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To determine whether prolonged, intense exercise training can improve left ventricular function in patients with coronary artery disease, we studied 25 patients, 52 ± 2 years old (mean + SE), who completed a 12 month program of endurance exercise training and 14 additional patients with comparable maximal exercise capacities and ejection fractions who did not exercise. The training program consisted of endurance exercise of progressively increasing intensity, frequency, and duration. During the last 3 months the patients were running an average of 18 miles/week, or doing an equivalent amount of exercise on a cycle ergometer. Maximal attainable V02 increased 37% (p < .001). Of the 10 patients with effort angina, five became asymptomatic, three experienced less angina, and two were unchanged after training. Ejection fraction was determined by equilibrium radionuclide ventriculography. At rest, ejection fraction was 53 + 3% before and 54 ± 3% after training (p = NS). Ejection fraction did not change during maximal supine exercise before training (52 ± 3%), but after training it increased to 58 + 3% (p < .01). During maximal exercise, systolic blood pressure and the rate-pressure product were higher after training. The systolic blood pressure-end-systolic volume relationship was shifted upward and to the left, with an increase in maximal systolic blood pressure (p < .001) and a smaller end-systolic volume (p < .05), providing evidence for an improvement in contractile state after training. In patients who did not participate in training neither this relationship nor the ejection fraction response to exercise was changed after 12 months. Exercise-induced regional wall motion disorders worsened in the training group. Our finding that prolonged, intense exercise training can bring about an improvement in left ventricular contractile function essentially independent of cardiac loading conditions in some patients with coronary artery disease provides evidence for a reduction in the severity of myocardial ischemia despite an increase in the myocardial 02 requirement. Circulation 74, No. 2, 350-358, 1986. EXERCISE TRAINING increases maximal exercise capacity, endurance, and the minimal work rate required to induce myocardial ischemia in patients with coronary artery disease.'-4 These effects have been attributed to adaptations in skeletal muscle and the autonomic nervous system2' 7 that result in smaller increases in heart rate and systolic blood pressure, and

SUMMARY We previously showed that the extent of infarction is virtually identical in patients with anterior and inferior infarction despite the more favorable prognosis associated with the latter. We postulated that the damage associated with inferior infarction is shared by both ventricles, thereby causing less hemodynamic impairment than anterior infarction, which involves only the left ventricle. To further explore this hypothesis, global and regional function of both right and left ventricles was assessed by gated radionuclide ventriculography in 50 patients with infarction within 48 hours after admission and again on the tenth day. Radionuclide ventriculography was also performed in 10 normal subjects. In 22 patients who had anterior infarction, the mean global left ventricular ejection fraction was decreased (27 ± 15% [± SD] vs 64 ± 10% in normal subjects, p < 0.05), reflecting regional abnormalities, and increased only slightly by the tenth day (33 ± 11%, p < 0.05). The global right ventricular ejection fraction was decreased (28 ± 11% vs 43 ± 9% in normal subjects, p < 0.05), reflecting a uniform depression of function without localized abnormalities, and returned to normal by the tenth day (43 ± 12, p < 0.05). In 20 patients who had inferior infarction, global left ventricular ejection fraction was only slightly decreased (51 ± 11%), reflecting inferoapical dysfunction, and did not change (55 ± 10). In contrast, global right ventricular ejection fraction was severely and persistently decreased (23 ± 9 vs 28 ± 9, p > 0.05), reflecting abnormalities primarily of the inferior region. The decreased right ventricular ejection fraction after inferior infarction correlated inversely with enzymatic estimates of infarct size (r --0.85, p < 0.01), although there was no correlation between left ventricular ejection fraction and infarct size. Thus, the functional responses of the ventricles to myocardial infarction are markedly influenced by the site of damage.

The purpose of this study was to examine the relationship between maximal 02 uptake (VO2max) and left ventricular systolic function in patients with coronary artery disease. We studied 27 patients, age 50 10 years (mean + SD), who were asymptomatic and able to attain true VO2max. VO2max was defined by the leveling-off criterion and/or a respiratory exchange ratio of 1.15 or greater. Left ventricular ejection fraction was determined, by gated cardiac blood pool imaging. In patients whose ejection fraction decreased with exercise, VO2max was 21 + 4 vs 27 + 4 ml/kg/min in those whose ejection fraction increased (p < .001). Systolic blood pressure/end-systolic volume relation was shifted upward and to the right in the former group in response to peak exercise. In contrast, the pressure-volume relation was shifted upward and to the left in patients whose ejection fraction increased with exercise. Ejection fraction at rest did not correlate with VO2max. There was a significant but weak correlation between peak exercise ejection fraction and VO2max (r .43, p < .025). Left ventricular exercise reserve, i.e., the change in ejection fraction from rest to exercise, correlated with VO2max (r .77, p < .0002), maximal 02 pulse (r = .50, p < .005), and maximal heart rate during treadmill exercise (r = .61, p < .001). Maximal heart rate during treadmill exercise correlated with VO2max (r = .70, p < .0002). These data suggest that impaired left ventricular function can limit VO2max and that maximal heart rate and left ventricular exercise reserve are among the variables affecting VO2max in patients with coronary artery disease who are not limited by angina. Circulation 70, No. 4, 552-560, 1984. MAXIMAL 02 uptake capacity (VO2max), the best available objective measure of aerobic exercise capacity, 1 is generally lower in patients with coronary artery disease than in age-matched healthy subjects.