To elucidate the effects of ventricular asynchrony with or without myocardial ischemia on the time constant of left ventricular pressure decay and asymptote, that is, the level to which pressure would decrease if isovolumic pressure decrease continued infinitely, left ventriculography and pressure measurements were investigated in 14 normal subjects and 25 patients with coronary artery disease. Ventricular asynchrony was quantitated by the segmental area-time curve. This study consisted of two parts. 1) After a right atrial pacing stress test, the time constant and asymptote remained unchanged in eight normal subjects. In 18 patients with coronary artery disease and pacing-induced angina, asynchrony increased, the time constant was prolonged (64 +/- 13 to 94 +/- 17 ms, p less than 0.01) and the asymptote decreased (-22 +/- 10 to -46 +/- 20 mm Hg, p less than 0.01) after the pacing. 2) During right ventricular pacing at 80, 100 and 120 beats/min in the patients, asynchrony increased and the time constant was prolonged (55 +/- 7 versus 70 +/- 10, 47 +/- 11 versus 66 +/- 19, 36 +/- 7 versus 53 +/- 13 ms, respectively, p less than 0.01 versus right atrial pacing), whereas the asymptote was unchanged in six normal subjects compared with the value during right atrial pacing at each pacing rate. In seven patients with coronary artery disease, right ventricular pacing at 80, 100 and 120 beats/min also produced an increase in the time constant, while the asymptote was unchanged. Thus, prolongation of the time constant of left ventricular pressure decay may result from ventricular asynchrony even in the absence of myocardial ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)

SUMMARYTo evaluate ventricular filling and interactions between right and left ventricles in patients with old myocardial infarction, right and left ventricular time-volume curves were analyzed from a cineangiographic study of 10 normal subjects (Group 1), 10 patients with old anterior myocardial infarction (Group 2) and 10 patients with old inferior myocardial infarction (Group 3). Volumes of both ventricles were calculated from each frame over an entire cardiac cycle using Simpson's method. From timevolume curves, peak ejection rates, peak filling rates and atrial kick rates were obtained for both ventricles and these parameters were normalized by end-diastolic volume. All patients were in sinus rhythm with heart rates less than 80 beats/min. There were no significant differences among the 3 groups in end-diastolic pressure of both ventricles and mean pulmonary artery pressure. Left ventricular ejection fractions were significantly lower in Groups 2 and 3 than in Group 1 (p<0.001, p<0.005, respectively), although there were no significant differences in end-diastolic volume indexes of either ventricle among the 3 groups. Peak left ventricular ejection rate and peak filling rates of the left and right ventricles were lower in Group 2 than in Group 1 (p<0.01, p<0.05, p<0.01, respectively) and peak filling rate of the right ventricle in Group 2 correlated with the peak filling rate of the left ventricle and left ventricular ejection fraction (r=0.64, r=0.64, respectively). Peak filling rate of the right ventricle in Group 2 correlated inversely with left ventricular peak negative dp/dt (r=-0.72), but no correlation was found between peak filling rate of the right ventricle and left ventricular end-diastolic volume index or mean pulmonary artery pressure. Peak ejection rate of the left ventricle and peak filling rates of both ventricles in Group 3 were lower than in Group 1 (p<0.02, p<0.02, p<0.01, respectively) and no correlation was found between peak filling rates of both ventricles. Wall motion of the right ventricular septal portion was slightly reduced in 5 patients in Group 2. In all patients in Group 3, right ventricular wall motion centering around the right ventricular diaphragmatic portion was re-

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