an apnoea/hypopnoea index>10.h(-1), obstructive sleep apnoea (OSA) occurred in 43% (n=88) and CSR in 28% (n=57) of patients. The prevalence of sleep-disordered breathing is high in patients with stable severe congestive heart failure from a European population. As sleep-disordered breathing may have a negative impact on the prognosis of congestive heart failure, a sleep study should be performed in every patient with congestive heart failure and a left ventricular ejection fraction of <40%. This diagnostic approach should probably be adopted for all of these patients irrespective of the presence of sleep-related symptoms.

The Influence of a High Salt Diet on a Rat Model of Isoproterenol-Induced Heart Failure

EPA Science Inventory

Rat models of heart failure (HF) show varied pathology and time to disease outcome, dependent on induction method. We found that subchronic (4 weeks) isoproterenol (ISO) infusion exacerbated cardiomyopathy in Spontaneously Hypertensive Heart Failure (SHHF) rats. Others have shown...

Tachycardia | Fast Heart Rate

MedlinePlus

... sinoatrial (SA) node --- the heart's natural pacemaker. A series of early beats in the atria speeds up the heart rate. The rapid heartbeat does not allow enough time for the heart to fill before it contracts ...

Rate of change of heart size before congestive heart failure in dogs with mitral regurgitation.

PubMed

Lord, P; Hansson, K; Kvart, C; Häggström, J

2010-04-01

The objective of the study was to examine the changes in vertebral heart scale, and left atrial and ventricular dimensions before and at onset of congestive heart failure in cavalier King Charles spaniels with mitral regurgitation. Records and radiographs from 24 cavalier King Charles spaniels with mitral regurgitation were used. Vertebral heart scale (24 dogs), and left atrial dimension and left ventricular end diastolic and end systolic diameters (18 dogs) and their rate of increase were measured at intervals over years to the onset of congestive heart failure. They were plotted against time to onset of congestive heart failure. Dimensions and rates of change of all parameters were highest at onset of congestive heart failure, the difference between observed and chance outcome being highly significant using a two-tailed chi-square test (P<0.001). The left heart chambers increase in size rapidly only in the last year before the onset of congestive heart failure. Increasing left ventricular end systolic dimension is suggestive of myocardial failure before the onset of congestive heart failure. Rate of increase of heart dimensions may be a useful indicator of impending congestive heart failure.

[Atrial fibrillation as a comorbidity of heart failure].

PubMed

Wachter, R

2018-05-01

Atrial fibrillation and heart failure are diseases that frequently occur together in patients, and the prevalence of the two diseases will continue to increase in the future. Unfortunately, they exacerbate each other: the prognosis of patients with atrial fibrillation is poorer if there is heart failure, and the prognosis of heart failure patients with atrial fibrillation is poorer than the prognosis of heart failure patients without atrial fibrillation. In the past, studies on drug stabilization of sinus rhythm with antiarrhythmic drugs were not able to show any influence on the prognosis of patients. In these patients, it seems to be better to treat the atrial fibrillation interventionally. The CASTLE-AF study has just shown for the first time that isolation of the pulmonary vein to treat atrial fibrillation in heart failure patients has positive effects: hospital admissions for heart failure decreased and the overall survival improved. Further studies have shown that quality of life improves and performance is increased.

Persistent tachycardia in clozapine treated patients: A 24-hour ambulatory electrocardiogram study.

PubMed

Nilsson, Björn M; Lindström, Leif; Mohsen, Issam; Holmlöv, Karolina; Bodén, Robert

2018-03-27

Tachycardia is associated with cardiovascular mortality. Tachycardia is also a known clozapine adverse effect. However, whether clozapine-associated tachycardia is persistent is not known. Thirty clozapine-treated patients with clinical tachycardia were investigated with 24-hour ambulatory electrocardiography (ECG). Baseline peripheral heart rate (HR) was 106.7±7.8. The ambulatory ECG 24-hour-HR was 98.7±9.7. Baseline HR and 24-hour-HR correlated strongly (r=0.74, p=0.000003). Daytime HR was 106.4±9.9 and nighttime HR 89.2±12.0. Low dose bisoprolol reduced HR significantly. The high 24-hour-HR indicates a persistent tachycardia. Tachycardia should not discourage from clozapine use but the findings indicate a need of guidelines for detection and treatment of clozapine-associated tachycardia. Copyright © 2018 The Authors. Published by Elsevier B.V. All rights reserved.

Farnesoid-X-receptor expression in monocrotaline-induced pulmonary arterial hypertension and right heart failure

DOE Office of Scientific and Technical Information (OSTI.GOV)

Ye, Lusi; Department of Rheumatology, The First Affiliated Hospital, Wenzhou Medical University, Wenzhou, Zhejiang 325015; Jiang, Ying

Objective: The farnesoid-X-receptor (FXR) is a metabolic nuclear receptor superfamily member that is highly expressed in enterohepatic tissue and is also expressed in the cardiovascular system. Multiple nuclear receptors, including FXR, play a pivotal role in cardiovascular disease (CVD). Pulmonary arterial hypertension (PAH) is an untreatable cardiovascular system disease that leads to right heart failure (RHF). However, the potential physiological/pathological roles of FXR in PAH and RHF are unknown. We therefore compared FXR expression in the cardiovascular system in PAH, RHF and a control. Methods and results: Hemodynamic parameters and morphology were assessed in blank solution-exposed control, monocrotaline (MCT)-exposed PAHmore » (4 weeks) and RHF (7 weeks) Sprague–Dawley rats. Real-time reverse transcription polymerase chain reaction (real-time RT-PCR), Western blot (WB), immunohistochemistry (IHC) analysis and immunofluorescence (IF) analysis were performed to assess FXR levels in the lung and heart tissues of MCT-induced PAH and RHF rats. In normal rats, low FXR levels were detected in the heart, and nearly no FXR was expressed in rat lungs. However, FXR expression was significantly elevated in PAH and RHF rat lungs but reduced in PAH and RHF rat right ventricular (RV) tissues. FXR expression was reduced only in RHF rat left ventricular (LV) tissues. Conclusions: The differential expression of FXR in MCT-induced PAH lungs and heart tissues in parallel with PAH pathophysiological processes suggests that FXR contributes to PAH. - Highlights: • FXR was expressed in rat lung and heart tissues. • FXR expression increased sharply in the lung tissues of PAH and RHF rats. • FXR expression was reduced in PAH and RHF rat RV tissue. • FXR expression was unaltered in PAH LV but reduced in RHF rat LV tissue. • FXR expression was prominent in the neovascularization region.« less

Genetic determinants of heart failure: facts and numbers.

PubMed

Czepluch, Frauke S; Wollnik, Bernd; Hasenfuß, Gerd

2018-06-01

The relevance of gene mutations leading to heart diseases and hence heart failure has become evident. The risk for and the course of heart failure depends on genomic variants and mutations underlying the so-called genetic predisposition. Genetic contribution to heart failure is highly heterogenous and complex. For any patient with a likely inherited heart failure syndrome, genetic counselling is recommended and important. In the last few years, novel sequencing technologies (named next-generation sequencing - NGS) have dramatically improved the availability of molecular testing, the efficiency of genetic analyses, and moreover reduced the cost for genetic testing. Due to this development, genetic testing has become increasingly accessible and NGS-based sequencing is now applied in clinical routine diagnostics. One of the most common reasons of heart failure are cardiomyopathies such as the dilated or the hypertrophic cardiomyopathy. Nearly 100 disease-associated genes have been identified for cardiomyopathies. The knowledge of a pathogenic mutation can be used for genetic counselling, risk and prognosis determination, therapy guidance and hence for a more effective treatment. Besides, family cascade screening for a known familial, pathogenic mutation can lead to an early diagnosis in affected individuals. At that timepoint, a preventative intervention could be used to avoid or delay disease onset or delay disease progression. Understanding the cellular basis of genetic heart failure syndromes in more detail may provide new insights into the molecular biology of physiological and impaired cardiac (cell) function. As our understanding of the molecular and genetic pathophysiology of heart failure will increase, this might help to identify novel therapeutic targets and may lead to the development of new and specific treatment options in patients with heart failure. © 2018 The Authors. ESC Heart Failure published by John Wiley & Sons Ltd on behalf of the European

Anabolic steroid-induced cardiomyopathy underlying acute liver failure in a young bodybuilder.

PubMed

Bispo, Miguel; Valente, Ana; Maldonado, Rosário; Palma, Rui; Glória, Helena; Nóbrega, João; Alexandrino, Paula

2009-06-21

Heart failure may lead to subclinical circulatory disturbances and remain an unrecognized cause of ischemic liver injury. We present the case of a previously healthy 40-year-old bodybuilder, referred to our Intensive-Care Unit of Hepatology for treatment of severe acute liver failure, with the suspicion of toxic hepatitis associated with anabolic steroid abuse. Despite the absence of symptoms and signs of congestive heart failure at admission, an anabolic steroid-induced dilated cardiomyopathy with a large thrombus in both ventricles was found to be the underlying cause of the liver injury. Treatment for the initially unrecognized heart failure rapidly restored liver function to normal. To our knowledge, this is the first reported case of severe acute liver failure due to an unrecognized anabolic steroid-induced cardiomyopathy. Awareness of this unique presentation will allow for prompt treatment of this potentially fatal cause of liver failure.

New diagnostic and therapeutic possibilities for diastolic heart failure.

PubMed

Jeong, Euy-Myoung; Dudley, Samuel C

2014-02-03

Despite the fact that up to half of all heart failure occurs in patients without evidence of systolic cardiac dysfunction, there are no universally accepted diagnostic markers and no approved therapies for heart failure with preserved ejection fraction (HFpEF). HFpEF, otherwise known as diastolic heart failure, has nearly the same grim prognosis as systolic heart failure, and diastolic heart failure is increasing in incidence and prevalence. Major trials have shown that many of the treatments that are salutary in systolic heart failure have no beneficial effects in diastolic heart failure, suggesting different underlying mechanisms for these two disorders. Even criteria for diagnosis of HFpEF are still debated, and there is still no gold standard marker to detect diastolic dysfunction. Here, we will review some promising new insights into the pathogenesis of diastolic dysfunction that may lead to new diagnostic and therapeutic tools.

Heart failure disease management: implementation and outcomes.

PubMed

Whellan, David J

2005-01-01

Millions of dollars are being spent to identify new therapies to improve mortality and morbidity for the growing epidemic of patients sustaining heart failure. However, in clinical practice, these therapies are currently underused. To bridge the gap between proven therapies and clinical practice, the medical community has turned to disease management. Heart failure disease management interventions vary from vital-sign monitoring to multidisciplinary approaches involving a pharmacist, nutritionist, nurse practitioner, and physician. This review attempts to categorize these inventions based on location. We compared the published results from randomized, controlled trials of the following types of heart failure disease management interventions: inpatient, clinic visits, home visits, and telephone follow up. Although research shows an improvement in the quality of care and a decrease in hospitalizations for patients sustaining heart failure, the economic impact of disease management is still unclear. The current reimbursement structure is a disincentive to providers wanting to offer disease management services to patients sustaining heart failure. Additionally, the cost of providing disease management services such as additional clinical visits, patient education materials, or additional personnel time has not been well documented. Most heart failure disease management studies do confirm the concept that providing increased access to healthcare providers for an at-risk group of patients sustaining heart failure does improve outcomes. However, a large-scale randomized, controlled clinical trial based in the United States is needed to prove that this concept can be implemented beyond a single center and to determine how much it will cost patients, providers, healthcare systems, and payers.

Challenges in Treatment of Inappropriate Sinus Tachycardia.

PubMed

Ruzieh, Mohammed; Moustafa, Abdelmoniem; Sabbagh, Ebrahim; Karim, Mohammad M; Karim, Saima

2018-03-14

Inappropriate Sinus Tachycardia (IST) is a clinical syndrome characterized by a sinus heart rate inexplicably higher than one hundred beats per minute at rest that is associated with symptoms like palpitations, dyspnea or dizziness in the absence of primary causes of tachycardia. The diagnosis requires exclusion of other causes of tachycardia including medications/substances (such as anti-cholinergic, beta-blocker withdrawal, caffeine, and alcohol) or medical conditions (such as panic attacks, pulmonary embolism, fever, hyperthyroidism, hypovolemia, anemia, and pain). Work up should include an EKG to differentiate other causes of tachycardia, 24 hour- Holter monitor if indicated, serum thyroid levels, hemoglobin levels and toxicology screen. Electrophysiological studies are not routinely recommended, but should be considered in certain patients in whom concurrent supraventricular tachycardia is suspected. The underlying pathology in IST is yet to be completely understood. However, it is thought that the causes of IST can be broadly classified into two groups; either as an intrinsic increase in sinus node automaticity or an extrinsic cause. Among extrinsic causes, there is evolving evidence that IgG anti-β receptor antibodies are found in IST causing tachycardia. Managing patients with IST includes lifestyle modification, non-pharmacological and pharmacological interventions. Ivabradine has recently emerged as an effective treatment of IST and was shown to be superior to beta-blockers. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.org.

Right ventricular strain in heart failure: Clinical perspective.

PubMed

Tadic, Marijana; Pieske-Kraigher, Elisabeth; Cuspidi, Cesare; Morris, Daniel A; Burkhardt, Franziska; Baudisch, Ana; Haßfeld, Sabine; Tschöpe, Carsten; Pieske, Burket

2017-10-01

The number of studies demonstrating the importance of right ventricular remodelling in a wide range of cardiovascular diseases has increased in the past two decades. Speckle-tracking imaging provides new variables that give comprehensive information about right ventricular function and mechanics. In this review, we summarize current knowledge of right ventricular mechanics in heart failure with reduced ejection fraction and preserved ejection fraction. We searched PubMed, MEDLINE, Ovid and Embase databases for studies published from January 2000 to December 2016 in the English language using the following keywords: "right ventricle"; "strain"; "speckle tracking"; "heart failure with reduced ejection fraction"; and "heart failure with preserved ejection fraction". Investigations showed that right ventricular dysfunction is associated with higher cardiovascular and overall mortality in patients with heart failure, irrespective of ejection fraction. The number of studies investigating right ventricular strain in patients with heart failure with reduced ejection fraction is constantly increasing, whereas data on right ventricular mechanics in patients with heart failure with preserved ejection fraction are limited. Given the high feasibility, accuracy and clinical implications of right ventricular strain in the population with heart failure, it is of great importance to try to include the evaluation of right ventricular strain as a regular part of each echocardiographic examination in patients with heart failure. However, further investigations are necessary to establish right ventricular strain as a standard variable for decision-making. Copyright © 2017 Elsevier Masson SAS. All rights reserved.

The total artificial heart for biventricular heart failure and beyond.

PubMed

Kasirajan, Vigneshwar; Tang, Daniel G; Katlaps, Gundars J; Shah, Keyur B

2012-05-01

Treatment options for late-stage biventricular heart failure are limited but include medical therapy with intravenous inotropes, biventricular assist devices (Bi-VADs) and the total artificial heart (TAH). In this manuscript, we review the indications, surgical techniques and outcomes for the TAH. The TAH offers biventricular replacement, rather than 'assistance', as the device is placed orthotopically after excision of the entire ventricular myocardium and all four native valves. In contrast to patients with Bi-VADs, patients with the TAH have no postoperative inotrope requirements, arrhythmias or inflow/outflow cannulae-related complications. Additionally, patients participate in rehabilitation early after device placement and the development of a portable drive may facilitate hospital discharge in the USA. Furthermore, total heart replacement may be ideal for heart failure associated with unique anatomical and mechanical complications. The TAH is an effective therapeutic option for the treatment of patients dying of heart failure who may not be suitable candidates for left ventricular assist devices.

Levosimendan Prevents Pressure-Overload-induced Right Ventricular Failure.

PubMed

Hillgaard, Thomas Krarup; Andersen, Asger; Andersen, Stine; Vildbrad, Mads D; Ringgaard, Steffen; Nielsen, Jan M; Nielsen-Kudsk, Jens E

2016-04-01

We investigated if chronic levosimendan treatment can prevent and revert pressure-overload-induced right ventricular hypertrophy and failure in rats. Right ventricular hypertrophy and failure was induced in Wistar rats by pulmonary trunk banding (PTB). The PTB rats were treated with levosimendan (3 mg·kg·d) 3 days before surgery [n = 10, prevention (PREV)], 3 weeks after surgery [n = 10, reversal (REV)] or vehicle (n = 10, VEH). Sham-operated rats received vehicle (n = 16, SHAM). Right ventricular function was evaluated 7 weeks after surgery by echocardiography, magnetic resonance imaging, pressure-volume relations, gross anatomy, and histology. PTB induced right ventricular hypertrophy and compensated heart failure evident by reduced cardiac index (CI) without extra cardiac signs of heart failure. Levosimendan treatment prevented deterioration of right ventricular function measured by CI and right ventricular ejection fraction (RVEF) (CI: VEH vs. PREV 281 ± 17 vs. 362 ± 34 mL·min·kg, P ≤ 0.05, RVEF: VEH vs. PREV 57 ± 2% vs. 68 ± 3%, P ≤ 0.01) to values similar to SHAM (CI: 345 ± 21 mL·min·kg, RVEF: 71 ± 2%). RV contractility was improved in the REV group measured by preload recruitable stroke work (VEH vs. REV 39 ± 3 vs. 66 ± 10 mmHg P ≤ 0.05). Chronic treatment with levosimendan prevents the development of right ventricular failure and improves contractility in established pressure-overload-induced right ventricular failure.

LCZ696 (Valsartan/Sacubitril)--A Possible New Treatment for Hypertension and Heart Failure.

PubMed

Andersen, Mathilde Borring; Simonsen, Ulf; Wehland, Markus; Pietsch, Jessica; Grimm, Daniela

2016-01-01

The aim of this MiniReview was to introduce the newly invented dual-acting drug valsartan/sacubitril (LCZ696), which combines an angiotensin receptor blocker (valsartan) with sacubitril, a specific inhibitor of the neutral endopeptidase (NEP) that degrades vasoactive peptides, including natriuretic peptides ANP and BNP, but also glucagon, enkephalins and bradykinin, among others. The MiniReview presents the data of four available trials NCT01193101, NCT00549770, NCT00887588 and NCT01035255 and provides the current knowledge about LCZ696 effects in patients with hypertension and heart failure. Presently, patients suffering from hypertension and heart failure are treated with ACE inhibitors or angiotensin receptor antagonists often in combination with other drugs. These current medications lead to a reduction in blood pressure in hypertensive patients and a decreased mortality and morbidity in patients with heart failure with reduced ejection fraction, but not in patients with heart failure with preserved ejection fraction. LCZ696 had been tested to utilize the beneficial properties of natriuretic peptides in combination with angiotensin receptor antagonism. It induces even greater blood pressure reductions and decreased mortality and morbidity in patients with heart failure with reduced ejection fraction, while patients with heart failure with preserved ejection fraction show lowered blood pressure and decreased NT-pro-BNP levels. Although long-term studies remain to be performed, these initial data suggest that there is a potential clinical benefit of LCZ696 in the treatment of hypertension and heart failure. © 2015 Nordic Association for the Publication of BCPT (former Nordic Pharmacological Society).

