[Sympathetic activity in patients with heart failure due to idiopathic dilated cardiomyopathy: modification by beta receptor blockers--a therapeutic approach?].
Increased sympatho-adrenergic activity is a compensatory mechanism in cardiac failure. Accordingly, beta-receptor blockers are generally regarded as contraindicated for use in heart failure. In 1975, Waagstein reported the first successful use of beta-receptor blockers in patients with idiopathic dilated cardiomyopathy. It was shown that the prognosis of patients with dilated cardiomyopathy could be improved by beta-receptor blockade. In this regard, most experience is associated with metoprolol. It should be stressed that the initial, and long-term dosage, as well, was maintained at a very low level (beginning, for example, with 6.25 mg metoprolol daily). An on-going, international, multicenter study is intended to clarify which patients with dilated cardiomyopathy may benefit from treatment with beta-receptor blockers. Additionally, further information is anticipated with respect to the complex mechanism of action. Beside the direct cardiac action with blockade of the cardiotoxic effect of the extremely high levels of plasma catecholamines, induction of an upregulation of the down-regulated beta-1-receptors there is attenuation of the activity of the renin-angiotensin-aldosterone system. Overall, this leads to interruption of the vicious cycle of maladaption associated with chronic heart failure and its attendant unfavorable vasoconstriction and sodium and water retention. This positive aspect of beta-1-receptor blockade in dilated cardiomyopathy carries with its initially and unavoidable negative inotropic effect and thus, in the individual patient, the net effect is difficult to predict. Consequently, the indication must be established on an individual basis.(ABSTRACT TRUNCATED AT 250 WORDS)
Lohmann
F W
FW
I. Innere Abteilung des Krankenhauses Berlin-Neukölln.
D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use*; D002311:Cardiomyopathy, Dilated / Q000188:drug therapy*; D002395:Catecholamines / Q000097:blood; D006333:Heart Failure / Q000188:drug therapy*; D006439:Hemodynamics / Q000187:drug effects; D006801:Humans; D013564:Sympathetic Nervous System / Q000187:drug effects*
D000319:Adrenergic beta-Antagonists; D002395:Catecholamines