No abstract

Cardiovascular reactivity to stress is hypothesized to be a marker for subsequent neurogenic cardiovascular disease, but few prospective studies of this hypothesis are available. We studied 910 white male medical students who had their blood pressure and pulse rate measured before and during a cold pressor test in the years [1948][1949][1950][1951][1952][1953][1954][1955][1956][1957][1958][1959][1960][1961][1962][1963][1964]. Hypertensive status (requiring drug treatment) was ascertained by annual questionnaires in the 20-to 36-year follow-up period. An association was observed between maximum change in systolic blood pressure and later hypertension, with a cumulative incidence of hypertension by age 44 of 6.7%, 3.0%, and 2.4% for a change in systolic blood pressure in the upper, middle two, and lowest quartiles, respectively (Kaplan-Meier, p<0.02). After adjustment for study entry age, Quetelet Index, cigarette smoking, pretest systolic blood pressure, and paternal or maternal history of hypertension in a Cox model, the association persisted. The excess risk associated with systolic blood pressure reactivity was not apparent until the population aged some 20 years and was most apparent among those in whom hypertension developed before age 45 (relative risk=2.5, 95% confidence intervals=1.47, 4.71 for a 20 mm Hg change). Diastolic blood pressure and heart rate changes were not associated with later hypertension. These data suggest that persons prone to later hypertension manifest an altered physiology at a young age. (Hypertension 1989;14:524-530)

Mental stress during daily life, including reported feelings of tension, frustration, and sadness, can more than double the risk of myocardial ischemia in the subsequent hour. The clinical significance of mental stress-induced ischemia during daily life needs to be further evaluated.

Mental stress-induced myocardial ischemia is associated with a significant increase in systemic vascular resistance and a relatively minor increase in heart rate and rate-pressure product compared with ischemia induced by exercise. These hemodynamic responses to mental stress can be mediated by the adrenal secretion of epinephrine. The pathophysiological mechanism involved are important in the understanding of the etiology of myocardial ischemia and perhaps in the selection of appropriate anti-ischemic therapy.

This report evaluates the relationships of hemodynamic reactivity and determinants of myocardial oxygen demand to myocardial ischemia during mental stress in coronary artery disease patients. Thirty-nine patients and 12 controls were studied by radionuclide ventriculography during three mental tasks (arithmetic, Stroop task, and simulated public speaking). Patients were subdivided into three groups based on the severity of ischemic wall motion responses to the mental stressors. Results revealed that systolic blood pressure (SBP) levels during the mental tasks and SBP reactivity (increases) to stress were highest for the severely ischemic group, lowest for controls, with the mild-moderate ischemic and nonischemic patients in between. Severely ischemic patients started out with lower double product (heart rate x SBP) levels, and reached higher levels during the Stroop and speech tasks. There were no reliable group effects for diastolic blood pressure, heart rate, or left ventricular end-diastolic volumes. Among severely ischemic patients, the most potent task in eliciting ischemia (the speech) was associated with higher cardiovascular levels and elicited greater heart rate, double product, and ventricular volume responses. The present data indicate a relationship between cardiovascular levels and reactivity and the magnitude of ischemia induced by mental stress.