The National Heart Failure Project: a health care financing administration initiative to improve the care of Medicare beneficiaries with heart failure.

PubMed

Masoudi, F A; Ordin, D L; Delaney, R J; Krumholz, H M; Havranek, E P

2000-01-01

This is the second in a series describing Health Care Financing Administration (HCFA) initiatives to improve care for Medicare beneficiaries with heart failure. The first article outlined the history of HCFA quality-improvement projects and current initiatives to improve care in six priority areas: heart failure, acute myocardial infarction, stroke, pneumonia, diabetes, and breast cancer. This article details the objectives and design of the Medicare National Heart Failure Quality Improvement Project (NHF), which has as its goal the improvement of inpatient heart failure care. (c)2000 by CHF, Inc.

Ventricular arrhythmias and changes in heart rate preceding ventricular tachycardia in patients with an implantable cardioverter defibrillator.

PubMed

Lerma, Claudia; Wessel, Niels; Schirdewan, Alexander; Kurths, Jürgen; Glass, Leon

2008-07-01

The objective was to determine the characteristics of heart rate variability and ventricular arrhythmias prior to the onset of ventricular tachycardia (VT) in patients with an implantable cardioverter defibrillator (ICD). Sixty-eight beat-to-beat time series from 13 patients with an ICD were analyzed to quantify heart rate variability and ventricular arrhythmias. The episodes of VT were classified in one of two groups depending on whether the sinus rate in the 1 min preceding the VT was greater or less than 90 beats per minute. In a subset of patients, increased heart rate and reduced heart rate variability was often observed up to 20 min prior to the VT. There was a non-significant trend to higher incidence of premature ventricular complexes (PVCs) before VT compared to control recordings. The patterns of the ventricular arrhythmias were highly heterogeneous among different patients and even within the same patient. Analysis of the changes of heart rate and heart rate variability may have predictive value about the onset of VT in selected patients. The patterns of ventricular arrhythmia could not be used to predict onset of VT in this group of patients.

TLR2 and TLR3 expression as a biomarker for the risk of doxorubicin-induced heart failure.

PubMed

Liang, Shao; Xinyong, Cai; Hongmin, Zhu; Jing, Wang; Lang, Hong; Ping, Zhang

2018-06-27

Doxorubicin (Dox) is limited in its use because of its adverse effect of inducing irreversible heart dysfunction. Innate immune factors, including toll-like receptors (TLRs), play important roles in most cardiac diseases and doxorubicin-induced cardiotoxicity. In this study, subjects were divided into the following groups: healthy controls (n = 62), HF group (n = 60), Dox group (n = 82), and Dox-HF group (n = 32). Expressions of TLR mRNAs in peripheral blood mononuclear cells were detected by RT-PCR. Western blotting was used to quantify protein expressions of Peripheral blood mononuclear cells (PBMCs) TLRs and their downstream signal proteins. The release of inflammatory factors was detected by ELISA. Results indicated that TLR2 was increased and TLR3 was decreased between the control group and Dox group, and between the Dox group and Dox-HF group. Serum inflammatory factors were comparable between the HF group, the Dox group, and the Dox-HF group. This study suggested that TLR2 and TLR3 are up- and down-regulated, respectively, in doxorubicin-treated patients who develop heart dysfunctions. This may suggest a predictive role for TLR2-TLR3 imbalance in doxorubicin-induced heart failure. Copyright © 2018. Published by Elsevier B.V.

Decongestion: Diuretics and other therapies for hospitalized heart failure

PubMed Central

Vazir, Ali; Cowie, Martin R.

2016-01-01

Acute heart failure (AHF) is a potentially life-threatening clinical syndrome, usually requiring hospital admission. Often the syndrome is characterized by congestion, and is associated with long hospital admissions and high risk of readmission and further healthcare expenditure. Despite a limited evidence-base, diuretics remain the first-line treatment for congestion. Loop diuretics are typically the first-line diuretic strategy with some evidence that initial treatment with continuous infusion or boluses of high-dose loop diuretic is superior to an initial lower dose strategy. In patients who have impaired responsiveness to diuretics, the addition of an oral thiazide or thiazide-like diuretic to induce sequential nephron blockade can be beneficial. The use of intravenous low-dose dopamine is no longer supported in heart failure patients with preserved systolic blood pressure and its use to assist diuresis in patients with low systolic blood pressures requires further study. Mechanical ultrafiltration has been used to treat patients with heart failure and fluid retention, but the evidence-base is not robust, and its place in clinical practice is yet to be established. Several novel pharmacological agents remain under investigation. PMID:27056656

Extracellular high-mobility group box 1 mediates pressure overload-induced cardiac hypertrophy and heart failure.

PubMed

Zhang, Lei; Liu, Ming; Jiang, Hong; Yu, Ying; Yu, Peng; Tong, Rui; Wu, Jian; Zhang, Shuning; Yao, Kang; Zou, Yunzeng; Ge, Junbo

2016-03-01

Inflammation plays a key role in pressure overload-induced cardiac hypertrophy and heart failure, but the mechanisms have not been fully elucidated. High-mobility group box 1 (HMGB1), which is increased in myocardium under pressure overload, may be involved in pressure overload-induced cardiac injury. The objectives of this study are to determine the role of HMGB1 in cardiac hypertrophy and cardiac dysfunction under pressure overload. Pressure overload was imposed on the heart of male wild-type mice by transverse aortic constriction (TAC), while recombinant HMGB1, HMGB1 box A (a competitive antagonist of HMGB1) or PBS was injected into the LV wall. Moreover, cardiac myocytes were cultured and given sustained mechanical stress. Transthoracic echocardiography was performed after the operation and sections for histological analyses were generated from paraffin-embedded hearts. Relevant proteins and genes were detected. Cardiac HMGB1 expression was increased after TAC, which was accompanied by its translocation from nucleus to both cytoplasm and intercellular space. Exogenous HMGB1 aggravated TAC-induced cardiac hypertrophy and cardiac dysfunction, as demonstrated by echocardiographic analyses, histological analyses and foetal cardiac genes detection. Nevertheless, the aforementioned pathological change induced by TAC could partially be reversed by HMGB1 inhibition. Consistent with the in vivo observations, mechanical stress evoked the release and synthesis of HMGB1 in cultured cardiac myocytes. This study indicates that the activated and up-regulated HMGB1 in myocardium, which might partially be derived from cardiac myocytes under pressure overload, may be of crucial importance in pressure overload-induced cardiac hypertrophy and cardiac dysfunction. © 2015 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.

[Obesity and heart failure].

PubMed

Weismann, D; Wiedmann, S; Bala, M; Frantz, S; Fassnacht, M

2015-02-01

Obesity is an important risk factor for the development of heart failure. In normotensive obese patients, a reduced peripheral resistance is typically observed and is accompanied by an increased fluid volume and an increase in cardiac work, resulting in hypertrophy and diastolic heart failure, which can be visualized with echocardiography. However, in the presence of arterial hypertension cardiac geometry is not different to hypertensive heart disease without obesity. Furthermore, the typical changes found with obesity, such as reduced peripheral resistance and increased blood volume, are no longer present. Obstructive sleep apnea (OSA) is very common in obesity and warrants screening but levels of the heart failure marker N-terminal pro-brain natriuretic peptide (NT-ProBNP) might be misleading as the values are lower in obesity than in normal weight controls. Body weight reduction is advisable but difficult to achieve and much more difficult to maintain. Furthermore, diet and exercise has not been proven to enhance life expectancy in obesity. However, with bariatric surgery, long-term weight reduction can be achieved and mortality can be reduced. With effective weight loss and improved clinical outcome after bariatric surgery, treatment of obesity has shifted much more into focus. Regardless of technical challenges in the work-up of obese patients, clinical symptoms suggestive of cardiac disorders warrant prompt investigation with standard techniques following recommendations as established for normal weight patients.

Warning Signs of Heart Failure

MedlinePlus

... the two terms are used interchangeably. View an animation of heart failure . If you have been diagnosed ... resources here Popular Articles 1 Understanding Blood Pressure Readings 2 Sodium and Salt 3 Heart Attack Symptoms ...

The Obesity and Heart Failure Epidemics Among African Americans: Insights From the Jackson Heart Study.

PubMed

Krishnamoorthy, Arun; Greiner, Melissa A; Bertoni, Alain G; Eapen, Zubin J; O'Brien, Emily C; Curtis, Lesley H; Hernandez, Adrian F; Mentz, Robert J

2016-08-01

Higher rates of obesity and heart failure have been observed in African Americans, but associations with mortality are not well-described. We examined intermediate and long-term clinical implications of obesity in African Americans and associations between obesity and all-cause mortality, heart failure, and heart failure hospitalization. We conducted a retrospective analysis of a community sample of 5292 African Americans participating in the Jackson Heart Study between September 2000 and January 2013. The main outcomes were associations between body mass index (BMI) and all-cause mortality at 9 years and heart failure hospitalization at 7 years using Cox proportional hazards models and interval development of heart failure (median 8 years' follow-up) using a modified Poisson model. At baseline, 1406 (27%) participants were obese and 1416 (27%) were morbidly obese. With increasing BMI, the cumulative incidence of mortality decreased (P= .007), whereas heart failure increased (P < .001). Heart failure hospitalization was more common among morbidly obese participants (9.0%; 95% confidence interval [CI] 7.6-11.7) than among normal-weight patients (6.3%; 95% CI 4.7-8.4). After risk adjustment, BMI was not associated with mortality. Each 1-point increase in BMI was associated with a 5% increase in the risk of heart failure (hazard ratio 1.05; 95% CI 1.03-1.06; P < .001) and the risk of heart failure hospitalization for BMI greater than 32 kg/m(2) (hazard ratio 1.05; 95% CI 1.03-1.07; P < .001). Obesity and morbid obesity were common in a community sample of African Americans, and both were associated with increased heart failure and heart failure hospitalization. Copyright © 2016 Elsevier Inc. All rights reserved.

The effect of heart failure nurse consultations on heart failure patients' illness beliefs, mood and quality of life over a six-month period.

PubMed

Lucas, Rebecca; Riley, Jillian P; Mehta, Paresh A; Goodman, Helen; Banya, Winston; Mulligan, Kathleen; Newman, Stanton; Cowie, Martin R

2015-01-01

To explore the effect contact with a heart failure nurse can have on patients' illness beliefs, mood and quality of life. There is growing interest in patients' illness beliefs and the part they play in a patients understanding of chronic disease. Secondary analysis on two independent datasets. Patients were recruited from five UK hospitals, four in London and one in Sussex. Patients were recruited from an inpatient and outpatient setting. The first dataset recruited 174 patients with newly diagnosed heart failure, whilst the second dataset recruited 88 patients with an existing diagnosis of heart failure. Patients completed the Minnesota Living with Heart Failure Questionnaire, Hospital Anxiety and Depression Scale, Illness Perception Questionnaire and the Treatment Representations Inventory at baseline and six months. We used a linear regression model to assess the association that contact with a heart failure nurse had on mood, illness beliefs and quality of life over a six-month period. Patients who had contact with a heart failure nurse were more satisfied with their treatment and more likely to believe that their heart failure was treatable. Contact with a heart failure nurse did not make a statistically significant difference to mood or quality of life. This study has shown that contact with a heart failure nurse can improve patient satisfaction with treatment decisions but has less influence on a patient's beliefs about their personal control, treatment control and treatment concerns. With appropriate support, skills and training, heart failure nurses could play an important role in addressing individual patient's beliefs. There is a need to further investigate this. Exploring patients' illness beliefs and mood could help to enhance person-centred care. Heart failure nurses would need additional training in the techniques used. © 2014 John Wiley & Sons Ltd.

Surgical treatment for ectopic atrial tachycardia.

PubMed

Graffigna, A; Vigano, M; Pagani, F; Salerno, G

1992-08-01

Atrial tachycardia is an infrequent but potentially dangerous arrhythmia which often determines cardiac enlargement. Surgical ablation of the arrhythmia is effective and safe, provided a careful atrial mapping is performed and the surgical technique is tailored to the individual focus location. Eight patients underwent surgical ablation of ectopic atrial tachycardia between 1977 and 1990. Different techniques were adopted for each patient according to the anatomical location of the focus and possibly associated arrhythmias. Whenever possible, a closed heart procedure was chosen. In 1 patient a double focal origin was found and treated by separate procedures. In 1 patient with ostium secundum atrial septal defect and atrial flutter, surgical isolation of the right appendage and the ectopic focus was performed. In all patients ectopic atrial tachycardia was ablated with maintenance of the sinoatrial and atrioventricular nodal function as well as internodal conduction. In follow-up up to December 1991, no recurrency was recorded.

Model for heart failure education.

PubMed

Baldonado, Analiza; Dutra, Danette; Abriam-Yago, Katherine

2014-01-01

Heart failure (HF) is the heart's inability to meet the body's need for blood and oxygen. According to the American Heart Association 2013 update, approximately 5.1 million people are diagnosed with HF in the United States in 2006. Heart failure is the most common diagnosis for hospitalization. In the United States, the HF direct and indirect costs are estimated to be US $39.2 billion in 2010. To address this issue, nursing educators designed innovative teaching frameworks on HF management both in academia and in clinical settings. The model was based on 2 resources: the American Association of Heart Failure Nurses (2012) national nursing certification and the award-winning Pierce County Responsive Care Coordination Program. The HF educational program is divided into 4 modules. The initial modules offer foundational levels of Bloom's Taxonomy then progress to incorporate higher-levels of learning when modules 3 and 4 are reached. The applicability of the key components within each module allows formatting to enhance learning in all areas of nursing, from the emergency department to intensive care units to the medical-surgical step-down units. Also applicable would be to provide specific aspects of the modules to nurses who care for HF patients in skilled nursing facility, rehabilitation centers, and in the home-health care setting.

Surgical approach to end-stage heart failure.

PubMed

Klotz, Stefan; Scheld, Hans H

2011-02-01

End-stage heart failure is a challenging disease with growing incidence. With decreasing heart transplant rates worldwide organ preserving therapies become, again, of interest. The purpose of the present review is to examine the potential challenges of surgical therapies in patients with end-stage heart failure. The gold-standard for end-stage heart failure is and will be cardiac transplantation. However, due to organ shortage this therapy is limited to a few patients. Therefore implantation of ventricular assist devices (VADs) or long-term minimal-invasive partial support devices will increase. Improvements in device design with smaller devices, easier implantation techniques, and modified anticoagulation outcome and long-term success will likely improve. In addition, good quality of life as destination therapy is almost available. Organ conservation surgery (coronary artery bypass grafting and surgical ventricular restoration or surgical repair of mitral valve regurgitation) in end-stage heart failure patients could not prove the expected results. Transcatheter or minimal-invasive approaches of these therapies might become routine in the near future. Due to the overwhelming outcome rates, cardiac transplantation is the most established surgical therapy for end-stage heart failure. VAD therapy is increasing and minimized VADs might further open the market for destination therapy/permanent support.

Idiopathic Paroxysmal Ventricular Tachycardia in Infants and Children

ERIC Educational Resources Information Center

Hernandez, Antonio; And Others

1975-01-01

Laboratory tests including blood count serum electrolyte measures, and electroencephalograms were performed on seven children ages 1 day to 18 years with recurrent attacks of rapid heart action known as idiopathic paroxysmal ventricular tachycardia. (CL)

Is depressed myocyte contractility centrally involved in heart failure?

PubMed

Houser, Steven R; Margulies, Kenneth B

2003-03-07

This review examines the evidence for and against the hypothesis that abnormalities in cardiac contractility initiate the heart failure syndrome and drive its progression. There is substantial evidence that the contractility of failing human hearts is depressed and that abnormalities of basal Ca2+ regulation and adrenergic regulation of Ca2+ signaling are responsible. The cellular and molecular defects that cause depressed myocyte contractility are not well established but seem to culminate in abnormal sarcoplasmic reticulum uptake, storage, and release. There are also strong links between Ca2+ regulation, Ca2+ signaling pathways, hypertrophy, and heart failure that need to be more clearly delineated. There is not substantial direct evidence for a causative role for depressed contractility in the initiation and progression of human heart failure, and some studies show that heart failure can occur without depressed myocyte contractility. Stronger support for a causal role for depressed contractility in the initiation of heart failure comes from animal studies where maintaining or improving contractility can prevent heart failure. Recent clinical studies in humans also support the idea that beneficial heart failure treatments, such as beta-adrenergic antagonists, involve improved contractility. Current or previously used heart failure treatments that increase contractility, primarily by increasing cAMP, have generally increased mortality. Novel heart failure therapies that increase or maintain contractility or adrenergic signaling by selectively modulating specific molecules have produced promising results in animal experiments. How to reliably implement these potentially beneficial inotropic therapies in humans without introducing negative side effects is the major unanswered question in this field.

A Zebrafish Heart Failure Model for Assessing Therapeutic Agents.

PubMed

Zhu, Xiao-Yu; Wu, Si-Qi; Guo, Sheng-Ya; Yang, Hua; Xia, Bo; Li, Ping; Li, Chun-Qi

2018-03-20

Heart failure is a leading cause of death and the development of effective and safe therapeutic agents for heart failure has been proven challenging. In this study, taking advantage of larval zebrafish, we developed a zebrafish heart failure model for drug screening and efficacy assessment. Zebrafish at 2 dpf (days postfertilization) were treated with verapamil at a concentration of 200 μM for 30 min, which were determined as optimum conditions for model development. Tested drugs were administered into zebrafish either by direct soaking or circulation microinjection. After treatment, zebrafish were randomly selected and subjected to either visual observation and image acquisition or record videos under a Zebralab Blood Flow System. The therapeutic effects of drugs on zebrafish heart failure were quantified by calculating the efficiency of heart dilatation, venous congestion, cardiac output, and blood flow dynamics. All 8 human heart failure therapeutic drugs (LCZ696, digoxin, irbesartan, metoprolol, qiliqiangxin capsule, enalapril, shenmai injection, and hydrochlorothiazide) showed significant preventive and therapeutic effects on zebrafish heart failure (p < 0.05, p < 0.01, and p < 0.001) in the zebrafish model. The larval zebrafish heart failure model developed and validated in this study could be used for in vivo heart failure studies and for rapid screening and efficacy assessment of preventive and therapeutic drugs.

