Stress-induced and sympathetically-mediated electrocardiographic and circulatory variations in the primary hyperkinetic heart syndrome

Abstract

As shown by the inotropic changes, the sympathetic discharge on the heart, is selectively enhanced by mental stimuli, and inhibited by pain in the primary hyperkinetic heart syndrome. In the steady state the electrocardiogram shows flat, diphasic, or 'tucked' T waves. Mental stimulation or isoproterenol, and, respectively, pain or beta blockade induce changes of the repolarization phase divergent from steady state. The former causes ST depression and deep T-wave inversion and the latter fully normalizes the repolarization phase. It is concluded that the electrical activity of the heart is directly influenced by the adrenergic drive in this disorder, and that different stressful factors can alter the repolarization phase in opposite ways in relation to the influence of the stimulus on the cardiac sympathetic tone.