Prevention of Myocardial Damage Following Acute Brain Injuries by Beta-Blockade

Abstract

Ancient man was heavily dependent upon his sympathetic nervous system for survival in a “fright, flight or fight” environment. Stress in modern man is more subtle and insidious and is often maintained over prolonged periods of time: high catecholamine production can, over a period of time (maybe as short as a few hours) cause myocardial damage. In animals catecholamine administration can cause subendocardial necrotic lesions [1] and similar lesions, or “stress cardiomyopathy”, have been identified in a) the hearts of patients with phaeochromocytoma [2, 3], b) homicide victims who had been subjected to very high levels of stress [4], and c) patients with ischaemic heart disease who die suddenly [5]. It is of interest that plasma catecholamine concentration in man reaches a peak at about 10.00 a.m. to noon [6, 7] and this time point coincides with the peak incidence of myocardial infarction and sudden death [6,8]. Silent ischaemia also peaks at this late morning period and can be significantly inhibited by beta1-selective blockade (atenolol) [9] (Fig. 1). Ischaemic stroke also peaks at this vulnerable period [10] but the effects of treatment are unknown (Fig. 2).