Type 2 Diabetes and Heart Failure: Challenges and Solutions

PubMed Central

Thomas, Merlin C.

2016-01-01

Increasing numbers of older patients with type 2 diabetes, and their improved survival from cardiovascular events is seeing a massive increase in patients with both diabetes and heart failure. Already, at least a third of all patients with heart failure have diabetes. This close association is partly because all the major risk factors for heart failure also cluster in patients with type 2 diabetes, including obesity, hypertension, advanced age, sleep apnoea, dyslipidaemia, anaemia, chronic kidney disease, and coronary heart disease. However, diabetes may also cause cardiac dysfunction in the absence of overt macrovascular disease, as well as complicate the response to therapy. Current management is focused on targeting modifiable risk factors for heart failure including hyperglycaemia, dyslipidaemia, hypertension, obesity and anemia. But although these are important risk markers, none of these interventions substantially prevents heart failure or improves its outcomes. Much more needs to be done to focus on this issue, including the inclusion of hospital admission for heart failure as a pre-specified component of the primary composite cardiovascular outcomes and new trials in heart failure management specifically in the context of diabetes. PMID:27280301

Circulating proteins as predictors of incident heart failure in the elderly.

PubMed

Stenemo, Markus; Nowak, Christoph; Byberg, Liisa; Sundström, Johan; Giedraitis, Vilmantas; Lind, Lars; Ingelsson, Erik; Fall, Tove; Ärnlöv, Johan

2018-01-01

To identify novel risk markers for incident heart failure using proteomic profiling of 80 proteins previously associated with cardiovascular pathology. Proteomic profiling (proximity extension assay) was performed in two community-based prospective cohorts of elderly individuals without heart failure at baseline: the Prospective Investigation of the Vasculature in Uppsala Seniors [PIVUS, n = 901, median age 70.2 (interquartile range 70.0-70.3) years, 80 events]; and the Uppsala Longitudinal Study of Adult Men [ULSAM, n = 685, median age 77.8 (interquartile range 76.9-78.1) years, 90 events]. Twenty-nine proteins were associated with incident heart failure in the discovery cohort PIVUS after adjustment for age and sex, and correction for multiple testing. Eighteen associations replicated in ULSAM. In pooled analysis of both cohorts, higher levels of nine proteins were associated with incident heart failure after adjustment for established risk factors: growth differentiation factor 15 (GDF-15), T-cell immunoglobulin and mucin domain 1 (TIM-1), tumour necrosis factor-related apoptosis-inducing ligand receptor 2 (TRAIL-R2), spondin-1 (SPON1), matrix metalloproteinase-12 (MMP-12), follistatin (FS), urokinase-type plasminogen activator surface receptor (U-PAR), osteoprotegerin (OPG), and suppression of tumorigenicity 2 (ST2). Of these, GDF-15, U-PAR, MMP-12, TRAIL-R2, SPON1 and FS were associated with worsened echocardiographic left ventricular systolic function at baseline, while only TIM-1 was positively associated with worsened diastolic function (P < 0.02 for all). Proteomic profiling identified several novel associations between proteins involved in apoptosis, inflammation, matrix remodelling, and fibrinolysis with incident heart failure in elderly individuals. Our results encourage additional studies investigating the underlying mechanisms and the clinical utility of our findings. © 2017 The Authors. European Journal of Heart Failure © 2017 European

Heart failure in children - overview

MedlinePlus

... heart failure worse Monitor for side effects of medicines your child may be taking ... a safe and effective exercise and activity plan. MEDICINES, SURGERY, AND DEVICES Your child will need to take medicines to treat heart ...

The Role of Beta-Blocker in Heart Failure in Adults with Congenital Heart Disease.

PubMed

Norozi, Kambiz

2014-01-01

Thanks to the enormous progress in the field of cardiac surgery and paediatric cardiology since the mid of 20th century, more and more children with congenital heart defects reach the adulthood. This on the other hand encounter physician and patients various problems due to late complications after the heart surgery like congestive heart failure, arrhythmia and sudden death. One of the challenging area is the medical management of heart failure in these patients with complex anatomy and hemodynamics. The lack of evidence of the effectiveness of the anti congestive medications in this population in from of large randomized controlled trials, makes it difficult to establish universally accepted therapy guidelines. In this article we will review the evidence of the beta-blockers in heart failure in patients with congenital heart disease. Also we will discuss the mechanisms of heart failure in this patient's cohort and will review the literature with respect to the use of neurohormonal antagonists in congenital heart disease. There is an urgent need to initiate well-designed clinical trials to prove if the positive results of neurohormonal blockade in acquired heart failure in adults can be translated in patients with congenital heart disease.

Outcome of Radiofrequency Catheter Ablation as a non-pharmacological therapy for idiopathic Ventricular Tachycardia.

PubMed

Samore, Naseer Ahmed; Imran Majeed, Syed Muhammad; Kayani, Azhar Mahmud; Bhalli, Muhammad Asif; Shabbir, Muhammad

2009-09-01

To determine the outcome of Radiofrequency Catheter Ablation (RFCA) as a non-pharmacological curative therapy for idiopathic Ventricular Tachycardia (VT) and to identify procedure-related complications. Descriptive study. The Armed Forces Institute of Cardiology and National Institute of Heart Diseases, Rawalpindi, from February 2001 to October 2008. Ninety eight consecutive patients with idiopathic VT, resistant to drug therapy, who underwent Electrophysiology Studies (EPS) radiofrequency catheter ablation were enrolled. Clinical and electrophysiological variables were recorded and a descriptive analysis was done. Out of the 98 patients, 79 were males (80.6%). The mean age was 33.29+11.93 years. Modes of presentation were sustained VT, Repetitive Monomorphic VT (RMVT), Non-sustained VT (NSVT) and Ventricular Premature Beats (VPBs). Right Ventricular Outflow Tract (RVOT) VT was found in 37 patients, 37 had Idiopathic Left Ventricular Tachycardia (ILVT), 20 had Left Ventricular Outflow Tract (LVOT) VT, and Inflow Right Ventricular Tachycardia (IRVT) was found in 7 patients. Other sites of origin of VT were infrequent. Eight patients had dual morphologies of VT. Atrioventricular Nodal Re-entry Tachycardia (AVNRT) was found in 8 patients. RFCA was successful in abolishing inducible VT in 88 patients. One patient developed complete AV block requiring a permanent pacemaker. Results of this study confirm a high degree of success and safety of radiofrequency catheter ablation as curative therapy for idiopathic ventricular tachycardia.

Economic impact of heart failure according to the effects of kidney failure.

PubMed

Sicras Mainar, Antoni; Navarro Artieda, Ruth; Ibáñez Nolla, Jordi

2015-01-01

To evaluate the use of health care resources and their cost according to the effects of kidney failure in heart failure patients during 2-year follow-up in a population setting. Observational retrospective study based on a review of medical records. The study included patients ≥ 45 years treated for heart failure from 2008 to 2010. The patients were divided into 2 groups according to the presence/absence of KF. Main outcome variables were comorbidity, clinical status (functional class, etiology), metabolic syndrome, costs, and new cases of cardiovascular events and kidney failure. The cost model included direct and indirect health care costs. Statistical analysis included multiple regression models. The study recruited 1600 patients (prevalence, 4.0%; mean age 72.4 years; women, 59.7%). Of these patients, 70.1% had hypertension, 47.1% had dyslipidemia, and 36.2% had diabetes mellitus. We analyzed 433 patients (27.1%) with kidney failure and 1167 (72.9%) without kidney failure. Patients with kidney failure were associated with functional class III-IV (54.1% vs 40.8%) and metabolic syndrome (65.3% vs 51.9%, P<.01). The average unit cost was €10,711.40. The corrected cost in the presence of kidney failure was €14,868.20 vs €9,364.50 (P=.001). During follow-up, 11.7% patients developed ischemic heart disease, 18.8% developed kidney failure, and 36.1% developed heart failure exacerbation. Comorbidity associated with heart failure is high. The presence of kidney failure increases the use of health resources and leads to higher costs within the National Health System. Copyright © 2014 Sociedad Española de Cardiología. Published by Elsevier Espana. All rights reserved.

Bidirectional Cardio-Respiratory Interactions in Heart Failure.

PubMed

Radovanović, Nikola N; Pavlović, Siniša U; Milašinović, Goran; Kirćanski, Bratislav; Platiša, Mirjana M

2018-01-01

We investigated cardio-respiratory coupling in patients with heart failure by quantification of bidirectional interactions between cardiac (RR intervals) and respiratory signals with complementary measures of time series analysis. Heart failure patients were divided into three groups of twenty, age and gender matched, subjects: with sinus rhythm (HF-Sin), with sinus rhythm and ventricular extrasystoles (HF-VES), and with permanent atrial fibrillation (HF-AF). We included patients with indication for implantation of implantable cardioverter defibrillator or cardiac resynchronization therapy device. ECG and respiratory signals were simultaneously acquired during 20 min in supine position at spontaneous breathing frequency in 20 healthy control subjects and in patients before device implantation. We used coherence, Granger causality and cross-sample entropy analysis as complementary measures of bidirectional interactions between RR intervals and respiratory rhythm. In heart failure patients with arrhythmias (HF-VES and HF-AF) there is no coherence between signals ( p < 0.01), while in HF-Sin it is reduced ( p < 0.05), compared with control subjects. In all heart failure groups causality between signals is diminished, but with significantly stronger causality of RR signal in respiratory signal in HF-VES. Cross-sample entropy analysis revealed the strongest synchrony between respiratory and RR signal in HF-VES group. Beside respiratory sinus arrhythmia there is another type of cardio-respiratory interaction based on the synchrony between cardiac and respiratory rhythm. Both of them are altered in heart failure patients. Respiratory sinus arrhythmia is reduced in HF-Sin patients and vanished in heart failure patients with arrhythmias. Contrary, in HF-Sin and HF-VES groups, synchrony increased, probably as consequence of some dominant neural compensatory mechanisms. The coupling of cardiac and respiratory rhythm in heart failure patients varies depending on the presence

Role of HSF1-upregulated AC6 in ameliorating heart failure in mice.

PubMed

The, Erlinda; Du, Peizhao; Chang, Yaowei; Dai, Fangjie; Wei, Chunyan; Li, Jiming

2016-10-01

Our previous studies discovered that Heat shock factor 1(HSF1) can alleviate pressure overload induced heart failure in mice. However, its molecular mechanisms are yet to be further explained. Many studies have already verified that Adenylyl Cyclase 6 (AC6) can ameliorate heart failure, but it is still unknown whether or not the pathway HSF1 is involved in the process. Our preliminary experiment showed that the expression level of AC6 is positively associated with HSF1. Therefore, in the present study, we aimed to explore whether HSF1 can play its role in ameliorating heart failure by regulating AC6, and how the potential internal mechanisms work. We applied the Transverse Aortic Constriction (TAC) for 4 weeks to develop the C57BL/6 mice pressure overload induced heart failure model. First, the mice were divided into TAC group and SHAM group. Changes in the cardiac function and morphology of the mice were observed by an ultrasonic device and Masson staining slices, expressions of AC6 mRNA were observed by RT-QPCR, expressions of HSF1 and proteinkinase A (PKA) were examined by Western Blotting, and the levels of cyclic adenosine monophosphate (cAMP) from aortic blood were measured by ELISA. Second, the TAC group were further divided into subgroups of HSF1 transgene mice, HSF1 knockout mice and wild type mice, followed by the aforesaid observations. In the SHAM group, no obvious variations of cardiac function, AC6 mRNAHSF1, PKA, cAMP and other test results were found among each of the subgroups. Compared to the SHAM group, the TAC group presented clearly weakened heart functions, while, expressions of AC6 mRNA, HSF1, PKA and cAMP all recorded obvious increases. In the TAC group, compared to the WT subgroup, the HSF1 KO subgroup presented decreases in expressions of AC6 mRNA, HSF1, PKA and cAMP, and at the same time, the heart functions were weaker, while, the HSF1 TG subgroup recorded the contrary results. In the pressure overload heart failure model, HSF1 can

Atrial Fibrillation and Heart Failure - Cause or Effect?

PubMed

Prabhu, Sandeep; Voskoboinik, Aleksandr; Kaye, David M; Kistler, Peter M

2017-09-01

There are emerging epidemics of atrial fibrillation (AF) and heart failure in most developed countries, with a significant health burden. Due to many shared pathophysiological mechanisms, which facilitate the maintenance of each condition, AF and heart failure co-exist in up to 30% of patients. In the circumstance where known structural causes of heart failure (such as myocardial infarction) are absent, patients presenting with both conditions present a unique challenge, particularly as the temporal relationship of each condition can often remain elusive from the clinical history. The question of whether the AF is driving, or significantly contributing to the left ventricular (LV) dysfunction, rather than merely a consequence of heart failure, has become ever more pertinent, especially as catheter ablation now offers a significant advancement over existing rhythm control strategies. This paper will review the inter-related physiological drivers of AF and heart failure before considering the implications from the outcomes of recent clinical trials in patients with AF and heart failure. Copyright © 2017 Australian and New Zealand Society of Cardiac and Thoracic Surgeons (ANZSCTS) and the Cardiac Society of Australia and New Zealand (CSANZ). Published by Elsevier B.V. All rights reserved.

The role of the autonomic nervous system in the resting tachycardia of human hyperthyroidism.

PubMed

Maciel, B C; Gallo, L; Marin Neto, J A; Maciel, L M; Alves, M L; Paccola, G M; Iazigi, N

1987-02-01

The mechanisms that control resting heart rate in hyperthyroidism were evaluated in six patients before and after treatment with propylthiouracil. The patients were subjected to pharmacological blockade under resting conditions in two experimental sessions: first session, propranolol (0.2 mg/kg body weight); second session, atropine (0.04 mg/kg body weight) followed by propranolol (0.2 mg/kg body weight). All drugs were administered intravenously. Resting heart rate was significantly reduced from 100 +/- 6.5 beats/min to 72 +/- 2.5 beats/min (P less than 0.005) after clinical and laboratory control of the disease. After double blockade, intrinsic heart rate was reduced from 105 +/- 6.8 beats/min before treatment to 98 +/- 6.0 beats/min after treatment (P less than 0.025). The reduction in heart rate caused by propranolol was not significantly different before (-13 +/- 1.4 beats/min) and after (-9 +/- 1.0 beats/min) propylthiouracil. In contrast, atropine induced a higher elevation of heart rate after treatment (45 +/- 8.6 beats/min) than before treatment (26 +/- 4.0 beats/min). The present results suggest no appreciable participation of the sympathetic component of the autonomic nervous system in the tachycardia of hyperthyroidism, at least under the conditions of the present study. The small change observed in intrinsic heart rate, although significant, seems to indicate that this is not the most important mechanism involved in this tachycardia. Our results suggest that an important reduction in the efferent activity of the parasympathetic component participates in the mechanisms that modify resting heart rte in hyperthyroidism.

Postural tachycardia syndrome and inappropriate sinus tachycardia: role of autonomic modulation and sinus node automaticity.

PubMed

Nwazue, Victor C; Paranjape, Sachin Y; Black, Bonnie K; Biaggioni, Italo; Diedrich, André; Dupont, William D; Robertson, David; Raj, Satish R

2014-04-10

Inappropriate sinus tachycardia (IST) and postural tachycardia syndrome (POTS) are 2 disorders characterized by sinus tachycardia. It is debated whether the pathophysiology of IST and POTS results from abnormal autonomic regulation or abnormal sinus node function. We hypothesized that intrinsic heart rate (IHR) after autonomic blockade would be increased in patients with IST but not POTS. We enrolled 48 POTS patients, 8 IST patients, and 17 healthy control (HC) subjects. Intravenous propranolol and atropine were given to block the sympathetic and parasympathetic limbs of the autonomic nervous system in order to determine the IHR. Patients with IST have a higher sympathetic contribution to heart rate when compared with POTS patients (31±13 bpm versus 12±7 bpm, P<0.001) and HC (8±4 bpm; P<0.001) and a trend to less parasympathetic contribution than POTS and HC (IST: 31±11 bpm versus POTS: 46±11 bpm versus HC: 48±11 bpm, ANOVA P=0.108). IHR was not significantly different between IST and either POTS or HC (IST: 111±11 bpm versus POTS: 108±11 bpm versus HC: 106±12 bpm, ANOVA P=0.237). IST patients have more sympathetic tone when compared with either POTS or HC, but IST patients do not have abnormal sinus node automaticity. These data suggest that the treatment of IST and POTS should focus on sympatholysis, reserving sinus node modification for patients with continued debilitating symptoms after beta-blockade and possibly ivabradine. http://clinicaltrials.gov/. Unique identifier: NCT00262470.

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

Influenza infection and heart failure-vaccination may change heart failure prognosis?

PubMed

Kadoglou, Nikolaos P E; Bracke, Frank; Simmers, Tim; Tsiodras, Sotirios; Parissis, John

2017-05-01

The interaction of influenza infection with the pathogenesis of acute heart failure (AHF) and the worsening of chronic heart failure (CHF) is rather complex. The deleterious effects of influenza infection on AHF/CHF can be attenuated by specific immunization. Our review aimed to summarize the efficacy, effectiveness, safety, and dosage of anti-influenza vaccination in HF. In this literature review, we searched MEDLINE and EMBASE from January 1st 1966 to December 31st, 2016, for studies examining the association between AHF/CHF, influenza infections, and anti-influenza immunizations. We used broad criteria to increase the sensitivity of the search. HF was a prerequisite for our search. The search fields used included "heart failure," "vaccination," "influenza," "immunization" along with variants of these terms. No restrictions on the type of study design were applied. The most common clinical scenario is exacerbation of pre-existing CHF by influenza infection. Scarce evidence supports a potential positive association of influenza infection with AHF. Vaccinated patients with pre-existing CHF have reduced all-cause morbidity and mortality, but effects are not consistently documented. Immunization with higher antigen quantity may confer additional protection, but such aggressive approach has not been generally advocated. Further studies are needed to delineate the role of influenza infection on AHF/CHF pathogenesis and maintenance. Annual anti-influenza vaccination appears to be an effective measure for secondary prevention in HF. Better immunization strategies and more efficacious vaccines are urgently necessary.

