1987 Volume 51 Issue 1 Pages 83-89
Mechanisms related to increased left ventricular filling pressure associated with myocardial ischemia were studied in 13 patients with coronary artery disease. Single-plane left ventriculograms were obtained using a high fidelity micromanometer-tipped catheter in the control and post-pacing periods. All patients developed typical anginal pain during pacing tachycardia. Seven patients (group I) demonstrated no significant changes in ejection fraction (EF) and peak systolic pressure-end-systolic volume ratio (P/Ves) after rapid pacing. End-diastolic pressure (EDP), however, increased significantly from 14.9±4.9 to 24.4±8.5 mmHg (p<0.01). The regional myocardial function was expressed by a radial coordinate system with its origin at the center of gravity of the end-diastolic contour. In the normal segment, the end-diastolic length (EDL) was augmented by 13.6%, associated with a 22.4% increase in stroke excursion with pacing stress. In the ischemic segment, EDL remained unchanged, but stroke excursion was significantly reduced. The diastolic pressure-volume curve shifted directly upward or more to the right, while the diastolic pressure-length curve moved up on the single curve in the normal segment and shifted directly upward or more to the right, while the diastolic pressure-length curve moved up on the single curve in the normal segment and shifted directly upward in the ischemic segment, so that pressure was higher at any given segment length in the ischemic segment, indicating regional alteration of the diastolic properties. Thus, an ischemic response to pacing tachycardia Changes in the regional myocardial performance are consistent and the global function is determined by the interaction of changes in regional function of both normal and ischemic myocardium.
