Adrenergic Arrhythmogenicity

  • E. M. Vaughan Williams
Part of the Handbook of Experimental Pharmacology book series (HEP, volume 89)

Abstract

An association between stress or emotion and a “heart attack” has long been recognized. A reasonable explanation would be that an increase in blood pressure, or pulse pressure, in a coronary artery already containing an atheromatous plaque could cause the latter to split and expose underlying collagen to platelets, which in turn would initiate thrombosis. The protection offerred by long-term beta-blockade to postmyocardial infarction (MI) patients against reinfarction and sudden death has been claimed to be due to a blunting of hypertensive surges, thus obviating the wall-stress which could split a plaque. If this explanation is correct in attributing the prophylactic benefits of beta-blockers solely to protection of coronary arteries, the alpha-adrenoceptor blockers or other antihypertensive agents not acting on adrenergic receptors would be expected to provide similar prophylaxis.

Keywords

Ischemia Adenosine Noradrenaline Adrenaline Glycoside 

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Copyright information

© Springer-Verlag Berlin Heidelberg 1989

Authors and Affiliations

  • E. M. Vaughan Williams

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