Nurses' attitudes toward family importance in heart failure care.

PubMed

Gusdal, Annelie K; Josefsson, Karin; Thors Adolfsson, Eva; Martin, Lene

2017-03-01

Support from the family positively affects self-management, patient outcomes and the incidence of hospitalizations among patients with heart failure. To involve family members in heart failure care is thus valuable for the patients. Registered nurses frequently meet family members of patients with heart failure and the quality of these encounters is likely to be influenced by the attitudes registered nurses hold toward families. To explore registered nurses' attitudes toward the importance of families' involvement in heart failure nursing care and to identify factors that predict the most supportive attitudes. Cross-sectional, multicentre web-survey study. A sample of 303 registered nurses from 47 hospitals and 30 primary health care centres completed the instrument Families' Importance in Nursing Care - Nurses' Attitudes. Overall, registered nurses were supportive of families' involvement. Nonetheless, attitudes toward inviting families to actively take part in heart failure nursing care and involve families in planning of care were less supportive. Factors predicting the most supportive attitudes were to work in a primary health care centre, a heart failure clinic, a workplace with a general approach toward families, to have a postgraduate specialization, education in cardiac and/or heart failure nursing care, and a competence to work with families. Experienced registered nurses in heart failure nursing care can be encouraged to mentor their younger and less experienced colleagues to strengthen their supportive attitudes toward families. Registered nurses who have designated consultation time with patients and families, as in a nurse-led heart failure clinic, may have the most favourable condition for implementing a more supportive approach to families.

The Impact of Worsening Heart Failure in the United States

PubMed Central

Cooper, Lauren B.; DeVore, Adam D.; Felker, G. Michael

2015-01-01

Synopsis In-hospital worsening heart failure represents a clinical scenario in which a patient hospitalized for treatment of acute heart failure experiences a worsening of their condition while in the hospital, requiring escalation of therapy. In-hospital worsening heart failure is associated with worse in-hospital and post-discharge outcomes. In-hospital worsening heart failure is increasingly being used as an endpoint, or as part of a combined endpoint, in many clinical trials in acute heart failure. This endpoint has advantages over other endpoints commonly used in acute and chronic heart failure trials, such as dyspnea relief and mortality or rehospitalization. Despite the extensive study of this condition, no treatment strategies have been approved for the prevention of this condition. However, several prediction models have been developed to identify worsening heart failure. Continued study in this area is warranted. PMID:26462100

Loeffler Endocarditis: A Unique Presentation of Right-Sided Heart Failure Due to Eosinophil-Induced Endomyocardial Fibrosis.

PubMed

Alam, Amit; Thampi, Shankar; Saba, Shahryar G; Jermyn, Rita

2017-01-01

Loeffler endocarditis is a rare restrictive cardiomyopathy caused by abnormal endomyocardial infiltration of eosinophils, with subsequent tissue damage from degranulation, eventually leading to fibrosis. Although an uncommon entity, it is still a disease with significant morbidity and mortality. Often identified only at late stages, treatment options are limited once fibrosis occurs, usually requiring heart failure medications or surgical intervention. We present a unique case of a woman with remote history of hypereosinophilic syndrome, attributed to treatment of rheumatoid arthritis with infliximab, who presented with symptoms of heart failure refractory to medical management and was found to have Loeffler endocarditis. The severe progression of the disease required surgical intervention with endocardial stripping to treat the right-sided diastolic heart failure.

Improving Patient Outcomes With Oral Heart Failure Medications.

PubMed

Sherrod, Melissa M; Cheek, Dennis J; Seale, Ashlie

2016-05-01

Hospitals are under immense pressure to reduce heart failure readmissions that occur within 30 days of discharge, and to improve the quality of care for these patients. Penalties mandated by the Affordable Care Act decrease hospital reimbursement and ultimately the overall cost of caring for these patients increases if they are not well managed. Approximately 25% of patients hospitalized for heart failure are at high risk for readmission and these rates have not changed over the past decade. As a result of an aging population, the incidence of heart failure is expected to increase to one in five Americans over the age of 65. Pharmacologic management can reduce the risk of death and help prevent unnecessary hospitalizations. Healthcare providers who have knowledge of heart failure medications and drug interactions and share this information with their patients contribute to improved long-term survival and physical functioning as well as fewer hospitalizations and a delay of progressive worsening of heart failure.

Novel prognostic tissue markers in congestive heart failure.

PubMed

Stone, James R

2015-01-01

Heart failure is a relatively common disorder associated with high morbidity, mortality, and economic burden. Better tools to predict outcomes for patients with heart failure could allow for better decision making concerning patient treatment and management and better utilization of health care resources. Endomyocardial biopsy offers a mechanism to pathologically diagnose specific diseases in patients with heart failure, but such biopsies can often be negative, with no specific diagnostic information. Novel tissue markers in endomyocardial biopsies have been identified that may be useful in assessing prognosis in heart failure patients. Such tissue markers include ubiquitin, Gremlin-1, cyclophilin A, and heterogeneous nuclear ribonucleoprotein C. In some cases, tissue markers have been found to be independent of and even superior to clinical indices and serum markers in predicting prognosis for heart failure patients. In some cases, these novel tissue markers appear to offer prognostic information even in the setting of an otherwise negative endomyocardial biopsy. Copyright © 2014 Elsevier Inc. All rights reserved.

Systems Biology and Biomechanical Model of Heart Failure

PubMed Central

Louridas, George E; Lourida, Katerina G

2012-01-01

Heart failure is seen as a complex disease caused by a combination of a mechanical disorder, cardiac remodeling and neurohormonal activation. To define heart failure the systems biology approach integrates genes and molecules, interprets the relationship of the molecular networks with modular functional units, and explains the interaction between mechanical dysfunction and cardiac remodeling. The biomechanical model of heart failure explains satisfactorily the progression of myocardial dysfunction and the development of clinical phenotypes. The earliest mechanical changes and stresses applied in myocardial cells and/or myocardial loss or dysfunction activate left ventricular cavity remodeling and other neurohormonal regulatory mechanisms such as early release of natriuretic peptides followed by SAS and RAAS mobilization. Eventually the neurohormonal activation and the left ventricular remodeling process are leading to clinical deterioration of heart failure towards a multi-organic damage. It is hypothesized that approaching heart failure with the methodology of systems biology we promote the elucidation of its complex pathophysiology and most probably we can invent new therapeutic strategies. PMID:22935019

Heart failure and atrial fibrillation: current concepts and controversies.

PubMed Central

Van den Berg, M. P.; Tuinenburg, A. E.; Crijns, H. J.; Van Gelder, I. C.; Gosselink, A. T.; Lie, K. I.

1997-01-01

Heart failure and atrial fibrillation are very common, particularly in the elderly. Owing to common risk factors both disorders are often present in the same patient. In addition, there is increasing evidence of a complex, reciprocal relation between heart failure and atrial fibrillation. Thus heart failure may cause atrial fibrillation, with electromechanical feedback and neurohumoral activation playing an important mediating role. In addition, atrial fibrillation may promote heart failure; in particular, when there is an uncontrolled ventricular rate, tachycardiomyopathy may develop and thereby heart failure. Eventually, a vicious circle between heart failure and atrial fibrillation may form, in which neurohumoral activation and subtle derangement of rate control are involved. Treatment should aim at unloading of the heart, adequate control of ventricular rate, and correction of neurohumoral activation. Angiotensin converting enzyme inhibitors may help to achieve these goals. Treatment should also include an attempt to restore sinus rhythm through electrical cardioversion, though appropriate timing of cardioversion is difficult. His bundle ablation may be used to achieve adequate rate control in drug refractory cases. PMID:9155607

Effects of intravenous home dobutamine in palliative end-stage heart failure on quality of life, heart failure hospitalization, and cost expenditure.

PubMed

Martens, Pieter; Vercammen, Jan; Ceyssens, Wendy; Jacobs, Linda; Luwel, Evert; Van Aerde, Herwig; Potargent, Peter; Renaers, Monique; Dupont, Matthias; Mullens, Wilfried

2018-01-17

In patients with palliative end-stage heart failure, interventions that could provide symptomatic relief and prevent hospital admissions are important. Ambulatory continuous intravenous inotropes have been advocated by guidelines for such a purpose. We sought to determine the effect of intravenous dobutamine on symptomatic status, hospital stay, mortality, and cost expenditure. All consecutive end-stage heart failure patients not amenable for advanced therapies and discharged with continuous intravenous home dobutamine from a single tertiary centre between April 2011 and January 2017 were retrospectively analysed. Dobutamine (fixed dose) was infused through a single-lumen central venous catheter with a small pump that was refilled by a nurse on a daily basis. Symptomatic status was longitudinally assessed as the change in New York Heart Association class and patient global assessment scale. Antecedent and incident heart failure hospitalizations were determined in a paired fashion, and cost impact was assessed. A total of 21 patients (age 77 ± 9 years) were followed up for 869 ± 647 days. At first follow-up (6 ± 1 weeks) after the initiation of dobutamine, patients had a significant improvement in New York Heart Association class (-1.29 ± 0.64; P < 0.001), global assessment scale (<0.001), and N-terminal pro-brain natriuretic peptide (6247 vs. 2543 pg/mL; P = 0.033). Incident heart failure hospitalizations assessed at 3, 6, and 12 months were significantly reduced (P < 0.001 for all) in comparison with antecedent heart failure hospitalizations over the same time period. Cost expenditure was significantly lower at 3 (P < 0.001), 6 (P = 0.005), and 12 months (P = 0.001) after initiation of dobutamine. Mortality rate at 1 year was 48% with 9/12 (75%) patients dying at home, most often from progressive pump failure. Continuous intravenous home dobutamine in patients with palliative end-stage heart failure is feasible and associated with

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

Management of Sleep Disordered Breathing in Patients with Heart Failure.

PubMed

Oates, Connor P; Ananthram, Manjula; Gottlieb, Stephen S

2018-06-01

This paper reviews treatment options for sleep disordered breathing (SDB) in patients with heart failure. We sought to identify therapies for SDB with the best evidence for long-term use in patients with heart failure and to minimize uncertainties in clinical practice by examining frequently discussed questions: what is the role of continuous positive airway pressure (CPAP) in patients with heart failure? Is adaptive servo-ventilation (ASV) safe in patients with heart failure? To what extent is SDB a modifiable risk factor? Consistent evidence has demonstrated that the development of SDB in patients with heart failure is a poor prognostic indicator and a risk factor for cardiovascular mortality. However, despite numerous available interventions for obstructive sleep apnea and central sleep apnea, it remains unclear what effect these therapies have on patients with heart failure. To date, all major randomized clinical trials have failed to demonstrate a survival benefit with SDB therapy and one major study investigating the use of adaptive servo-ventilation demonstrated harm. Significant questions persist regarding the management of SDB in patients with heart failure. Until appropriately powered trials identify a treatment modality that increases cardiovascular survival in patients with SDB and heart failure, a patient's heart failure management should remain the priority of medical care.

Safe Hydration Volume to Prevent Contrast-induced Acute Kidney Injury and Worsening Heart Failure in Patients With Heart Failure and Preserved Ejection Fraction After Cardiac Catheterization.

PubMed

Bei, Wei-Jie; Wang, Kun; Li, Hua-Long; Lin, Kai-Yang; Guo, Xiao-Sheng; Chen, Shi-Qun; Liu, Yong; Yi, Shi-Xin; Luo, De-Mou; Chen, Ji-Yan; Tan, Ning

2017-09-01

Few studies have investigated the efficacy and safety of hydration to prevent contrast-induced acute kidney injury (CI-AKI) and worsening heart failure (WHF) after cardiac catheterization in heart failure and preserved ejection fraction (HFpEF; HF and EF ≥50%) patients. We recruited 1206 patients with HFpEF undergoing cardiac catheterization with periprocedural hydration volume/weight (HV/W) ratio data and investigated the relationship between hydration volumes and risk of CI-AKI and WHF. Incidence of CI-AKI was not significantly reduced in individuals with higher HV/W [quartile (Q) 1, Q2, Q3, and Q4: 9.7%, 10.2%, 12.7%, and 12.2%, respectively; P = 0.219]. Multivariate analysis indicated that higher HV/W ratios were not associated with decreased CI-AKI risks [Q2 vs. Q1: odds ratio (OR), 0.95; Q3 vs. Q1: OR, 1.07; Q4 vs. Q1: OR, 0.92; all P > 0.05]. According to multivariate analysis, higher HV/W significantly increased the WHF risk (Q4 vs. Q1: adjusted OR, 8.13 and 95% confidence interval, 1.03-64.02; P = 0.047). CI-AKI and WHF were associated with a significantly increased risk of long-term mortality (mean follow-up, 2.33 years). For HFpEF patients, an excessively high hydration volume might not be associated with lower risk of CI-AKI but may increase the risk of postprocedure WHF.

Heart Failure: From Research to Clinical Practice.

PubMed

Islam, Md Shahidul

2018-01-01

"Heart failure: from research to clinical practice", a collection of selected reviews, which comes out also as a book, covers essentially all important aspects of heart failure, including the pathogenesis, clinical features, biomarkers, imaging techniques, medical treatment and surgical treatments, use of pacemakers and implantable cardioverter defibrillators, and palliative care. The reviews include essential background information, state of the art, critical and in-depth analysis, and directions for future researches for elucidation of the unresolved issues. Everyone interested in heart failure is expected to find this compilation helpful for a deeper understanding of some of the complex issues.

Decongestion: Diuretics and other therapies for hospitalized heart failure.

PubMed

Vazir, Ali; Cowie, Martin R

2016-04-01

Acute heart failure (AHF) is a potentially life-threatening clinical syndrome, usually requiring hospital admission. Often the syndrome is characterized by congestion, and is associated with long hospital admissions and high risk of readmission and further healthcare expenditure. Despite a limited evidence-base, diuretics remain the first-line treatment for congestion. Loop diuretics are typically the first-line diuretic strategy with some evidence that initial treatment with continuous infusion or boluses of high-dose loop diuretic is superior to an initial lower dose strategy. In patients who have impaired responsiveness to diuretics, the addition of an oral thiazide or thiazide-like diuretic to induce sequential nephron blockade can be beneficial. The use of intravenous low-dose dopamine is no longer supported in heart failure patients with preserved systolic blood pressure and its use to assist diuresis in patients with low systolic blood pressures requires further study. Mechanical ultrafiltration has been used to treat patients with heart failure and fluid retention, but the evidence-base is not robust, and its place in clinical practice is yet to be established. Several novel pharmacological agents remain under investigation. Copyright © 2015 Cardiological Society of India. Published by Elsevier B.V. All rights reserved.

Fatigue in older adults with stable heart failure.

PubMed

Stephen, Sharon A

2008-01-01

The purpose of this study was to describe fatigue and the relationships among fatigue intensity, self-reported functional status, and quality of life in older adults with stable heart failure. A descriptive, correlational design was used to collect quantitative data with reliable and valid instruments. Fifty-three eligible volunteers completed a questionnaire during an interview. Those with recent changes in their medical regimen, other fatigue-inducing illnesses, and isolated diastolic dysfunction were excluded. Fatigue intensity (Profile of Mood States fatigue subscale) was associated with lower quality of life, perceived health, and satisfaction with life. Fatigue was common, and no relationship was found between fatigue intensity and self-reported functional status. Marital status was the only independent predictor of fatigue. In stable heart failure, fatigue is a persistent symptom. Clinicians need to ask patients about fatigue and assess the impact on quality of life. Self-reported functional status cannot serve as a proxy measure for fatigue.

Chronobiology of death in heart failure.

PubMed

Ribas, Nuria; Domingo, Maite; Gastelurrutia, Paloma; Ferrero-Gregori, Andreu; Rull, Pilar; Noguero, Mariana; Garcia, Carmen; Puig, Teresa; Cinca, Juan; Bayes-Genis, Antoni

2014-05-01

In the general population, heart events occur more often during early morning, on Mondays, and during winter. However, the chronobiology of death in heart failure has not been analyzed. The aim of this study was to determine the circadian, day of the week, and seasonal variability of all-cause mortality in chronic heart failure. This was an analysis of all consecutive heart failure patients followed in a heart failure unit from January 2003 to December 2008. The circadian moment of death was analyzed at 6-h intervals and was determined by reviewing medical records and by information provided by the relatives. Of 1196 patients (mean [standard deviation] age, 69 [13] years; 62% male), 418 (34.9%) died during a mean (standard deviation) follow-up of 29 (21) months. Survivors were younger, had higher body mass index, left ventricular ejection fraction, glomerular filtration rate, hemoglobin and sodium levels, and lower Framingham risk scores, amino-terminal pro-B type natriuretic peptide, troponin T, and urate values. They were more frequently treated with angiotensin receptor blockers, beta-blockers, mineralocorticoids receptor antagonists, digoxin, nitrates, hydralazine, statins, loop diuretics, and thiazides. The analysis of the circadian and weekly variability did not reveal significant differences between the four 6-h intervals or the days of the week. Mortality occurred more frequently during the winter (30.6%) compared with the other seasons (P = .024). All cause mortality does not follow a circadian pattern, but a seasonal rhythm in patients with heart failure. This finding is in contrast to the circadian rhythmicity of cardiovascular events reported in the general population. Copyright © 2013 Sociedad Española de Cardiología. Published by Elsevier Espana. All rights reserved.

[Surgical Regeneration Therapy Using Myoblast Sheets for Severe Heart Failure].

PubMed

Sawa, Yoshiki

2017-01-01

Heart failure is a life-threatening disorder worldwide, and the current end-stage therapies for severe heart failure are replacement therapies such as ventricular-assist devices and heart transplantation. Although these therapies have been reported to be useful, there are many issues in terms of the durability, complications, limited donors, adverse effect of continuous administration of immunosuppressive agents, and high costs involved. Recently, regenerative therapy based on genetic, cellular, or tissue engineering techniques has gained attention as a new therapy to overcome the challenges encountered in transplantation medicine. We focused on skeletal myoblasts as the source of progenitor cells for autologous cell transplantation and the cell-sheet technique for site-specific implantation. In vitro studies have reported that myoblast sheets secrete cytoprotective and angiogenic cytokines such as hepatocyte growth factor (HGF). Additionally, in vivo studies using large and small animal models of heart failure, we have shown that myoblast sheets could improve diastolic and systolic performance and enhance angiogenesis and antifibrosis as well as the expression of several cytokines including HGF and vascular endothelial growth factor(VEGF) in the tissues at the transplanted site. Based on the results of these studies, we performed clinical trials using autologous myoblast sheets in ischemic cardiomyopathy (ICM) and dilated cardiomyopathy patients. Some patients showed left ventricular reverse remodeling and improved symptoms and exercise tolerance. Recently, multiple medical institutions including our institution successfully conducted an exploratory, uncontrolled, open-label phase II study in subjects with ICM to validate the efficacy and safety of autologous myoblast sheets. Moreover, as a novel cell source for regenerative medicine, our recent studies demonstrated that induced pluripotent stem cell-derived cardiomyocyte sheets showed electrical and

In-hospital and 3-year outcomes of heart failure patients in South India: The Trivandrum Heart Failure Registry.

