Literature DB >> 11527116

Beta-blocking agents in heart failure: modern concepts and overview.

B E Strauer1.   

Abstract

Heart failure is characterized by the inability of the myocardium to shorten sufficiently or to eject an adequate stroke volume to maintain normal perfusion of both the cardiac and the extracardiac organs. Irrespective of etiologic reasons, the depression of myocardial contractility represents one of the major mechanisms that contributes to low output in heart failure. Despite their intrinsic negative inotropic effects, beta-receptor-blocking agents have been used in numerous studies for treating the failing heart, especially in dilated cardiomyopathy and ischemic heart disease. In this regard, specific therapeutic aims of the use of beta-receptor-blocking agents in chronic heart failure have been described. e.g., reduction of an increased heart rate in tachycardia, blood pressure reduction in hypertensive heart failure, improvement of supraventricular and ventricular arrhythmias, depression of an increased sympathetic tone (e.g., in hyperthyrioidism, pheochromocytoma), increase in the amount of downregulated beta-receptors, and anti-ischemic effects in coronary artery disease. For chronic heart failure, therefore, some special indications may be established and may be individually used; for acute heart failure, only very rare indications are present (e.g., hypertensive crisis, life-threatening cardiac arrhythmias). The actual rationale for the use of beta-receptor blocking agents in heart failure is therefore analyzed with regard to pathophysiology, clinical effects, and clinical outcome of treated patients.

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Year:  1990        PMID: 11527116

Source DB:  PubMed          Journal:  J Cardiovasc Pharmacol        ISSN: 0160-2446            Impact factor:   3.105


  1 in total

1.  Untangling ligand induced activation and desensitization of G-protein-coupled receptors.

Authors:  Peter J Woolf; Jennifer J Linderman
Journal:  Biophys J       Date:  2003-01       Impact factor: 4.033

  1 in total

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