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Heart Failure Treatment (heart + failure_treatment)

Distribution by Scientific Domains

Medical Sciences	100%

Selected Abstracts

The Usefulness of Chronic Heart Failure Treatments in Chronic Cardiac Graft Failure

CARDIOVASCULAR THERAPEUTICS, Issue 1 2010
Osman Najam
Following cardiac transplantation, registry data has demonstrated a gradual improvement in survival over the last several decades, which is testament to continual improvement in aftercare strategy. However, a significant number of patients will eventually develop a new syndrome of chronic heart failure, owing to the multitude of physiological processes that occur after transplantation. This condition, referred to as chronic graft failure (CGF) should be regarded as a unique illness rather than one that is simply analogous with chronic heart failure. In particular, the unique pathophysiological (and pharmacological) environment in the setting of CGF presents a challenging situation to the transplant physician. There is uncertainty over which treatments to offer given a paucity of clinical trial data to support the use of standard heart failure treatments in CGF. In this review, we discuss which chronic heart failure treatments could be considered in the setting of CGF based on their mechanisms of action, benefits within the native heart failure setting, and the relevant issues within the posttransplant environment. [source]

The importance of inhibiting free fatty acid metabolism in heart failure treatment

INTERNATIONAL JOURNAL OF CLINICAL PRACTICE, Issue 4 2007
Graham Jackson
No abstract is available for this article. [source]

Diuretic-Related Side Effects: Development and Treatment

JOURNAL OF CLINICAL HYPERTENSION, Issue 9 2004
Domenic A. Sica MD
Diuretics are important therapeutic tools. First, they effectively reduce blood pressure and have been shown in numerous hypertension clinical trials to reduce both cardiovascular and cerebrovascular morbidity and mortality. In addition, their use has been equally effective in controlling cardiovascular events as angiotensin-converting enzyme inhibitors or calcium channel blockers. Diuretics are currently recommended by the Seventh Report of the Joint National Commission on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure report as first-line therapy for the treatment of hypertension. In addition, they remain an important aspect of congestive heart failure treatment in that they improve the congestive symptomatology, which typifies the more advanced stages of congestive heart failure. This article reviews the commonly encountered side effects with the various diuretic classes. Where indicated, the mechanistic basis and treatment of such side effects is further discussed. [source]

HUMAN HEART ,-ADRENOCEPTORS: ,1 -ADRENOCEPTOR DIVERSIFICATION THROUGH ,AFFINITY STATES' AND POLYMORPHISM

CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 10 2007
P Molenaar
SUMMARY 1In atrium and ventricle from failing and non-failing human hearts, activation of ,1 - or ,2 -adrenoceptors causes increases in contractile force, hastening of relaxation, protein kinase A-catalysed phosphorylation of proteins implicated in the hastening of relaxation, phospholamban, troponin I and C-protein, consistent with coupling of both ,1 - and ,2 -adrenoceptors to stimulatory Gsa -protein but not inhibitory Gia -protein. 2Two ,affinity states', namely ,1H and ,1L, of the ,1 -adrenoceptor exist. In human heart, noradrenaline elicits powerful increases in contractile force and hastening of relaxation. These effects are blocked with high affinity by ,-adenoceptor antagonists, including propranolol, (,)-pindolol, (,)-CGP 12177 and carvedilol. Some beta-blockers, typified by (,)-pindolol and (,)-CGP 12177, not only block the receptor, but also activate it, albeit at much higher concentrations (approximately 2 log units) than those required to antagonize the effects of catecholamines. In human heart, both (,)-CGP 12177 and (,)-pindolol increase contractile force and hasten relaxation. However, the involvement of the ,1 -adrenoceptor was not immediately obvious because (,)-pindolol- and (,)-CGP 12177-evoked responses were relatively resistant to blockade by (,)-propranolol. Abrogation of cardiostimulant effects of (,)-CGP 12177 in ,1 -/,2 -adrenoceptor double-knockout mice, but not ,2 -adrenoceptor-knockout mice, revealed an obligatory role of the ,1 -adrenoceptor. On the basis of these results, two ,affinity states' have been designated, the ,1H - and ,1L -adrenoceptor, where the ,1H -adrenoceptor is activated by noradrenaline and blocked with high affinity by beta-blockers and the ,1L -adrenoceptor is activated by drugs such as (,)-CGP 12177 and (,)-pindolol and blocked with low affinity by beta-blockers such as (,)-propranolol. The ,1H - and ,1L -adrenoceptor states are consistent with high- and low-affinity binding sites for (,)-[3H]-CGP 12177 radioligand binding found in cardiac muscle and recombinant ,1 -adrenoceptors. 3There are two common polymorphic locations of the ,1 -adrenoceptor, at amino acids 49 (Ser/Gly) and 389 (Arg/Gly). Their existence has raised several questions, including their role in determining the effectiveness of heart failure treatment with beta-blockers. We have investigated the effect of long-term maximally tolerated carvedilol administration (> 1 year) on left ventricular ejection fraction (LVEF) in patients with non-ischaemic cardiomyopathy (mean left ventricular ejection fraction 23 ± 7%; n = 135 patients). The administration of carvedilol improved LVEF to 37 ± 13% (P < 0.005); however, the improvement was variable, with 32% of patients showing £ 5% improvement. Upon segregation of patients into Arg389Gly-,1 -adrenoceptors, it was found that carvedilol caused a greater increase in left ventricular ejection faction in patients carrying the Arg389 allele with Arg389Arg > Arg389Gly > Gly389Gly. [source]