PubMed

Sanjay, Ganapathi; Jeemon, Panniyammakal; Agarwal, Anubha; Viswanathan, Sunitha; Sreedharan, Madhu; Govindan, Vijayaraghavan; Gopalan, Bahuleyan Charantharalyil; Biju, R; Nair, Tiny; Prathapkumar, N; Krishnakumar, G; Rajalekshmi, N; Suresh, Krishnan; Park, Lawrence P; Huffman, Mark D; Harikrishnan, Sivadasanpillai

2018-06-06

Long-term data on outcomes of participants hospitalized with heart failure (HF) from low and middle-income countries are limited. In the Trivandrum Heart Failure Registry (THFR) in 2013, 1205 participants from 18 hospitals in Trivandrum, India were enrolled. Data were collected on demographics, clinical presentation, treatment and outcomes. We performed survival analyses, compared groups and evaluated the association between HF type and mortality, adjusting for covariates that predicted mortality in a global HF risk score. The mean (SD) age of participants was 61.2 (13.7) years. Ischemic heart disease was the most common etiology (72%). In-hospital mortality was higher for participants with heart-failure with reduced ejection fraction (HFrEF) (9.7%) compared to those with heart-failure with preserved ejection fraction (HFpEF) (4.8%, p = 0.003). After three years, 540 (44.8%) of all participants had died. All-cause mortality was lower for participants with HFpEF (40.8%) compared to HFrEF (46.2%, p = 0.049). In multivariable models, older age (hazard ratio [HR] 1.24 per decade, 95% CI 1.15, 1.33), NYHA class-IV symptoms (HR 2.80, 95% CI 1.43, 5.48), and higher serum creatinine (HR 1.12 per mg/dl, 95%CI 1.04, 1.22) were associated with all-cause mortality. Participants with HF in the THFR have high three-year all-cause mortality. Targeted hospital-based quality improvement initiatives are needed to improve survival during and after hospitalization for heart failure. Copyright © 2018 Elsevier Ltd. All rights reserved.

A holistic approach to managing a patient with heart failure.

PubMed

Duncan, Alison; Cunnington, Colin

2013-03-01

Despite varied and complex therapeutic strategies for managing patients with heart failure, the prognosis may remain poor in certain groups. Recognition that patients with heart failure frequently require input from many care groups formed the basis of The British Society of Heart Failure Annual Autumn Meeting in London (UK), in November 2012, entitled: 'Heart failure: a multidisciplinary approach'. Experts in cardiology, cardiac surgery, general practice, care of the elderly, palliative care and cardiac imaging shared their knowledge and expertise. The 2-day symposium was attended by over 500 participants from the UK, Europe and North America, and hosted physicians, nurses, scientists, trainees and representatives from the industry, as well as patient and community groups. The symposium, accredited by the Royal College of Physicians and the Royal College of Nursing, focused on the multidisciplinary approach to heart failure, in particular, current therapeutic advances, cardiac remodeling, palliative care, atrial fibrillation, heart rate-lowering therapies, management of acute heart failure and the management of patients with mitral regurgitation and heart failure.

Prolonged intra-aortic balloon pump support in biventricular heart failure induces right ventricular reverse remodeling.

PubMed

Ntalianis, Argyrios; Kapelios, Chris J; Kanakakis, John; Repasos, Evangelos; Pantsios, Christos; Nana, Emmeleia; Kontogiannis, Christos; Malliaras, Konstantinos; Tsamatsoulis, Michael; Kaldara, Elisabeth; Charitos, Christos; Nanas, John N

2015-08-01

Right ventricular dysfunction is associated with high morbidity and mortality in candidates for left ventricular assist device (LVAD) implantation or cardiac transplantation. We examined the effects of prolonged intra-aortic balloon pump (IABP) support on right ventricular, renal and hepatic functions in patients presenting with end-stage heart failure. Between March 2008 and June 2013, fifteen patients (mean age = 49.5 years; 14 men) with end-stage systolic heart failure (HF), contraindications for any life saving procedure (conventional cardiac surgery, heart transplantation, LVAD implantation) and right ventricular dysfunction were supported with the IABP. The patients remained on IABP support for a mean of 73 ± 50 days (median 72, range of 13-155). We measured the echocardiographic and hemodynamic changes in right ventricular function, and the changes in serum creatinine and bilirubin concentrations before and during IABP support. Mean right atrial pressure decreased from 12.7 ± 6.5 to 3.8 ± 3.3 (P < 0.001) and pulmonary artery pressure decreased from 35.7 ± 10.6 to 25 ± 8.4 mmHg (P = 0.001), while cardiac index increased from 1.5 ± 0.4 to 2.2 ± 0.7 l/m(2)/min (P = 0.003) and right ventricular stroke work index from 485 ± 228 to 688 ± 237 mmHg × ml/m(2) (P = 0.043). Right ventricular end-diastolic diameter decreased from 34.0 ± 6.5 mm to 27.8 ± 6.2 mm (P < 0.001) and tricuspid annular systolic tissue Doppler velocity increased from 9.6 ± 2.4 cm/s to 11.1 ± 2.3 cm/s (P = 0.029). Serum creatinine and bilirubin decreased from 2.1 ± 1.3 to 1.4 ± 0.6 mg/dl and 2.0 ± 1.0 to 0.9 ± 0.5 mg/dl, respectively (P = 0.002 and P < 0.001, respectively). Prolonged IABP support of patients presenting with end-stage heart failure and right ventricular dysfunction induced significant improvement in right ventricular and peripheral organ function. Copyright © 2015. Published by Elsevier Ireland Ltd.

Cyanobacteria blooms induce embryonic heart failure in an endangered fish species.

PubMed

Zi, Jinmei; Pan, Xiaofu; MacIsaac, Hugh J; Yang, Junxing; Xu, Runbing; Chen, Shanyuan; Chang, Xuexiu

2018-01-01

Cyanobacterial blooms drive water-quality and aquatic-ecosystem deterioration in eutrophic lakes worldwide, mainly owing to their harmful, secondary metabolites. The response of fish exposed to these cyanobacterial chemicals, however, remains largely unknown. In this paper, we employed an endangered fish species (Sinocyclocheilus grahami) in Dianchi Lake, China to evaluate the risks of cell-free exudates (MaE) produced by a dominant cyanobacterium (Microcystis aeruginosa) on embryo development, as well as the molecular mechanisms responsible. MaE (3d cultured) caused a reduction of fertilization (35.4%) and hatching (15.5%) rates, and increased mortality rates (≤90.0%) and malformation rate (27.6%), typically accompanied by heart failure. Proteomics analysis revealed that two greatest changed proteins - protein S100A1 (over-expressed 26 times compared with control) and myosin light chain (under-expressed 25 fold) - are closely associated with heart function. Further study revealed that heart failure was due to calcium ion imbalance and malformed cardiac structure. We conclude that harmful secondary metabolites from cyanobacteria may adversely affect embryo development in this endangered fish, and possibly contribute to its disappearance and unsuccessful recovery in Dianchi Lake. Hazardous consequences of substances released by cyanobacteria should raise concerns for managers addressing recovery of this and other imperiled species in affected lakes. Copyright © 2017 Elsevier B.V. All rights reserved.

A narrow QRS tachycardia and cannon A waves: What is the mechanism?

PubMed

Ali, Hussam; Epicoco, Gianluca; De Ambroggi, Guido; Lupo, Pierpaolo; Foresti, Sara; Cappato, Riccardo

2017-07-01

Regular narrow QRS tachycardia, particularly if well-tolerated, is usually considered a "benign" arrhythmia of a supraventricular origin. This case concerns an 82-year-old male with ischemic heart disease who presented with recurrent episodes of a narrow QRS tachycardia that was initially diagnosed and treated as atrial tachyarrhythmia. However, careful physical examination and ECG analysis established the correct diagnosis, and the patient was managed appropriately. Remarkably, the observation of irregular cannon A waves, and Lewis lead recording, confirmed atrioventricular dissociation during tachycardia and indicated its underlying mechanism. © 2016 Wiley Periodicals, Inc.

The renal nerves in chronic heart failure: efferent and afferent mechanisms

PubMed Central

Schiller, Alicia M.; Pellegrino, Peter R.; Zucker, Irving H.

2015-01-01

The function of the renal nerves has been an area of scientific and medical interest for many years. The recent advent of a minimally invasive catheter-based method of renal denervation has renewed excitement in understanding the afferent and efferent actions of the renal nerves in multiple diseases. While hypertension has been the focus of much this work, less attention has been given to the role of the renal nerves in the development of chronic heart failure (CHF). Recent studies from our laboratory and those of others implicate an essential role for the renal nerves in the development and progression of CHF. Using a rabbit tachycardia model of CHF and surgical unilateral renal denervation, we provide evidence for both renal efferent and afferent mechanisms in the pathogenesis of CHF. Renal denervation prevented the decrease in renal blood flow observed in CHF while also preventing increases in Angiotensin-II receptor protein in the microvasculature of the renal cortex. Renal denervation in CHF also reduced physiological markers of autonomic dysfunction including an improvement in arterial baroreflex function, heart rate variability, and decreased resting cardiac sympathetic tone. Taken together, the renal sympathetic nerves are necessary in the pathogenesis of CHF via both efferent and afferent mechanisms. Additional investigation is warranted to fully understand the role of these nerves and their role as a therapeutic target in CHF. PMID:26300788

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

Bmi1 limits dilated cardiomyopathy and heart failure by inhibiting cardiac senescence

PubMed Central

Gonzalez-Valdes, I.; Hidalgo, I.; Bujarrabal, A.; Lara-Pezzi, E.; Padron-Barthe, L.; Garcia-Pavia, P.; Gómez-del Arco, Pablo; Redondo, J.M.; Ruiz-Cabello, J.M.; Jimenez-Borreguero, L.J.; Enriquez, J.A.; de la Pompa, J.L.; Hidalgo, A.; Gonzalez, S.

2015-01-01

Dilated cardiomyopathy (DCM) is the most frequent cause of heart failure and the leading indication for heart transplantation. Here we show that epigenetic regulator and central transcriptional instructor in adult stem cells, Bmi1, protects against DCM by repressing cardiac senescence. Cardiac-specific Bmi1 deletion induces the development of DCM, which progresses to lung congestion and heart failure. In contrast, Bmi1 overexpression in the heart protects from hypertrophic stimuli. Transcriptome analysis of mouse and human DCM samples indicates that p16INK4a derepression, accompanied by a senescence-associated secretory phenotype (SASP), is linked to severely impaired ventricular dimensions and contractility. Genetic reduction of p16INK4a levels reverses the pathology of Bmi1-deficient hearts. In parabiosis assays, the paracrine senescence response underlying the DCM phenotype does not transmit to healthy mice. As senescence is implicated in tissue repair and the loss of regenerative potential in aging tissues, these findings suggest a source for cardiac rejuvenation. PMID:25751743

Heart Rate Dynamics During A Treadmill Cardiopulmonary Exercise Test in Optimized Beta-Blocked Heart Failure Patients

PubMed Central

Carvalho, Vitor Oliveira; Guimarães, Guilherme Veiga; Ciolac, Emmanuel Gomes; Bocchi, Edimar Alcides

2008-01-01

BACKGROUND Calculating the maximum heart rate for age is one method to characterize the maximum effort of an individual. Although this method is commonly used, little is known about heart rate dynamics in optimized beta-blocked heart failure patients. AIM The aim of this study was to evaluate heart rate dynamics (basal, peak and % heart rate increase) in optimized beta-blocked heart failure patients compared to sedentary, normal individuals (controls) during a treadmill cardiopulmonary exercise test. METHODS Twenty-five heart failure patients (49±11 years, 76% male), with an average LVEF of 30±7%, and fourteen controls were included in the study. Patients with atrial fibrillation, a pacemaker or noncardiovascular functional limitations or whose drug therapy was not optimized were excluded. Optimization was considered to be 50 mg/day or more of carvedilol, with a basal heart rate between 50 to 60 bpm that was maintained for 3 months. RESULTS Basal heart rate was lower in heart failure patients (57±3 bpm) compared to controls (89±14 bpm; p<0.0001). Similarly, the peak heart rate (% maximum predicted for age) was lower in HF patients (65.4±11.1%) compared to controls (98.6±2.2; p<0.0001). Maximum respiratory exchange ratio did not differ between the groups (1.2±0.5 for controls and 1.15±1 for heart failure patients; p=0.42). All controls reached the maximum heart rate for their age, while no patients in the heart failure group reached the maximum. Moreover, the % increase of heart rate from rest to peak exercise between heart failure (48±9%) and control (53±8%) was not different (p=0.157). CONCLUSION No patient in the heart failure group reached the maximum heart rate for their age during a treadmill cardiopulmonary exercise test, despite the fact that the percentage increase of heart rate was similar to sedentary normal subjects. A heart rate increase in optimized beta-blocked heart failure patients during cardiopulmonary exercise test over 65% of the

Natriuretic peptide-guided management in heart failure.

PubMed

Chioncel, Ovidiu; Collins, Sean P; Greene, Stephen J; Ambrosy, Andrew P; Vaduganathan, Muthiah; Macarie, Cezar; Butler, Javed; Gheorghiade, Mihai

2016-08-01

Heart failure is a clinical syndrome that manifests from various cardiac and noncardiac abnormalities. Accordingly, rapid and readily accessible methods for diagnosis and risk stratification are invaluable for providing clinical care, deciding allocation of scare resources, and designing selection criteria for clinical trials. Natriuretic peptides represent one of the most important diagnostic and prognostic tools available for the care of heart failure patients. Natriuretic peptide testing has the distinct advantage of objectivity, reproducibility, and widespread availability.The concept of tailoring heart failure management to achieve a target value of natriuretic peptides has been tested in various clinical trials and may be considered as an effective method for longitudinal biomonitoring and guiding escalation of heart failure therapies with overall favorable results.Although heart failure trials support efficacy and safety of natriuretic peptide-guided therapy as compared with usual care, the relationship between natriuretic peptide trajectory and clinical benefit has not been uniform across the trials, and certain subgroups have not shown robust benefit. Furthermore, the precise natriuretic peptide value ranges and time intervals of testing are still under investigation. If natriuretic peptides fail to decrease following intensification of therapy, further work is needed to clarify the optimal pharmacologic approach. Despite decreasing natriuretic peptide levels, some patients may present with other high-risk features (e.g. elevated troponin). A multimarker panel investigating multiple pathological processes will likely be an optimal alternative, but this will require prospective validation.Future research will be needed to clarify the type and magnitude of the target natriuretic peptide therapeutic response, as well as the duration of natriuretic peptide-guided therapy in heart failure patients.

Positive inotropes in heart failure: a review article

PubMed Central

Amin, Ahmad; Maleki, Majid

2012-01-01

Increasing myocardial contractility has long been considered a big help for patients with systolic heart failure, conferring an augmented haemodynamic profile in terms of higher cardiac output, lower cardiac filling pressure and better organ perfusion. Though concerns have been raised over the safety issues regarding the clinical trials of different inotropes in hearts with systolic dysfunction, they still stand as a main therapeutic strategy in many centres dealing with such patients. They must be used as short in duration, low in dose and stopped as early as possible. Evidence-based guidelines have provided clinicians with valuable data for better applying inotropes in heart failure patients. In this paper, the authors address clinical trials with different agents used for increasing cardiac contractility in heart failure patients. Furthermore, the authors focus on recent guidelines on making the most out of inotropes in heart failure patients. PMID:27326019

Interesting Electrophysiological Findings in a Patient With Coincidental Right Ventricular Outflow Tract and Atrioventricular Nodal Reentrant Tachycardia

PubMed Central

Ozin, Bulent; Pirat, Bahar; Muderrisoglu, Haldun

2004-01-01

Tachycardia induced tachycardias are not common in clinical practice, and it is believed that most cases of double tachycardia are coincidental. The existence of two different tachycardias in the same patient almost always poses problems in the electrophysiology laboratory. However, in rare instances, the emergence of a second tachycardia can actually provide invaluable information about the first one. In this report, we describe a 30-year-old woman who presented with palpitations. Electrophysiological study revealed that atrial programmed stimulation at baseline induced right ventricular outflow tract (RVOT) tachycardia and supraventricular tachycardia. The study also showed that each of the tachycardias was able to induce the other. A short run of RVOT tachycardia during supraventricular tachycardia was able to entrain the latter. This finding provided important information about the nature of the supraventricular tachycardia, which proved to be atrioventricular nodal reentrant tachycardia. Both of these tachycardias were successfully ablated, and the patient’s palpitations disappeared. PMID:16943976

Targeting Inflammation in Heart Failure with Histone Deacetylase Inhibitors

PubMed Central

McKinsey, Timothy A

2011-01-01

Cardiovascular insults such as myocardial infarction and chronic hypertension can trigger the heart to undergo a remodeling process characterized by myocyte hypertrophy, myocyte death and fibrosis, often resulting in impaired cardiac function and heart failure. Pathological cardiac remodeling is associated with inflammation, and therapeutic approaches targeting inflammatory cascades have shown promise in patients with heart failure. Small molecule histone deacetylase (HDAC) inhibitors block adverse cardiac remodeling in animal models, suggesting unforeseen potential for this class of compounds for the treatment of heart failure. In addition to their beneficial effects on myocardial cells, HDAC inhibitors have potent antiinflammatory actions. This review highlights the roles of HDACs in the heart and the potential for using HDAC inhibitors as broad-based immunomodulators for the treatment of human heart failure. PMID:21267510

Mitochondrial function as a therapeutic target in heart failure

PubMed Central

Brown, David A.; Perry, Justin B.; Allen, Mitchell E.; Sabbah, Hani N.; Stauffer, Brian L.; Shaikh, Saame Raza; Cleland, John G. F.; Colucci, Wilson S.; Butler, Javed; Voors, Adriaan A.; Anker, Stefan D.; Pitt, Bertram; Pieske, Burkert; Filippatos, Gerasimos; Greene, Stephen J.; Gheorghiade, Mihai

2017-01-01

Heart failure is a pressing worldwide public-health problem with millions of patients having worsening heart failure. Despite all the available therapies, the condition carries a very poor prognosis. Existing therapies provide symptomatic and clinical benefit, but do not fully address molecular abnormalities that occur in cardiomyocytes. This shortcoming is particularly important given that most patients with heart failure have viable dysfunctional myocardium, in which an improvement or normalization of function might be possible. Although the pathophysiology of heart failure is complex, mitochondrial dysfunction seems to be an important target for therapy to improve cardiac function directly. Mitochondrial abnormalities include impaired mitochondrial electron transport chain activity, increased formation of reactive oxygen species, shifted metabolic substrate utilization, aberrant mitochondrial dynamics, and altered ion homeostasis. In this Consensus Statement, insights into the mechanisms of mitochondrial dysfunction in heart failure are presented, along with an overview of emerging treatments with the potential to improve the function of the failing heart by targeting mitochondria. PMID:28004807

Primary health care nurses and heart failure education: a survey.

