The Adrenergic System and Prevention of Myocardial Damage by β-Blockade: A Clinical Overview


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Abstract

SummaryHigh sympathetic outflow, or stress, can cause cardiac damage. Sudden death and death from myocardial infarction peak at about 09.00–10.00 a.m., coincident with peak sympathetic drive. Catecholamines can cause ECG changes and myocardial necrotic changes—probably due to an excess of intracellular free calcium leading to mitochondrial damage. Such changes are seen in stress states such as subarachnoid hemorrhage and trauma and correlate positively with plasma catecholamine levels; β1-blockade prevents such cardiac damage. Sympathetic tone is probably raised in hypertensive patients. The most common cause of death in hypertensive patients is myocardial infarction. β-Blockers, compared to diuretics, probably prevent death from myocardial infarction, certainly in men: this benefit is probably confined to non-smokers if nonselective β-blockade is used. The possible mechanisms of the benefit of β-blockade in the prevention of cardiac damage are (a) reduction in the myocardial oxygen requirement by slowing the heart rate and lowering blood pressure and the velocity of left ventricular contraction, (b) reduction of infarct size, (c) prevention of catecholamine-induced myocardial necrosis, (d) prevention of catecholamine-induced life-threatening arrhythmias, (e) prevention of cardiac rupture, and (f) prevention of atheromatous plaque formation and rupture by reduction of arterial flow disturbance and wall stress. Possible reduction of endothelial permeability to lipids and inhibition of cholesterol esterification in the plaque may also be important.

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