Ischemic, hemodynamic, and neurohormonal responses to mental and exercise stress. Experience from the Psychophysiological Investigations of Myocardial Ischemia Study (PIMI).
BACKGROUND
The pathophysiology of mental stress-induced myocardial ischemia, which occurs at lower heart rates than during physical stress, is not well understood.


RESULTS
The Psychophysiological Investigations of Myocardial Ischemia Study (PIMI) evaluated the physiological and neuroendocrine functioning in unmedicated patients with stable 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, there were increases in heart rate, systolic blood pressure, cardiac output, and systemic vascular resistance that were correlated with increases in plasma epinephrine. During exercise, systemic vascular resistance fell, and there was no relationship between the hemodynamic changes and epinephrine levels. The fall in ejection fraction was greater with mental stress than exercise. During mental stress, the changes in ejection fraction were inversely correlated with the changes in systemic 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 norepinephrine occurred with ischemia during exercise, and greater increases in systemic vascular resistance occurred with ischemia during mental stress.


CONCLUSIONS
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.
Goldberg
A D
AD
Henry Ford Heart and Vascular Institute, Detroit, MI 48202, USA. DASH@AOL.COM
Becker
L C
LC
Bonsall
R
R
Cohen
J D
JD
Ketterer
M W
MW
Kaufman
P G
PG
Krantz
D S
DS
Light
K C
KC
McMahon
R P
RP
Noreuil
T
T
Pepine
C J
CJ
Raczynski
J
J
Stone
P H
PH
Strother
D
D
Taylor
H
H
Sheps
D S
DS
D000328:Adult; D000368:Aged; D002395:Catecholamines / Q000097:blood*; D004837:Epinephrine / Q000097:blood; D005260:Female; D006439:Hemodynamics; D006801:Humans; D008297:Male; D008875:Middle Aged; D017202:Myocardial Ischemia / Q000209:etiology*; D009638:Norepinephrine / Q000097:blood; D005082:Physical Exertion; D013312:Stress, Physiological / Q000097:blood / Q000150:complications* / Q000503:physiopathology; D013315:Stress, Psychological / Q000097:blood / Q000150:complications* / Q000503:physiopathology
D002395:Catecholamines; D009638:Norepinephrine; D004837:Epinephrine