PubMed

Gilmour, Jean; Strong, Alison; Chan, Helen; Hanna, Sue; Huntington, Annette

2014-09-01

Heart failure education contributes to effective self-management. New Zealand primary health care nurses' contributions to heart failure educational activities have not been researched. To identify primary health care nurses' heart failure educational activities in terms of duration and frequency, topics covered, resources used and strategies for Maori and other ethnic groups. A cross-sectional survey of a random sample of 961 primary health care nurses using a postal questionnaire. Of 630 respondents (65.5%), 369 worked with patients with heart failure and 339 provided heart failure education. One-third of respondents providing education (33.3%; n=113) delivered sessions from 16 to 60 minutes. The main educational topics covered were on the physical aspects of heart failure; prognosis, spiritual/existential and psychosocial topics were least often addressed. One-quarter of the group providing education did not use educational resources (n=86). The majority of respondents reported they would find more education about heart failure useful or very useful (80.2%; n=292), along with nurse practitioner support (64.7%; n=229). Maori-centred services and resources and involving whanau/family in education were the most frequently mentioned Maori-specific education strategies. A consistent approach to heart failure education is important to address knowledge gaps in a timely manner. This study affirms the contribution made by primary health care nurses in chronic illness education and highlights the need for further development and investment in ongoing heart failure nursing education and specialist nursing support.

Randomised controlled trial of specialist nurse intervention in heart failure

PubMed Central

Blue, Lynda; Lang, Elanor; McMurray, John J V; Davie, Andrew P; McDonagh, Theresa A; Murdoch, David R; Petrie, Mark C; Connolly, Eugene; Norrie, John; Round, Caroline E; Ford, Ian; Morrison, Caroline E

2001-01-01

Objectives To determine whether specialist nurse intervention improves outcome in patients with chronic heart failure. Design Randomised controlled trial. Setting Acute medical admissions unit in a teaching hospital. Participants 165 patients admitted with heart failure due to left ventricular systolic dysfunction. The intervention started before discharge and continued thereafter with home visits for up to 1 year. Main outcome measures Time to first event analysis of death from all causes or readmission to hospital with worsening heart failure. Results 31 patients (37%) in the intervention group died or were readmitted with heart failure compared with 45 (53%) in the usual care group (hazard ratio=0.61, 95% confidence interval 0.33 to 0.96).Compared with usual care, patients in the intervention group had fewer readmissions for any reason (86 v 114, P=0.018), fewer admissions for heart failure (19 v 45, P<0.001) and spent fewer days in hospital for heart failure (mean 3.43 v 7.46 days, P=0.0051). Conclusions Specially trained nurses can improve the outcome of patients admitted to hospital with heart failure. What is already known on this topicStudies have suggested that nurse intervention may reduce readmission in patients with heart failureWhat this study addsHome based intervention from nurses reduces readmissions for worsening heart failureRegular contact to review treatment and patient education are likely to contribute to this effect PMID:11576977

Air pollution and heart failure: Relationship with the ejection fraction

PubMed Central

Dominguez-Rodriguez, Alberto; Abreu-Afonso, Javier; Rodríguez, Sergio; Juarez-Prera, Ruben A; Arroyo-Ucar, Eduardo; Gonzalez, Yenny; Abreu-Gonzalez, Pedro; Avanzas, Pablo

2013-01-01

AIM: To study whether the concentrations of particulate matter in ambient air are associated with hospital admission due to heart failure in patients with heart failure with preserved ejection fraction and reduced ejection fraction. METHODS: We studied 353 consecutive patients admitted into a tertiary care hospital with a diagnosis of heart failure. Patients with ejection fraction of ≥ 45% were classified as having heart failure with preserved ejection fraction and those with an ejection fraction of < 45% were classified as having heart failure with reduced ejection fraction. We determined the average concentrations of different sizes of particulate matter (< 10, < 2.5, and < 1 μm) and the concentrations of gaseous pollutants (carbon monoxide, sulphur dioxide, nitrogen dioxide and ozone) from 1 d up to 7 d prior to admission. RESULTS: The heart failure with preserved ejection fraction population was exposed to higher nitrogen dioxide concentrations compared to the heart failure with reduced ejection fraction population (12.95 ± 8.22 μg/m3 vs 4.50 ± 2.34 μg/m3, P < 0.0001). Multivariate analysis showed that nitrogen dioxide was a significant predictor of heart failure with preserved ejection fraction (odds ratio ranging from (1.403, 95%CI: 1.003-2.007, P = 0.04) to (1.669, 95%CI: 1.043-2.671, P = 0.03). CONCLUSION: This study demonstrates that short-term nitrogen dioxide exposure is independently associated with admission in the heart failure with preserved ejection fraction population. PMID:23538391

An Educational Intervention to Evaluate Nurses' Knowledge of Heart Failure.

PubMed

Sundel, Siobhan; Ea, Emerson E

2018-07-01

Nurses are the main providers of patient education in inpatient and outpatient settings. Unfortunately, nurses may lack knowledge of chronic medical conditions, such as heart failure. The purpose of this one-group pretest-posttest intervention was to determine the effectiveness of teaching intervention on nurses' knowledge of heart failure self-care principles in an ambulatory care setting. The sample consisted of 40 staff nurses in ambulatory care. Nurse participants received a focused education intervention based on knowledge deficits revealed in the pretest and were then resurveyed within 30 days. Nurses were evaluated using the valid and reliable 20-item Nurses Knowledge of Heart Failure Education Principles Survey tool. The results of this project demonstrated that an education intervention on heart failure self-care principles improved nurses' knowledge of heart failure in an ambulatory care setting, which was statistically significant (p < .05). Results suggest that a teaching intervention could improve knowledge of heart failure, which could lead to better patient education and could reduce patient readmission for heart failure. J Contin Educ Nurs. 2018;49(7):315-321. Copyright 2018, SLACK Incorporated.

CD28/B7 deficiency attenuates systolic overload-induced congestive heart failure, myocardial and pulmonary inflammation, and activated T-cell accumulation in the heart and lungs

PubMed Central

Wang, Huan; Kwak, Dongmin; Fassett, John; Hou, Lei; Xu, Xin; Burbach, Brandon J.; Thenappan, Thenappan; Xu, Yawei; Ge, Jun-bo; Shimizu, Yoji; Bache, Robert J.; Chen, Yingjie

2017-01-01

The inflammatory response regulates congestive heart failure (CHF) development. T-cell activation plays an important role in tissue inflammation. We postulate that CD28 or B7 deficiency inhibits T-cell activation and attenuates CHF development by reducing systemic, cardiac and pulmonary inflammation. We demonstrated that chronic pressure overload-induced end-stage CHF in mice is characterized by profound accumulation of activated effector T-cells (CD3+CD44high cells) in the lungs and a mild but significant increase of these cells in the heart. In knockout (KO) mice lacking either CD28 or B7, there was a dramatic reduction in the accumulation of activated effector T cells in both hearts and lungs of mice under control conditions and after transverse aortic constriction (TAC). CD28 or B7 KO significantly attenuated TAC-induced CHF development, as indicated by less increase of heart and lung weight, and less reduction of LV contractility. CD28 or B7 KO also significantly reduced TAC-induced CD45+ leukocyte, T-cell and macrophage infiltration in hearts and lungs, lowered pro-inflammatory cytokine expression (such as TNF-α and IL-1β) in lungs. Furthermore, CD28/B7 blockade by CTLA4-Ig treatment (250μg/mouse every 3 days) attenuated TAC-induced T cell activation, LV hypertrophy, and LV dysfunction. Our data indicate that CD28/B7 deficiency inhibits activated effector T-cell accumulation, reduces myocardial and pulmonary inflammation, and attenuates the development of CHF. Our findings suggest that strategies targeting T-cell activation may be useful in treating CHF. PMID:27432861

Rational use of inotropic therapy in heart failure.

PubMed

Felker, G M; O'Connor, C M

2001-03-01

Despite their theoretic appeal, agents that increase cardiac contractility (positive inotropes) have consistently been shown to increase mortality when given chronically to patients with heart failure. The routine use of inotropes as heart failure therapy in either the acute or the chronic setting is not supported by the available data. Some appropriate uses of inotropes are as temporary treatment of diuretic-refractory acute heart failure decompensations, or as a bridge to definitive treatment such as revascularization or cardiac transplantation. Although controversial, the use of inotropes as a palliative measure in the small subset of patients with truly end-stage heart failure may be appropriate. An understanding of the appropriate goals of therapy is important for both patients and physicians if rational decisions about the use of inotropes are to be made.

Noninvasive reconstruction of the three-dimensional ventricular activation sequence during pacing and ventricular tachycardia in the rabbit heart.

PubMed

Han, Chengzong; Pogwizd, Steven M; Killingsworth, Cheryl R; He, Bin

2011-01-01

Ventricular arrhythmias represent one of leading causes for sudden cardiac death, a significant problem in public health. Noninvasive imaging of cardiac electric activities associated with ventricular arrhythmias plays an important role in better our understanding of the mechanisms and optimizing the treatment options. The present study aims to rigorously validate a novel three-dimensional (3-D) cardiac electrical imaging (3-DCEI) technique with the aid of 3-D intra-cardiac mapping during paced rhythm and ventricular tachycardia (VT) in the rabbit heart. Body surface potentials and intramural bipolar electrical recordings were simultaneously measured in a closed-chest condition in thirteen healthy rabbits. Single-site pacing and dual-site pacing were performed from ventricular walls and septum. VTs and premature ventricular complexes (PVCs) were induced by intravenous norepinephrine (NE). The non-invasively imaged activation sequence correlated well with invasively measured counterparts, with a correlation coefficient of 0.72 and a relative error of 0.30 averaged over all paced beats and NE-induced PVCs and VT beats. The averaged distance from imaged site of initial activation to measured site determined from intra-cardiac mapping was ∼5mm. These promising results suggest that 3-DCEI is feasible to non-invasively localize the origins and image activation sequence of focal ventricular arrhythmias.

Severe right heart failure in a patient with Grave's disease.

PubMed

Xenopoulos, N P; Braden, G A; Applegate, R J

1996-11-01

This brief report presents a patient with isolated right heart failure and two rare underlying causes, hyperthyroidism and dysplastic tricuspid valve. Repair of the tricuspid valve and treatment of the hyperthyroidism were both essential for successful treatment of the right heart failure. Most important, recrudescence of hyperthyroidism in this patient was associated with reappearance of florid right heart failure. This report provides further information about a potential linkage of hyperthyroidism and severe right heart failure.

Relative refractoriness of left ventricular contraction underlies human tachycardia-induced mechanical and electrical alternans.

PubMed

Kashimura, Takeshi; Kodama, Makoto; Watanabe, Tohru; Tanaka, Komei; Hayashi, Yuka; Ohno, Yukako; Obata, Hiroaki; Ito, Masahiro; Hirono, Satoru; Hanawa, Haruo; Minamino, Tohru

2014-02-01

Mechanical alternans (MA) and electrical alternans (EA) are predictors of cardiac events. Experimental studies have suggested that refractoriness of calcium cycling underlies these cardiac alternans. However, refractoriness of left ventricular contraction has not been examined in patients with cardiac alternans. In 51 patients with miscellaneous heart diseases, incremental right atrial pacing was performed to induce MA and EA. MA was quantified by alternans amplitude (AA: the difference between left ventricular dP/dt of a strong beat and that of a weak beat), and AA at 100/min (AA100) and maximal AA (AAmax) were measured. EA was defined as alternation of T wave morphology in 12-lead electrocardiogram. Relative refractoriness of left ventricular contraction was examined by drawing the mechanical restitution curve under a basal coupling interval (BCL) of 600 ms (100/min) and was assessed by the slope at BCL (Δmechanical restitution). Postextrasystolic potentiation (PESP) was also examined and the slope of PESP curve (ΔPESP) was assessed as a property to alternate strong and weak beats. MA and EA were induced in 19 patients and in none at 100/min or less, and at any heart rate in 32 and in 10, respectively. AA100 and AAmax correlated positively with Δmechanical restitution and negatively with ΔPESP. Patients with EA had a significantly larger Δmechanical restitution and a significantly larger absolute value of ΔPESP than those without. In patients with MA and EA, the left ventricular contractile force during tachycardia is under relative refractoriness and prone to cause large fluctuation of contractile force. ©2013, The Authors. Journal compilation ©2013 Wiley Periodicals, Inc.

Allopurinol improves endothelial dysfunction in chronic heart failure.

PubMed

Farquharson, Colin A J; Butler, Robert; Hill, Alexander; Belch, Jill J F; Struthers, Allan D

2002-07-09

Increased oxidative stress in chronic heart failure is thought to contribute to endothelial dysfunction. Xanthine oxidase produces oxidative stress and therefore we examined whether allopurinol improved endothelial dysfunction in chronic heart failure. We performed a randomized, placebo-controlled, double-blind crossover study on 11 patients with New York Heart Association class II-III chronic heart failure, comparing 300 mg allopurinol daily (1 month) versus placebo. Endothelial function was assessed by standard forearm venous occlusion plethysmography with acetylcholine, nitroprusside, and verapamil. Plasma malondialdehyde levels were also compared to assess significant changes in oxidative stress. Allopurinol significantly increased the forearm blood flow response to acetylcholine (percentage change in forearm blood flow [mean+/-SEM]: 181+/-19% versus 120+/-22% allopurinol versus placebo; P=0.003). There were no significant differences in the forearm blood flow changes between the placebo and allopurinol treatment arms with regard to sodium nitroprusside or verapamil. Plasma malondialdehyde was significantly reduced with allopurinol treatment (346+/-128 nmol/L versus 461+/-101 nmol/L, allopurinol versus placebo; P=0.03), consistent with reduced oxidative stress with allopurinol therapy. We have shown that allopurinol improves endothelial dysfunction in chronic heart failure. This raises the distinct possibility that allopurinol might reduce cardiovascular events and even improve exercise capacity in chronic heart failure.

Medical costs in patients with heart failure after acute heart failure events: one-year follow-up study.

PubMed

Kim, Eugene; Kwon, Hye-Young; Baek, Sang Hong; Lee, Haeyoung; Yoo, Byung-Su; Kang, Seok-Min; Ahn, Youngkeun; Yang, Bong-Min

2018-03-01

This study investigated annual medical costs using real-world data focusing on acute heart failure. The data were retrospectively collected from six tertiary hospitals in South Korea. Overall, 330 patients who were hospitalized for acute heart failure between January 2011 and July 2012 were selected. Data were collected on their follow-up medical visits for 1 year, including medical costs incurred toward treatment. Those who died within the observational period or who had no records of follow-up visits were excluded. Annual per patient medical costs were estimated according to the type of medical services, and factors contributing to the costs using Gamma Generalized Linear Models (GLM) with log link were analyzed. On average, total annual medical costs for each patient were USD 6,199 (±9,675), with hospitalization accounting for 95% of the total expenses. Hospitalization cost USD 5,904 (±9,666) per patient. Those who are re-admitted have 88.5% higher medical expenditure than those who have not been re-admitted in 1 year, and patients using intensive care units have 19.6% higher expenditure than those who do not. When the number of hospital days increased by 1 day, medical expenses increased by 6.7%. Outpatient drug costs were not included. There is a possibility that medical expenses for AHF may have been under-estimated. It was found that hospitalization resulted in substantial costs for treatment of heart failure in South Korea, especially in patients with an acute heart failure event. Prevention strategies and appropriate management programs that would reduce both frequency of hospitalization and length of stay for patients with the underlying risk of heart failure are needed.

Heart rate differentiates urgency and emergency in hypertensive crisis.

PubMed

Al Bannay, Rashed; Böhm, Michael; Husain, Aysha

2013-08-01

To study the clinical significance of presenting blood pressure parameters and heart rate in patients with hypertensive crisis. In patients admitted with hypertensive crisis between January 2011 and May 2011, demography, mode of presentation, co-morbidities, blood pressure readings, and heart rate at presentation were documented. Further clustering of hypertensive crisis into emergency or urgency was based on the presence or absence of target organ involvement. The relationship between blood pressure parameters, heart rate, and other variables was analyzed. 189 patients in sinus rhythm were enrolled in this pilot study. The rate of hypertensive urgency was 56 %, whereas the rate of hypertensive emergency was 44 %, respectively. Subjects with hypertensive emergency had a higher mean heart rate (93 ± 22.7 bpm) than those with urgency (81 ± 11.5 bpm) (P = 0.015). Women had higher heart rates (92 ± 18.5 bpm) than men (86 ± 17.6 bpm) (P = 0.014). Heart rates below 100 bpm had a specificity of 94 %, classifying patients as hypertensive urgency. Tachycardia had a powerful statistical association with hypertensive left ventricular failure (P < 0.0001). Other hemodynamic parameters, including systolic blood pressure, diastolic blood pressure, pulse pressure, and mean blood pressure relates neither to urgency nor to emergency. Diabetic patients with HBA1c levels of more than 53 mmol/mol had a heart rate of more than 100 bpm (P = 0.015) during hypertensive crisis. Normal heart rate is characteristic of hypertensive urgency. Tachycardia in this setting is an ominous sign and denotes hypertensive complications in particular left ventricular failure. Among diabetics, elevated heart rate is associated with poor glycemic control.

Hypertension as a risk factor for heart failure.

