Contemporary Medical Management of Systolic Heart Failure

Nair, Ajith; Timoh, Tendoh; Fuster, Valentín

doi:10.1253/circj.cj-11-1424

Cited by 22 publications

(14 citation statements)

References 94 publications

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“…Accurate risk stratification for the early identification of patients who are at higher risk for poor outcome is critical for the management of HF patients [2], [3]. Laboratory tests, imaging examinations, and clinical signs are three categories of tools widely used in HF prognosis estimation [4], [5].…”

Section: Introductionmentioning

confidence: 99%

Prognostic Value of Red Blood Cell Distribution Width for Patients with Heart Failure: A Systematic Review and Meta-Analysis of Cohort Studies

et al. 2014

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AimsMultiple studies have investigated the prognostic role of red blood cell distribution width (RDW) for patients with heart failure (HF), but the results have been inconsistent. The aim of the present study was to estimate the impact of RDW on the prognosis of HF by performing a systematic review and meta-analysis.Methods and ResultsThe Embase, PubMed, and Web of Science databases were searched up to November 16, 2013 to identify eligible cohort studies. The quality of each study was assessed using the Newcastle-Ottawa Scale (NOS). The association between RDW, either on admission or at discharge, and HF outcomes (all-cause mortality [ACM], heart transplantation, cardiovascular mortality, and rehospitalization, etc.) were reviewed. The overall hazard ratio (HR) for the effect of RDW on ACM was pooled using a random-effects model, and the publication bias was evaluated using funnel plots and Eggers' tests. Seventeen studies, with a total of 18288 HF patients, were included for systematic review. All eligible studies indicated that RDW on admission and RDW at discharge, as well as its change during treatment, were of prognostic significance for HF patients. The HR for the effect of a 1% increase in baseline RDW on ACM was 1.10 (95% confidence interval: 1.07–1.13), based on pooling of nine studies that provided related data. However, publication bias was observed among these studies.ConclusionsHF patients with higher RDW may have poorer prognosis than those with lower RDW. Further studies are needed to explore the potential mechanisms underlying this association.

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Section: Introductionmentioning

confidence: 99%

Prognostic Value of Red Blood Cell Distribution Width for Patients with Heart Failure: A Systematic Review and Meta-Analysis of Cohort Studies

et al. 2014

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“…Nevertheless, CHF mortality remains high, the quality of a patient's life low, and the economic burden on our health system is enormous (Morrissey et al, 2011;Nair et al, 2012). During the last decade, numerous reports have delineated cardioprotective properties of erythropoietin (EPO) in experimental animal models of acute myocardial infarction (MI) (Bogoyevitch, 2004;Lipsic et al, 2006;Koul et al, 2007;Latini et al, 2008;Riksen et al, 2008;Vogiatzi et al, 2010).…”

Section: Introductionmentioning

confidence: 99%

Chronic Administration of Small Nonerythropoietic Peptide Sequence of Erythropoietin Effectively Ameliorates the Progression of Postmyocardial Infarction–Dilated Cardiomyopathy

Ahmet

Tae

Brines

et al. 2013

J Pharmacol Exp Ther

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The cardioprotective properties of erythropoietin (EPO) in preclinical studies are well documented, but erythropoietic and prothrombotic properties of EPO preclude its use in chronic heart failure (CHF). We tested the effect of long-term treatment with a small peptide sequence within the EPO molecule, helix B surface peptide (HBSP), that possesses tissue-protective, but not erythropoietic properties of EPO, on mortality and cardiac remodeling in postmyocardial infarction-dilated cardiomyopathy in rats. Starting 2 weeks after permanent left coronary artery ligation, rats received i.p. injections of HBSP (60 mg/kg) or saline two times per week for 10 months. Treatment did not elicit an immune response, and did not affect the hematocrit. Compared with untreated rats, HBSP treatment reduced mortality by 50% (P , 0.05). Repeated echocardiography demonstrated remarkable attenuation of left ventricular dilatation (end-diastolic volume: 41 versus 86%; end-systolic volume: 44 versus 135%; P , 0.05), left ventricle functional deterioration (ejection fraction: 24 versus 263%; P , 0.05), and myocardial infarction (MI) expansion (3 versus 38%; P , 0.05). A hemodynamic assessment at study termination demonstrated normal preload independent stroke work (63 6 5 versus 40 6 4; P , 0.05) and arterioventricular coupling (1.2 6 0.2 versus 2.7 6 0.7; P , 0.05). Histologic analysis revealed reduced apoptosis (P , 0.05) and fibrosis (P , 0.05), increased cardiomyocyte density (P , 0.05), and increased number of cardiomyocytes in myocardium among HBSP-treated rats. The results indicate that HBSP effectively reduces mortality, ameliorates the MI expansion and CHF progression, and preserves systolic reserve in the rat post-MI model. There is also a possibility that HBSP promoted the increase of the myocytes number in the myocardial wall remote from the infarct. Thus, HBSP peptide merits consideration for clinical testing.

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“…In contrast, pharmacologic agents that block RAS and SNA not only improve exercise tolerance and QOL, but also reduce cardiovascular mortality. 14,18,19, 84 ACE inhibitors and ARB are established treatments for CHF, improving clinical symptoms and prognosis. 84 Both of these vasodilators essentially inhibit RAS and angiotensin II, resulting in improvements in skeletal muscle dysfunction in humans and animal models of CHF.…”

Section: Pharmacological Therapiesmentioning

confidence: 99%

“…14,18,19, 84 ACE inhibitors and ARB are established treatments for CHF, improving clinical symptoms and prognosis. 84 Both of these vasodilators essentially inhibit RAS and angiotensin II, resulting in improvements in skeletal muscle dysfunction in humans and animal models of CHF. 18, 19 Researchers in a previous study performed muscle biopsies in patients with CHF to investigate the effects of RAS inhibition on skeletal muscle abnormalities.…”

Section: Pharmacological Therapiesmentioning

confidence: 99%

Exercise Intolerance in Chronic Heart Failure

Okita

Kinugawa

Tsutsui

2013

Circ J

105

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Chronic heart failure (CHF) is characterized as a clinical disorder displaying exercise intolerance; patients typically complain of early muscular fatigue. Previously, it was thought to be simply a failure of perfusion to the exercising musculature and consequent early onset of intramuscular acidosis in CHF. However, improved hemodynamics by cardiotonic agents did not lead to an increase in exercise tolerance. Later studies have shown that intrinsic skeletal muscle abnormalities exist in patients with CHF and could induce the early anaerobic metabolism that limits exercise tolerance. We review the clinical importance of skeletal muscle abnormalities in patients with CHF. Considering the significance of peripheral muscle abnormalities and their development might help physicians and researchers better understand the mechanisms of well-established exercise training and pharmacological therapies that have been shown to improve the prognosis for CHF, and thus develop potential novel therapies. (Circ J 2013; 77: 293 -300)

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Contemporary Medical Management of Systolic Heart Failure

Cited by 22 publications

References 94 publications

Prognostic Value of Red Blood Cell Distribution Width for Patients with Heart Failure: A Systematic Review and Meta-Analysis of Cohort Studies

Prognostic Value of Red Blood Cell Distribution Width for Patients with Heart Failure: A Systematic Review and Meta-Analysis of Cohort Studies

Chronic Administration of Small Nonerythropoietic Peptide Sequence of Erythropoietin Effectively Ameliorates the Progression of Postmyocardial Infarction–Dilated Cardiomyopathy

Exercise Intolerance in Chronic Heart Failure

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