ISCHEMIC, HEMODYNAMIC, AND NEUROHORMONAL RESPONSES TO MENTAL AND EXERCISE STRESS - EXPERIENCE FROM THE PSYCHOPHYSIOLOGICAL INVESTIGATIONS OF MYOCARDIAL-ISCHEMIA STUDY (PIMI)
Ad. Goldberg et al., ISCHEMIC, HEMODYNAMIC, AND NEUROHORMONAL RESPONSES TO MENTAL AND EXERCISE STRESS - EXPERIENCE FROM THE PSYCHOPHYSIOLOGICAL INVESTIGATIONS OF MYOCARDIAL-ISCHEMIA STUDY (PIMI), Circulation, 94(10), 1996, pp. 2402-2409
Background The pathophysiology of mental stress-induced myocardial isc
hemia, which occurs at lower heart rates than during physical stress,
is not well understood. Methods and Results The Psychophysiological In
vestigations of Myocardial Ischemia Study (PIMI) evaluated the physiol
ogical and neuroendocrine functioning in unmedicated patients with sta
ble coronary artery disease and exercise-induced ischemia. Hemodynamic
and neurohormonal responses to bicycle exercise, public speaking, and
the Stroop test were measured by radionuclide ventriculography, ECG,
and blood pressure and catecholamine monitoring. With mental stress, t
here were increases in heart rate, systolic blood pressure, cardiac ou
tput, and systemic vascular resistance that were correlated with incre
ases in plasma epinephrine. During exercise, systemic vascular resista
nce fell, and there was no relationship between the hemodynamic change
s and epinephrine levels. The fall in ejection fraction was greater wi
th mental stress than exercise. During mental stress, the changes in e
jection fraction were inversely correlated with the changes in systemi
c vascular resistance. Evidence for myocardial ischemia was present in
92% of patients during bicycle exercise and in 58% of patients during
mental stress. Greater increases in plasma epinephrine and norepineph
rine occurred with ischemia during exercise, and greater increases in
systemic vascular resistance occurred with ischemia during mental stre
ss. Conclusions Mental stress-induced myocardial ischemia is associate
d with a significant increase in systemic vascular resistance and a re
latively minor increase in heart rate and rate-pressure product compar
ed with ischemia induced by exercise. These hemodynamic responses to m
ental stress can be mediated by the adrenal secretion of epinephrine.
The pathophysiological mechanisms involved are important in the unders
tanding of the etiology of myocardial ischemia and perhaps in the sele
ction of appropriate anti-ischemic therapy.