PubMed

Kannan, Arun; Janardhanan, Rajesh

2014-07-01

Hypertension remains a significant risk factor for development of congestive heart failure CHF), with various mechanisms contributing to both systolic and diastolic dysfunction. The pathogenesis of myocardial changes includes structural remodeling, left ventricular hypertrophy, and fibrosis. Activation of the sympathetic nervous system and renin-angiotensin system is a key contributing factor of hypertension, and thus interventions that antagonize these systems promote regression of hypertrophy and heart failure. Control of blood pressure is of paramount importance in improving the prognosis of patients with heart failure.

Nkx2.5 enhances the efficacy of mesenchymal stem cells transplantation in treatment heart failure in rats.

PubMed

Deng, Bo; Wang, Jin Xin; Hu, Xing Xing; Duan, Peng; Wang, Lin; Li, Yang; Zhu, Qing Lei

2017-08-01

The aim of this study is to determine whether Nkx2.5 transfection of transplanted bone marrow mesenchymal stem cells (MSCs) improves the efficacy of treatment of adriamycin-induced heart failure in a rat model. Nkx2.5 was transfected in MSCs by lentiviral vector transduction. The expressions of Nkx2.5 and cardiac specific genes in MSCs and Nkx2.5 transfected mesenchymal stem cells (MSCs-Nkx2.5) were analyzed with quantitative real-time PCR and Western blot in vitro. Heart failure models of rats were induced by adriamycin and were then randomly divided into 3 groups: injected saline, MSCs or MSCs-Nkx2.5 via the femoral vein respectively. Four weeks after injection, the cardiac function, expressions of cardiac specific gene, fibrosis formation and collagen volume fraction in the myocardium as well as the expressions of GATA4 and MEF2 in rats were analyzed with echocardiography, immunohistochemistry, Masson staining, quantitative real-time PCR and Western blot, respectively. Nkx2.5 enhanced cardiac specific gene expressions including α-MHC, TNI, CKMB, connexin-43 in MSCs-Nkx2.5 in vitro. Both MSCs and MSCs-Nkx2.5 improved cardiac function, promoted the differentiation of transplanted MSCs into cardiomyocyte-like cells, decreased fibrosis formation and collagen volume fraction in the myocardium, as well as increased the expressions of GATA4 and MEF2 in adriamycin-induced rat heart failure models. Moreover, the effect was much more remarkable in MSCs-Nkx2.5 than in MSCs group. This study has found that Nkx2.5 enhances the efficacy of MSCs transplantation in treatment adriamycin-induced heart failure in rats. Nkx2.5 transfected to transplanted MSCs provides a potential effective approach to heart failure. Copyright © 2017 Elsevier Inc. All rights reserved.

Maternal and fetal outcomes in pregnant women with heart failure.

PubMed

Ng, Angie T; Duan, Lewei; Win, Theresa; Spencer, Hillard T; Lee, Ming-Sum

2018-05-25

The goal of this study is to report the prevalence, aetiology and clinical outcome of pregnant women with heart failure. This is a retrospective community-based cohort study that included pregnant women in the Kaiser Permanente Health System between 2003 and 2014. Women with heart failure were identified using International Classification of Disease, Ninth Revision codes. Medical records were manually reviewed to confirm diagnosis and adjudicate outcomes. In a cohort of 385 935 pregnancies, 488 (0.13%) had a diagnosis of heart failure, corresponding to 126 cases per 100 000 pregnancies. Peripartum cardiomyopathy was the most common cause of heart failure, accounting for 333 (68.2%) cases. Preterm birth and caesarean delivery were more common in patients with heart failure. Neonatal death rate was higher in the heart failure group (1.0% vs 0.4%, p=0.03). Infants delivered to women with heart failure had lower birth weights (3112.0±774.0 g vs 3331.9±575.5 g, p<0.001) and lower Apgar score at 1 min (7.9±1.5 vs 8.3±1.1, p<0.001). Median follow-up was 6.2 years (IQR 3.2-9.2). During follow-up, 7 (1.4%) in the heart failure group and 423 (0.11%) in the control group died. Heart failure was associated with a 7.7-fold increase risk of death (adjusted HR 7.7, 95% CI 3.6 to 16.4, p<0.001). Heart failure during pregnancy is associated with unfavourable fetal outcomes including prematurity and low birth weight. While the overall mortality rate was low, pregnant women with heart failure carried an excess risk of death compared with controls. © Article author(s) (or their employer(s) unless otherwise stated in the text of the article) 2018. All rights reserved. No commercial use is permitted unless otherwise expressly granted.

Comprehensive in-hospital monitoring in acute heart failure: applications for clinical practice and future directions for research. A statement from the Acute Heart Failure Committee of the Heart Failure Association (HFA) of the European Society of Cardiology (ESC).

PubMed

Harjola, Veli-Pekka; Parissis, John; Brunner-La Rocca, Hans-Peter; Čelutkienė, Jelena; Chioncel, Ovidiu; Collins, Sean P; De Backer, Daniel; Filippatos, Gerasimos S; Gayat, Etienne; Hill, Loreena; Lainscak, Mitja; Lassus, Johan; Masip, Josep; Mebazaa, Alexandre; Miró, Òscar; Mortara, Andrea; Mueller, Christian; Mullens, Wilfried; Nieminen, Markku S; Rudiger, Alain; Ruschitzka, Frank; Seferovic, Petar M; Sionis, Alessandro; Vieillard-Baron, Antoine; Weinstein, Jean Marc; de Boer, Rudolf A; Crespo Leiro, Maria G; Piepoli, Massimo; Riley, Jillian P

2018-04-30

This paper provides a practical clinical application of guideline recommendations relating to the inpatient monitoring of patients with acute heart failure, through the evaluation of various clinical, biomarker, imaging, invasive and non-invasive approaches. Comprehensive inpatient monitoring is crucial to the optimal management of acute heart failure patients. The European Society of Cardiology heart failure guidelines provide recommendations for the inpatient monitoring of acute heart failure, but the level of evidence underpinning most recommendations is limited. Many tools are available for the in-hospital monitoring of patients with acute heart failure, and each plays a role at various points throughout the patient's treatment course, including the emergency department, intensive care or coronary care unit, and the general ward. Clinical judgment is the preeminent factor guiding application of inpatient monitoring tools, as the various techniques have different patient population targets. When applied appropriately, these techniques enable decision making. However, there is limited evidence demonstrating that implementation of these tools improves patient outcome. Research priorities are identified to address these gaps in evidence. Future research initiatives should aim to identify the optimal in-hospital monitoring strategies that decrease morbidity and prolong survival in patients with acute heart failure. © 2018 The Authors. European Journal of Heart Failure © 2018 European Society of Cardiology.

[Sleep apnea and heart failure: pathophysiology, diagnosis and therapy].

PubMed

Monda, Cinzia; Scala, Oriana; Paolillo, Stefania; Savarese, Gianluigi; Cecere, Milena; D'Amore, Carmen; Parente, Antonio; Musella, Francesca; Mosca, Susanna; Filardi, Pasquale Perrone

2010-11-01

Sleep apnea, defined as a pathologic pause in breathing during sleep >10 s, promotes the progression of chronic heart failure and may be a predictor of poor prognosis. It causes, in fact, several mechanical, hemodynamic, chemical and inflammatory changes that negatively compromise cardiovascular homeostasis of heart failure patients. Sleep apnea is recognized as sleep apnea syndrome when specific symptoms, such as sleepiness and headache during the daytime and snoring, are present and is diagnosed with an overnight test called polysomnography. There are two different forms of sleep apnea, central and obstructive. Breathing is interrupted by the loss of respiratory drive and the lack of respiratory effort in the central form, which affects about 40-60% of heart failure patients. In obstructive sleep apnea, breathing stops when throat muscles relax, despite respiratory effort. This form affects about 3% of the general population, while it is present in at least 30% of heart failure patients. The diagnosis of sleep disorders in heart failure becomes very important to help patients adopting lifestyle changes and starting specific therapies to improve quality of life and retard the progression of chronic heart failure.

Out-patient management of chronic heart failure.

PubMed

Terrovitis, John V; Anastasiou-Nana, Maria I; Nanas, John N

2005-09-01

Chronic heart failure is a clinical syndrome associated with an ominous long-term prognosis and major economic consequences for Western societies. In recent years, considerable progress has been made in the pharmacological management of heart failure, and several treatments have been confirmed to confer survival and symptomatic benefits. However, pharmaceuticals remain underutilised, and the combination of several different drugs present challenges for their optimal prescription, requiring a thorough knowledge of potential side effects and complex interactions. This article reviews in detail the evidence pertaining to the out-patient pharmacological management of chronic heart failure, and offers recommendations on the use of various drugs in complex clinical conditions, or in areas of ongoing controversy.

Renal Denervation for Chronic Heart Failure: Background and Pathophysiological Rationale.

PubMed

Böhm, Michael; Ewen, Sebastian; Mahfoud, Felix

2017-01-01

The activation of the sympathetic nervous system is associated with cardiovascular hospitalizations and death in heart failure. Renal denervation has been shown to effectively reduce sympathetic overdrive in certain patients with uncontrolled hypertension. Pilot trials investigating renal denervation as a potential treatment approach for heart failure were initiated. Heart failure comorbidities like obstructive sleep apnea, metabolic syndrome and arrhythmias could also be targets for renal denervation, because these occurrences are also mediated by the activation of the sympathetic nervous system. Therefore, renal denervation in heart failure is worthy of further investigation, although its effectiveness still has to be proven. Herein, we describe the pathophysiological rationale and the effect of renal denervation on surrogates of the heart failure syndrome.

Implantable automatic scanning pacemaker for termination of supraventricular tachycardia.

PubMed

Spurrell, R A; Nathan, A W; Bexton, R S; Hellestrand, K J; Nappholz, T; Camm, A J

1982-03-01

Thirteen patients suffering from reentrant supraventricular tachycardia have undergone implantation of a scanning extrastimulus pacemaker. This pacemaker is fully implanted and automatic, and it requires no external control device to activate or control it. The pacemaker is activated when tachycardia occurs. After four cycles an extrastimulus is induced with a preset coupling time from a sensed intracardiac potential, and every four cycles thereafter a further extrastimulus occurs, but on each occasion there is a decrement in coupling cycle by 6 ms until 90 ms of the cardiac cycle has been scanned by extrastimuli. When necessary, two extrastimuli can be introduced with a fixed but preset coupling time between them. Every four beats two extrastimuli are induced but the coupling time between the spontaneous cardiac potential and the first stimulus is decreased by 6 ms until 90 ms of the cardiac cycle has been scanned. The coupling time between the two stimuli is fixed throughout the scan. When termination of tachycardia occurs the successful timing variables are retained in the pacemaker memory so that at the onset of the next episode of tachycardia these settings are used first. Pacemaker pulse width, sensitivity, tachycardia trigger rate, coupling intervals for both stimuli and the use of single or double extrastimuli are all programmable transcutaneously. Three patients required single, and seven patients double ventricular premature stimuli; three patients required double atrial premature stimuli for termination of tachycardia. Despite frequent attacks of tachycardia before implantation, only two patients had a sustained attack of tachycardia after pacemaker implantation.

Quality of life improves in patients with chronic heart failure and Cheyne-Stokes respiration treated with adaptive servo-ventilation in a nurse-led heart failure clinic.

PubMed

Olseng, Margareth W; Olsen, Brita F; Hetland, Arild; Fagermoen, May S; Jacobsen, Morten

2017-05-01

The aim of this study was to investigate if quality of life improved in chronic heart failure patients with Cheyne-Stokes respiration treated with adaptive servo-ventilation in nurse-led heart failure clinic. Cheyne-Stokes respiration is associated with decreased quality of life in patients with chronic heart failure. Adaptive servo-ventilation is introduced to treat this sleep-disordered breathing. Randomised, controlled design. Fifty-one patients (ranging from 53-84 years), New York Heart Association III-IV and/or left ventricular ejection fraction ≤40% and Cheyne-Stokes respiration were randomised to an intervention group who received adaptive servo-ventilation or a control group. Minnesota Living with Heart Failure Questionnaire was used to assess quality of life at randomisation and after three months. Both groups were followed in the nurse-led heart failure clinic. Adaptive servo ventilation improved quality of life-scores both in a per protocol analysis and in an intention to treat analysis. Twenty-one patients dropped out of the study, nine in the control and 12 in the intervention group. Use of adaptive servo-ventilation improved quality of life in chronic heart failure patients with Cheyne-Stokes respiration. However, the drop-out rate was high. Chronic heart failure patients come regularly to the nurse-led heart failure clinic. The heart failure nurses' competency has to include knowledge of equipment to provide support and continuity of care to the patients. © 2016 John Wiley & Sons Ltd.

Diagnosis and management of heart failure in the elderly.

PubMed

King, D

1996-10-01

Heart failure is common in the elderly and is associated with a significant morbidity and mortality. It accounts for about 5% of adult medical admissions and the expenditure of 1% of the total National Health Service budget. Clinical presentation in old age may be with the classical symptoms of heart failure but often, due to multiple pathology and low functional ability, presentation is atypical. Both nonspecific symptoms and signs of heart failure, are often a delayed presentation in this population, make diagnosis difficult. Treatment of the failing heart in an older person is similar to the young however, diligence is required when prescribing due to age-related pharmacokinetic changes and co-existent morbidity. This may result in polypharmacy and an increase in drug interactions which themselves may have deleterious consequences. However, knowledge of the aetiology of heart failure in old age and the possible atypical presentation as well as available treatments, will result in better management and improved quality of life and reduced mortality in the elderly heart failure population.

Diagnosis and management of heart failure in the elderly.

PubMed Central

King, D.

1996-01-01

Heart failure is common in the elderly and is associated with a significant morbidity and mortality. It accounts for about 5% of adult medical admissions and the expenditure of 1% of the total National Health Service budget. Clinical presentation in old age may be with the classical symptoms of heart failure but often, due to multiple pathology and low functional ability, presentation is atypical. Both nonspecific symptoms and signs of heart failure, are often a delayed presentation in this population, make diagnosis difficult. Treatment of the failing heart in an older person is similar to the young however, diligence is required when prescribing due to age-related pharmacokinetic changes and co-existent morbidity. This may result in polypharmacy and an increase in drug interactions which themselves may have deleterious consequences. However, knowledge of the aetiology of heart failure in old age and the possible atypical presentation as well as available treatments, will result in better management and improved quality of life and reduced mortality in the elderly heart failure population. PMID:8977936

Reversible catecholamine-induced cardiomyopathy due to pheochromocytoma: case report.

PubMed

Satendra, Milan; de Jesus, Cláudia; Bordalo e Sá, Armando L; Rosário, Luís; Rocha, José; Bicha Castelo, Henrique; Correia, Maria José; Nunes Diogo, António

2014-03-01

Pheochromocytoma is a tumor originating from chromaffin tissue. It commonly presents with symptoms and signs of catecholamine excess, such as hypertension, tachycardia, headache and sweating. Cardiovascular manifestations include catecholamine-induced cardiomyopathy, which may present as severe left ventricular dysfunction and congestive heart failure. We report a case of pheochromocytoma which was diagnosed following investigation of dilated cardiomyopathy. We highlight the dramatic symptomatic improvement and reversal of cardiomyopathy, with recovery of left ventricular function after treatment. Copyright © 2013 Sociedade Portuguesa de Cardiologia. Published by Elsevier España. All rights reserved.

Crosstalk between the heart and peripheral organs in heart failure

PubMed Central

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

Clinical phenotypes and outcome of patients hospitalized for acute heart failure: the ESC Heart Failure Long-Term Registry.

PubMed

Chioncel, Ovidiu; Mebazaa, Alexandre; Harjola, Veli-Pekka; Coats, Andrew J; Piepoli, Massimo Francesco; Crespo-Leiro, Maria G; Laroche, Cecile; Seferovic, Petar M; Anker, Stefan D; Ferrari, Roberto; Ruschitzka, Frank; Lopez-Fernandez, Silvia; Miani, Daniela; Filippatos, Gerasimos; Maggioni, Aldo P

2017-10-01

To identify differences in clinical epidemiology, in-hospital management and 1-year outcomes among patients hospitalized for acute heart failure (AHF) and enrolled in the European Society of Cardiology Heart Failure Long-Term (ESC-HF-LT) Registry, stratified by clinical profile at admission. The ESC-HF-LT Registry is a prospective, observational study collecting hospitalization and 1-year follow-up data from 6629 AHF patients. Among AHF patients enrolled in the registry, 13.2% presented with pulmonary oedema (PO), 2.9% with cardiogenic shock (CS), 61.1% with decompensated heart failure (DHF), 4.8% with hypertensive heart failure (HT-HF), 3.5% with right heart failure (RHF) and 14.4% with AHF and associated acute coronary syndromes (ACS-HF). The 1-year mortality rate was 28.1% in PO, 54.0% in CS, 27.2% in DHF, 12.8% in HT-HF, 34.0% in RHF and 20.6% in ACS-HF patients. When patients were classified by systolic blood pressure (SBP) at initial presentation, 1-year mortality was 34.8% in patients with SBP <85 mmHg, 29.0% in those with SBP 85-110 mmHg, 21.2% in patients with SBP 110-140 mmHg and 17.4% in those with SBP >140 mmHg. These differences tended to diminish in the months post-discharge, and 1-year mortality for the patients who survived at least 6 months post-discharge did not vary significantly by either clinical profile or SBP classification. Rates of adverse outcomes in AHF remain high, and substantial differences have been found when patients were stratified by clinical profile or SBP. However, patients who survived at least 6 months post-discharge represent a more homogeneous group and their 1-year outcome is less influenced by clinical profile or SBP at admission. © 2017 The Authors. European Journal of Heart Failure © 2017 European Society of Cardiology.

[Orthostatic postural tachycardia: study of 8 patients].

PubMed

Santiago Pérez, S; Ferrer Gila, T

1998-02-07

The occurrence of syncopal episodes is a very frequent event. In the absence of a structural systemic or cardiac disease, syncope is resulting of an anomalous cardiovascular response neurally mediated by the autonomic nervous system. It is the final common manifestation of different abnormal mechanisms and is frequently precipitated by orthostatism. Orthostatic intolerance syndrome refers to the development of symptoms during the upright posture that disappear in supine position. Tachycardia may be one of the clinical features of the syndrome. During orthostatic stress a hyperadrenergic response, with maintained increment of heart rate and associated symptoms, is developed. Changes in blood pressure may be diverse and in some cases hypotension and syncope occurs. Eight patients with symptoms of orthostatic intolerance who underwent autonomic evaluation and were diagnosed from postural tachycardia are presented. In all the cases an abnormal increment of heart rate during tilting was found and it was associated to hyperadrenergic symptoms. Evidence of restricted sympathetic impairment was observed in six cases with distal reduction of sudomotor function and abnormal adrenergic response during Valsalva manoeuvre. Symptoms disappeared or mostly subsided with pharmacological (amitriptyline in one case, phenobarbital in another one and non-cardioselective beta-blockers in six patients) and non-pharmacological treatment. In further examinations heart rate and blood pressure were normal.

