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.
KeywordsAction Potential Duration Postmyocardial Infarction Cardiac Purkinje Fibre Maximum Diastolic Potential Repolarization Time
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