To assess the causal relation between acute mental stress and myocardial ischemia, we evaluated cardiac function in selected patients during a series of mental tasks (arithmetic, the Stroop color--word task, simulated public speaking, and reading) and compared the responses with those induced by exercise. Thirty-nine patients with coronary artery disease and 12 controls were studied by radionuclide ventriculography. Of the patients with coronary artery disease, 23 (59 percent) had wall-motion abnormalities during periods of mental stress and 14 (36 percent) had a fall in ejection fraction of more than 5 percentage points. Ischemia induced by mental stress was symptomatically "silent" in 19 of the 23 patients with wall-motion abnormalities (83 percent) and occurred at lower heart rates than exercise-induced ischemia (P less than 0.05). In contrast, we observed comparable elevations in arterial pressure during ischemia induced by mental stress and ischemia induced by exercise. A personally relevant, emotionally arousing speaking task induced more frequent and greater regional wall-motion abnormalities than did less specific cognitive tasks causing mental stress (P less than 0.05). The magnitude of cardiac dysfunction induced by the speaking task was similar to that induced by exercise. Personally relevant mental stress may be an important precipitant of myocardial ischemia--often silent--in patients with coronary artery disease. Further examination of the pathophysiologic mechanisms responsible for myocardial ischemia induced by mental stress could have important implications for the treatment of transient myocardial ischemia.

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.

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Two studies assess relationships of hostility to extent and severity of exercise-induced cardiac ischemia and daily life ischemia in patients with coronary artery disease (CAD). CAD patients (N = 80) who underwent exercise tomographic thallium testing to assess myocardial perfusion completed the Cook-Medley Hostility Inventory (Ho). A Composite Hostility (Chost) score obtained from the Ho scale was also used. Statistically controlling for the effects of gender in the full sample (N = 80), Chost was positively correlated with severity of perfusion defects (r = 0.22, p < 0.05). This relationship was nonsignificant in the 63 male patients, but was significant among women (N = 17, r = 0.42, p < 0.05) and among middle-aged men (less than 60 years, N = 17, r = 0.55, p < 0.05). In an overlapping sample of 42 CAD patients with ischemia (ST-segment depression > or = 1 mm) during 24 to 48 hours of ambulatory electrocardiographic monitoring, after controlling for gender, both Ho and Chost were positively correlated with total minutes of ischemia (r = 0.28 and r = 0.29, respectively, p < 0.05). In addition, there was a significant gender x hostility interaction, with stronger relationships with hostility evident for women. Results from these two studies indicate that in patients with coronary artery disease, hostility traits are significantly correlated with extent of daily life ischemia and with severity of exercise-induced myocardial ischemia. These relationships appear to be significant among female and middle aged male patients, but may be less evident among older male patients.

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To explore the effect of beta-adrenergic blockade on low heart rate-related (mental stress) ischemia, 19 patients with coronary artery disease were randomized into a double-blind crossover trial of metoprolol, 100 mg twice daily, and underwent serial mental stress/bicycle exercise studies. Mental stress-induced wall motion abnormalities occurred at a lower heart rate than exercise-induced wall motion abnormalities during placebo administration (81 +/- 16 vs. 123 +/- 20 beats/min, p less than 0.05). Metoprolol reduced the mean magnitude of exercise-induced wall motion abnormalities (2.8 +/- 2.0 vs. 1.6 +/- 2.4, p = 0.003); improvement was related to the magnitude of hemodynamic beta-blockade effect. Metoprolol did not significantly reduce the mean magnitude of mental stress-induced wall motion abnormalities (3.0 +/- 2.2 vs. 2.6 +/- 2.2), although individual responses predominantly either improved (50%) or worsened (29%). Unlike exercise, the magnitude of hemodynamic beta-blockade did not predict mental stress response and metoprolol did not block mental stress-induced blood pressure elevations. Patients with abolition of exercise-induced ischemia were more likely to have reduction of mental stress-induced ischemia. Patients whose ischemia worsened with metoprolol during mental stress had more easily inducible ischemia, as assessed by exercise-induced placebo wall motion abnormality, chest pain and prior myocardial infarction. Beta-blockade was associated with a lowering of ischemia-related hemodynamic thresholds compared with placebo. These results suggest that beta-blockade has a variable effect on low heart rate-related ischemia that may be due to a lack of effect on mental stress-induced blood pressure elevation in patients with easily induced ischemia or to effects on coronary vasomotor tone, or both.

The recent development of the VEST, an ambulatory radionuclide detector, to measure left ventricular ejection fraction may enhance the detection of ischemia during daily activities in patients with coronary artery disease. The normal range and determinants of ejection fraction responses to stimuli other than physical exercise, however, are not adequately characterized. Therefore, ejection fraction responses to various activities were measured in 18 normal subjects utilizing the VEST. Uniform increases (greater than 5%) in ejection fraction were seen during physical exercise, uniform decreases were seen during cold pressor testing and modest changes (including decreases greater than 5%) were seen in ejection fraction during mental stress, micturition and hyperventilation. Different forms of stress produced significantly different changes in ejection fraction, even when values were controlled for changes in heart rate. Ventricular loading conditions in the form of enhanced blood pressure responses during mental stress may have contributed to the relatively smaller changes in ejection fraction compared with those during exercise. Subjects demonstrating a decrease in ejection fraction during mental stress did not differ from other subjects in hemodynamic reactivity during mental testing but did have evidence of increased parasympathetic tone during cold pressor and bicycle exercise testing. The results reveal that normal ejection fraction response differs among varying physiologic stimuli. These changes are in part related to changes in heart rate and blood pressure; however, other factors, such as neurohumoral regulation, may also play a role. These findings indicate that the patient's activity and the setting in which it occurs must be considered when interpreting ambulatory ejection fraction responses.