Spironolactone for heart failure with preserved ejection fraction.

PubMed

Pitt, Bertram; Pfeffer, Marc A; Assmann, Susan F; Boineau, Robin; Anand, Inder S; Claggett, Brian; Clausell, Nadine; Desai, Akshay S; Diaz, Rafael; Fleg, Jerome L; Gordeev, Ivan; Harty, Brian; Heitner, John F; Kenwood, Christopher T; Lewis, Eldrin F; O'Meara, Eileen; Probstfield, Jeffrey L; Shaburishvili, Tamaz; Shah, Sanjiv J; Solomon, Scott D; Sweitzer, Nancy K; Yang, Song; McKinlay, Sonja M

2014-04-10

Mineralocorticoid-receptor antagonists improve the prognosis for patients with heart failure and a reduced left ventricular ejection fraction. We evaluated the effects of spironolactone in patients with heart failure and a preserved left ventricular ejection fraction. In this randomized, double-blind trial, we assigned 3445 patients with symptomatic heart failure and a left ventricular ejection fraction of 45% or more to receive either spironolactone (15 to 45 mg daily) or placebo. The primary outcome was a composite of death from cardiovascular causes, aborted cardiac arrest, or hospitalization for the management of heart failure. With a mean follow-up of 3.3 years, the primary outcome occurred in 320 of 1722 patients in the spironolactone group (18.6%) and 351 of 1723 patients in the placebo group (20.4%) (hazard ratio, 0.89; 95% confidence interval [CI], 0.77 to 1.04; P=0.14). Of the components of the primary outcome, only hospitalization for heart failure had a significantly lower incidence in the spironolactone group than in the placebo group (206 patients [12.0%] vs. 245 patients [14.2%]; hazard ratio, 0.83; 95% CI, 0.69 to 0.99, P=0.04). Neither total deaths nor hospitalizations for any reason were significantly reduced by spironolactone. Treatment with spironolactone was associated with increased serum creatinine levels and a doubling of the rate of hyperkalemia (18.7%, vs. 9.1% in the placebo group) but reduced hypokalemia. With frequent monitoring, there were no significant differences in the incidence of serious adverse events, a serum creatinine level of 3.0 mg per deciliter (265 μmol per liter) or higher, or dialysis. In patients with heart failure and a preserved ejection fraction, treatment with spironolactone did not significantly reduce the incidence of the primary composite outcome of death from cardiovascular causes, aborted cardiac arrest, or hospitalization for the management of heart failure. (Funded by the National Heart, Lung, and Blood

Severe tricuspid regurgitation and isolated right heart failure due to thyrotoxicosis

PubMed Central

Bonou, Maria; Lampropoulos, Konstantinos M.; Andriopoulou, Maria; Kotsas, Dimitrios; Lakoumentas, John; Barbetseas, John

2012-01-01

We describe the case of a patient presented with isolated right heart failure with atrial fibrillation and severe tricuspid regurgitation due to hyperthyroidism. Treatment of the thyroid disease resulted in the disappearance of signs of right heart failure and resolution of the valve incompetence and normalization of the heart rhythm. Although thyrotoxicosis may be associated with congestive heart failure, isolated right heart failure with marked tricuspid regurgitation is rarely seen. PMID:23253416

Pregnancy in women with heart disease: risk assessment and management of heart failure.

PubMed

Grewal, Jasmine; Silversides, Candice K; Colman, Jack M

2014-01-01

Heart disease, present in 0.5% to 3% of pregnant women, is an important cause of morbidity and the leading cause of death among pregnant women in the developed world. Certain heart conditions are associated with an increased risk of heart failure during pregnancy or the postpartum period; for these conditions, management during pregnancy benefits from multidisciplinary care at a center with expertise in pregnancy and heart disease. This article focuses on cardiac risks and management strategies for women with acquired and congenital heart disease who are at increased risk of heart failure during pregnancy. Crown Copyright © 2014. Published by Elsevier Inc. All rights reserved.

Tachycardia in patients treated with clozapine versus antipsychotic long-acting injections.

PubMed

Nilsson, Björn M; Edström, Oscar; Lindström, Leif; Wernegren, Petter; Bodén, Robert

2017-07-01

Tachycardia is a known adverse effect during clozapine treatment. However, prevalence reported differs widely between studies and hitherto there are no studies comparing clozapine-treated patients with a similar control group. The present study was carried out to assess the prevalence of tachycardia in patients treated with clozapine and antipsychotic long-acting injections (LAI). Data on heart rate (HR), concomitant medication, and relevant anthropometric and laboratory measurements were collected for all clozapine-treated patients (n=174) in a defined catchment area and compared with data on patients treated with LAI (n=87). In total, 33% of patients on long-term clozapine treatment had tachycardia (HR>100) compared with 16% in the LAI group (P<0.001). The mean HR was 91 in the clozapine group and 82 in the LAI group (P<0.001). Clozapine dose correlated with HR. The majority of patients with HR more than 100 received no specific treatment for tachycardia. In conclusion, the prevalence of tachycardia was twice as high in patients treated with clozapine as in a similar patient group with severe schizophrenia spectrum disorder. The tachycardia was in many cases clinically unnoticed. Tachycardia during antipsychotic treatment is a common phenomenon that must be monitored for actively and, when noticed, further investigated and treated.

[AV-reentrant tachycardia and Wolff-Parkinson-White syndrome : Diagnosis and treatment].

PubMed

Voss, Frederik; Eckardt, Lars; Busch, Sonia; Estner, Heidi L; Steven, Daniel; Sommer, Philipp; von Bary, Christian; Neuberger, Hans-Ruprecht

2016-12-01

The AV-reentrant tachycardia (AVRT) is a supraventricular tachycardia with an incidence of 1-3/1000. The pathophysiological basis is an accessory atrioventricular pathway (AP). Patients with AVRT typically present with palpitations, an on-off characteristic, anxiety, dyspnea, and polyuria. This type of tachycardia may often be terminated by vagal maneuvers. Although the clinical presentation of AVRT is quite similar to AV-nodal reentrant tachycardias, the correct diagnosis is often facilitated by analyzing a standard 12-lead ECG at normal heart rate showing ventricular preexcitation. Curative catheter ablation of the AP represents the therapy of choice in symptomatic patients. This article is the fourth part of a series written to improve the professional education of young electrophysiologists. It explains pathophysiology, symptoms, and electrophysiological findings of an invasive EP study. It focusses on mapping and ablation of accessory pathways.

Heart failure after conventional metal-on-metal hip replacements

PubMed Central

Gillam, Marianne H; Pratt, Nicole L; Inacio, Maria C S; Roughead, Elizabeth E; Shakib, Sepehr; Nicholls, Stephen J; Graves, Stephen E

2017-01-01

Background and purpose — It is unclear whether metal particles and ions produced by mechanical wear and corrosion of hip prostheses with metal-on-metal (MoM) bearings have systemic adverse effects on health. We compared the risk of heart failure in patients with conventional MoM total hip arthroplasty (THA) and in those with metal-on-polyethylene (MoP) THA. Patients and methods — We conducted a retrospective cohort study using data from the Australian Government Department of Veterans’ Affairs health claims database on patients who received conventional THA for osteoarthritis between 2004 and 2012. The MoM THAs were classified into groups: Articular Surface Replacement (ASR) XL Acetabular System, other large-head (LH) (> 32 mm) MoM, and small-head (SH) (≤ 32 mm) MoM. The primary outcome was hospitalization for heart failure after THA. Results — 4,019 patients with no history of heart failure were included (56% women). Men with an ASR XL THA had a higher rate of hospitalization for heart failure than men with MoP THA (hazard ratio (HR) = 3.2, 95% CI: 1.6–6.5). No statistically significant difference in the rate of heart failure was found with the other LH MoM or SH MoM compared to MoP in men. There was no statistically significant difference in heart failure rate between exposure groups in women. Interpretation — An association between ASR XL and hospitalization for heart failure was found in men. While causality between ASR XL and heart failure could not be established in this study, it highlights an urgent need for further studies to investigate the possibility of systemic effects associated with MoM THA. PMID:27759468

Idiopathic ventricular tachycardia and fibrillation.

PubMed

Belhassen, B; Viskin, S

1993-06-01

Important data have recently been added to our understanding of sustained ventricular tachyarrhythmias occurring in the absence of demonstrable heart disease. Idiopathic ventricular tachycardia (VT) is usually of monomorphic configuration and can be classified according to its site of origin as either right monomorphic (70% of all idiopathic VTs) or left monomorphic VT. Several physiopathological types of monomorphic VT can be presently individualized, according to their mode of presentation, their relationship to adrenergic stress, or their response to various drugs. The long-term prognosis is usually good. Idiopathic polymorphic VT is a much rarer type of arrhythmia with a less favorable prognosis. Idiopathic ventricular fibrillation may represent an underestimated cause of sudden cardiac death in ostensibly healty patients. A high incidence of inducibility of sustained polymorphic VT with programmed ventricular stimulation has been found by our group, but not by others. Long-term prognosis on Class IA antiarrhythmic medications that are highly effective at electrophysiologic study appears excellent.

What Is New in Heart Failure Management in 2017? Update on ACC/AHA Heart Failure Guidelines.

PubMed

Bozkurt, Biykem

2018-04-17

The goal of this paper is to provide a summary of the new recommendations in the most recent 2017 ACC/AHA/HFSA Focused Update of the 2013 ACCF/AHA Guideline for the Management of Heart Failure: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Failure Society of America. The intent is to provide the background and the supporting evidence for the recommendations and to provide practical guidance for management strategies in treatment of heart failure patients. In the 2017 ACC/AHA/HFSA Focused Update of HF guidelines, important additions include new information on biomarkers, specifically on the topics of the diagnostic, prognostic role of natriuretic peptides in heart failure, and the role of natriuretic peptides in screening in patients high risk for HF and prevention of HF. There are important recommendations for treatment of patients with HF with reduced EF (HFrEF), including the beneficial role of angiotensin receptor blocker and neprilysin inhibition (ARNI) treatment in reducing outcomes including mortality, ivabradine in reducing heart failure hospitalizations in stable HFrEF patients with sinus rhythm and heart rate ≥ 70 bpm despite β-blockers. In patients with HF with preserved EF (HFpEF), though there are no studies demonstrating survival benefit, potential benefit with aldosterone antagonism in reducing HF hospitalizations is noted. In treatment of comorbidities, optimization of blood pressure control to less than 130 mmHg is recommended in hypertensive patients to prevent HF or in patients with hypertension and HFrEF or HFpEF. In addition to recognition on the potential role of treatment of iron deficiency anemia to improve symptoms and functional capacity, caution against use of adaptive servo-ventilation in patients with HFrEF and central sleep apnea and against use of erythropoietin stimulating agents in patients with HFrEF is provided. There are new treatment

Renal Denervation for Chronic Heart Failure: Background and Pathophysiological Rationale

PubMed Central

Ewen, Sebastian; Mahfoud, Felix

2017-01-01

The activation of the sympathetic nervous system is associated with cardiovascular hospitalizations and death in heart failure. Renal denervation has been shown to effectively reduce sympathetic overdrive in certain patients with uncontrolled hypertension. Pilot trials investigating renal denervation as a potential treatment approach for heart failure were initiated. Heart failure comorbidities like obstructive sleep apnea, metabolic syndrome and arrhythmias could also be targets for renal denervation, because these occurrences are also mediated by the activation of the sympathetic nervous system. Therefore, renal denervation in heart failure is worthy of further investigation, although its effectiveness still has to be proven. Herein, we describe the pathophysiological rationale and the effect of renal denervation on surrogates of the heart failure syndrome. PMID:28154583

[A case of systemic lupus erythematosus discovered from left heart failure due to lupus induced mitral regurgitation].

PubMed

Ueno, K; Fujimoto, S; Fujimoto, T; Nakano, H; Nakajima, T; Yamano, S; Shiiki, H; Hashimoto, T; Imoto, K; Miyagawa, S; Dohi, K

1999-10-01

A 50-year-old female was admitted to a local hospital because of dyspnea, and diagnosed as having left heart failure secondary to mitral regurgitation. After the improvement of congestive heart failure, polyarthralgia, fever, and positive anti-nuclear antibody were pointed out. She was referred to our hospital for the further evaluation. Serological test showed anti-double stranded DNA antibodies, anti-SS-A antibodies, anti-beta 2-GPI antibodies and biological false positive for syphilis. The diagnosis of SLE has been made from the clinical signs and the serology. Therefore mitral valvular lesion of this patient was considered to be one of the symptoms of SLE. We reported a rare case in which left heart failure was a initial clinical manifestation of SLE.

BMI change during puberty and the risk of heart failure.

PubMed

Kindblom, J M; Bygdell, M; Sondén, A; Célind, J; Rosengren, A; Ohlsson, C

2018-03-12

Hospitalization for heart failure amongst younger men has increased. The reason for this is unknown but it coincides with the obesity epidemic. The aim of this study was to evaluate the association between childhood BMI (Body Mass Index) and BMI change during puberty for risk of adult heart failure in men. Using the BMI Epidemiology Study (BEST), a population-based study in Gothenburg, Sweden, we collected information on childhood BMI at age 8 years and BMI change during puberty (BMI at age 20 - BMI at 8) for men born 1945-1961, followed until December 2013 (n = 37 670). BMI was collected from paediatric growth charts and mandatory military conscription tests. Information on heart failure was retrieved from high-quality national registers (342 first hospitalizations for heart failure). BMI change during puberty was independently of childhood BMI associated with risk of heart failure in a nonlinear J-shaped manner. Subjects in the upper quartile of BMI change during puberty (Q4) had more than twofold increased risk of heart failure compared with subjects in Q1 [HR (Hazard Ratio) = 2.29, 95% CI (Confidence Interval) 1.68-3.12]. Childhood BMI was not independently associated with risk of heart failure. Boys developing overweight during puberty (HR 3.14; 95% CI 2.25-4.38) but not boys with childhood overweight that normalized during puberty (HR 1.12, 95% CI 0.63-2.00) had increased risk of heart failure compared with boys without childhood or young adult overweight. BMI change during puberty is a novel risk factor for adult heart failure in men. © 2018 The Association for the Publication of the Journal of Internal Medicine.

Women-specific risk factors for heart failure: A genetic approach.

PubMed

van der Kemp, Jet; van der Schouw, Yvonne T; Asselbergs, Folkert W; Onland-Moret, N Charlotte

2018-03-01

Heart failure is a complex disease, which is presented differently by men and women. Several studies have shown that reproductive factors, such as age at natural menopause, parity and polycystic ovarian syndrome (PCOS), may play a role in the development of heart failure. Shared genetics may provide clues to underlying mechanisms; however, this has never been examined. Therefore, the aim of the current study was to explore whether any reproductive factor is potentially related to heart failure in women, based on genetic similarities. Conducting a systematic literature review, single nucleotide polymorphisms (SNPs) associated with reproductive factors, heart failure and its risk factors were extracted from recent genome-wide association studies. We tested whether there was any overlap between the SNPs and their proxies of reproductive risk factors with those known for heart failure or its risk factors. In total, 520 genetic variants were found that are associated with reproductive factors, namely age at menarche, age at natural menopause, menstrual cycle length, PCOS, preeclampsia, preterm delivery and spontaneous dizygotic twinning. For heart failure and associated phenotypes, 25 variants were found. Genetic variants for reproductive factors did not overlap with those for heart failure. However, age at menarche, gestational diabetes and PCOS were found to be genetically linked to risk factors for heart failure, such as atrial fibrillation, diabetes and smoking. Corresponding implicated genes, such as TNNI3K, ErbB3, MKL2, MTNR1B and PRKD1, may explain the associations between reproductive factors and heart failure. Exact effector mechanisms of these genes remain to be investigated further. Copyright © 2017. Published by Elsevier B.V.

Reparative resynchronization in ischemic heart failure: an emerging strategy.

PubMed

Yamada, Satsuki; Terzic, Andre

2014-08-01

Cardiac dyssynchrony refers to disparity in cardiac wall motion, a serious consequence of myocardial infarction associated with poor outcome. Infarct-induced scar is refractory to device-based cardiac resynchronization therapy, which relies on viable tissue. Leveraging the prospect of structural and functional regeneration, reparative resynchronization has emerged as a potentially achievable strategy. In proof-of-concept studies, stem-cell therapy eliminates contractile deficit originating from infarcted regions and secures long-term synchronization with tissue repair. Limited clinical experience suggests benefit of cell interventions in acute and chronic ischemic heart disease as adjuvant to standard of care. A regenerative resynchronization option for dyssynchronous heart failure thus merits validation.

The 'aerobic/resistance/inspiratory muscle training hypothesis in heart failure'.

PubMed

Laoutaris, Ioannis D

2018-01-01

Evidence from large multicentre exercise intervention trials in heart failure patients, investigating both moderate continuous aerobic training and high intensity interval training, indicates that the 'crème de la crème' exercise programme for this population remains to be found. The 'aerobic/resistance/inspiratory (ARIS) muscle training hypothesis in heart failure' is introduced, suggesting that combined ARIS muscle training may result in maximal exercise pathophysiological and functional benefits in heart failure patients. The hypothesis is based on the decoding of the 'skeletal muscle hypothesis in heart failure' and on revision of experimental evidence to date showing that exercise and functional intolerance in heart failure patients are associated not only with reduced muscle endurance, indication for aerobic training (AT), but also with reduced muscle strength and decreased inspiratory muscle function contributing to weakness, dyspnoea, fatigue and low aerobic capacity, forming the grounds for the addition of both resistance training (RT) and inspiratory muscle training (IMT) to AT. The hypothesis will be tested by comparing all potential exercise combinations, ARIS, AT/RT, AT/IMT, AT, evaluating both functional and cardiac indices in a large sample of heart failure patients of New York Heart Association class II-III and left ventricular ejection fraction ≤35% ad hoc by the multicentre randomized clinical trial, Aerobic Resistance, InSpiratory Training OutcomeS in Heart Failure (ARISTOS-HF trial).

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