Basic mechanisms of disease progression in the failing heart: the role of excessive adrenergic drive.
This review examines experimental evidence that suggests that excessive adrenergic stimulation of the heart may actually contribute to the untoward natural history of congestive heart failure. The basic mechanisms for catecholamine-mediated cardiac toxicity are discussed, as well as relatively new evidence that catecholamine-mediated toxicity is the result of beta-adrenoceptor-mediated cyclic adenosine monophosphate-dependent calcium overload of the cardiac myocyte. The studies reviewed herein provide a plausible biological rationale for the use of beta-adrenergic blocking agents in patients with heart failure.
Department of Medicine, Veterans Administration Medical Center, and Baylor College of Medicine, Houston, TX 77030, USA.
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D000818:Animals; D002395:Catecholamines / Q000378:metabolism*; D018450:Disease Progression; D006333:Heart Failure / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology*; D006439:Hemodynamics; D006801:Humans; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D009490:Neurosecretory Systems / Q000503:physiopathology; D011941:Receptors, Adrenergic / Q000378:metabolism*
D002395:Catecholamines; D011941:Receptors, Adrenergic