Author + information
- Received July 24, 1997
- Revision received January 30, 1998
- Accepted February 5, 1998
- Published online May 1, 1998.
- Diwakar Jain, MD, FACCA,* (, )
- Sheriff M Shaker, MDA,
- Matthew Burg, PhDA,
- Frans J.Th Wackers, MD, FACCA,
- Robert Soufer, MD, FACCA and
- Barry L Zaret, MD, FACCA
- ↵*Dr. Diwakar Jain, 3 FMP Section of Cardiovascular Medicine, Yale University School of Medicine, 333 Cedar Street, New Haven, Connecticut 06520.
Objectives. We sought to investigate the mechanism of a mental stress–induced fall in left ventricular ejection fraction (LVEF) in patients with coronary artery disease.
Background. Mental stress induces a fall in LVEF in a significant proportion of patients with coronary artery disease. This is accompanied by an increase in heart rate, blood pressure and rate–pressure product. Whether the mental stress–induced fall in LVEF is due to myocardial ischemia, altered loading conditions or a combination of both is not clear.
Methods. Left ventricular (LV) function was studied noninvasively by serial equilibrium radionuclide angiocardiography and simultaneous measurement of peak power, a relatively afterload-independent index of LV contractility, in 21 patients with coronary artery disease (17 men, 4 women) and 9 normal subjects (6 men, 3 women) at baseline, during mental stress and during exercise. Peripheral vascular resistance (PVR), cardiac output (CO), arterial and end-systolic ventricular elastance (Ea, Ees) and ventriculoarterial coupling (V/AC) were also calculated. Patients underwent two types of mental stress—mental arithmetic and anger recall—as well as symptom-limited semisupine bicycle exercise.
Results. Nine patients (43%) had an absolute fall in LVEF of ≥5% (Group I) in response to at least one of the mental stressors, whereas the remaining patients did not (Group II). Group I and Group II patients were similar in terms of baseline characteristics. Both groups showed a significant but comparable increase in systolic blood pressure (15 ± 7 vs. 9 ± 10 mm Hg, p = 0.12) and a slight increase in heart rate (7 ± 4 vs. 8 ± 7 beats/min, p = 0.6) and a comparable increase in rate–presure product (2.2 ± 0.9 vs. 1.9 ± 1.2 beats/min × mm Hg, p = 0.6) with mental stress. However, PVR increased in Group I and decreased in Group II (252 ± 205 vs. −42 ± 230 dynes·s·cm−5, p = 0.006), and CO decreased in Group I and increased in Group II (−0.2 ± 0.4 vs. 0.6 ± 0.7 liters/min, p = 0.02) with mental stress. There was no difference in the change in peak power (p = 0.4) with mental stress. With exercise, an increase in systolic blood pressure, heart rate, rate–pressure product and CO and a fall in PVR were similar in both groups. Of the two mental stressors, anger recall resulted in a greater fall in LVEF and a greater increase in diastolic blood pressure. Exercise resulted in a fall in LVEF in 7 patients (33%). However, exercise-induced changes in LVEF and hemodynamic variables were not predictive of mental stress–induced changes in LVEF and hemodynamic variables.
Conclusions. Abnormal PVR and Earesponses to mental stress and exercise are observed in patients with a mental stress–induced fall in LVEF. Peripheral vasoconstrictive responses to mental stress contribute significantly toward a mental stress–induced fall in LVEF.
- Received July 24, 1997.
- Revision received January 30, 1998.
- Accepted February 5, 1998.
- The American College of Cardiology