Sympathoadrenal and cardiovascular responses to mental stress, isometric handgrip, and cold pressor test in asymptomatic young men with primary T wave abnormalities in the electrocardiogram.

Abstract

Sympathoadrenal activity was evaluated by the determination of plasma catecholamines at rest and during stressful provocations in 12 young asymptomatic men with primary T wave abnormalities in the electrocardiogram and without a history or signs of cardiac disease (group T) and in 13 matched controls. The T wave abnormalities consisted of notching, flattening, or inversion without concomitant ST depression in leads II, V4, and V6. At rest, plasma noradrenaline was approximately twice as high in group T as in the controls, whereas plasma adrenaline and dopamine levels were similar in the two groups. Non-invasive haemodynamic monitoring (blood pressure and impedance cardiography) showed a significantly higher systolic blood pressure and impedance signs of increased cardiac contractility without tachycardia in group T. A standardised mental stress test, isometric hand grip, and a cold pressor test all significantly increased blood pressure, as well as noradrenaline and adrenaline in both groups. The increases in diastolic blood pressure and adrenaline tended to be larger in group T in connection with stressful provocations, indicating increased sympathoadrenal reactivity. The increases in systolic blood pressure and noradrenaline persisted during provocations. In both groups the cold pressor test, which raises blood pressure mainly by vasoconstriction, increased noradrenaline more than did the other two tests, which are believed to act mainly by cardiac stimulation. Because of the low adrenaline levels found, neurogenic mechanisms appear to be of greater importance than adrenaline for the circulatory responses to each of these provocations. The study provides evidence in favour of increased sympathetic activity at rest and enhanced sympathoadrenal reactivity during stress in subjects with primary T wave abnormalities. These electrocardiographic findings may therefore be explained by increased sympathoadrenal activity.