Left ventricular function in coronary artery disease. Evaluation of slope of end-systolic pressure-volume line (Emax) and ratio of peak systolic pressure to end-systolic volume (P/Ves).

Left ventricular function was assessed by measurement of systolic pressure-volume variables and ejection fraction in seven normal subjects (group I), five patients with coronary artery disease and normal symmetric left ventricular wall motion (group II) and eight patients with remote myocardial infarction and segmental akinesia (group III). Left ventricular volumes were obtained from right anterior oblique ventriculograms and pressures from catheter-tip micromanometer (14 patients) or fluid-filled catheters (6 patients) at two different systolic loads. P/Ves was calculated as the ratio of peak systolic pressure (P) to end-systolic volume (Ves) at rest, Emax as the slope of the end-systolic pressure volume line constructed at two systolic loads, and Vo as the volume axis intercept of this line. Emax was significantly (p less than 0.01) lower in patients with segmental akinesia (group III) (5.0 +/- 0.5) than in normal subjects (group I) (10.4 +/- 0.8) or patients with coronary artery disease and normal wall motion (group II) (9.9 +/- 0.8). In contrast, there was no significant difference in P/Ves among the three groups (6 +/- 1.0 in group I, 5 +/- 0.8 in group II, 3.7 +/- 0.5 in group III). Similarly, Ves and Vo failed to separate the three groups. Although ejection fraction was significantly (p less than 0.05) lower in group III (0.56 +/- 0.03) than in groups I and II (0.67 +/- 0.03 in both groups), there was considerable overlap of individual values in the three groups. In eight patients, measurements were repeated during isometric exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

Captopril in congestive heart failure resistant to other vasodilators.

In an attempt to study the possible mechanism(s) by which captopril controls resistant heart failure, sequential haemodynamic studies (radioisotope technique) and humoral measurements (plasma renin activity, plasma aldosterone and plasma catecholamines) were obtained in 11 such patients. The studies were made at the time patients became unresponsive to other vasodilators (hydralazine or prazosin); the vasodilator drug was then discontinued and five days later, the 'no-vasodilator' studies were obtained. Captopril therapy was then started. Optimum daily maintenance dose of captopril varied from 75 to 200 mg in different patients. Studies were again repeated after a period of time equal to the duration of the previous vasodilator therapy. Digitalis and diuretic doses were kept constant throughout. Captopril improved effort tolerance in ten patients. Haemodynamically, mean blood pressure and peripheral resistance were lower than during vasodilator therapy (85 +/- 3.1 v. 92 +/- 3.3 mmHg and 47 +/- 4.4 v. 59 +/- 4.4 U.M2, respectively; p less than 0.05 for both). Cardiac index was higher during captopril treatment (1.95 +/- 0.15 v. 1.63 +/- 0.10 l/m2, p less than 0.01) and pulmonary mean transit was normalized by captopril (14.6 +/- 1.7 v. 18.4 +/- 1.3 s, p less than 0.05). Humoral indices revealed a significant (p less than 0.05) reduction in plasma aldosterone during captopril therapy (25.9 +/- 5.6 ng/dl during captopril, v. 62 +/- 22 ng/dl with no vasodilators and 50.9 +/- 6.1 ng/dl with other vasodilators). Moreover, there was a decrease in circulating plasma catecholamines during captopril treatment, but differences between the three treatment periods were not statistically significant.(ABSTRACT TRUNCATED AT 250 WORDS)