Increased afterload intensifies asynchronous wall motion and impairs ventricular relaxation.

To clarify whether impaired left ventricular relaxation elicited by increased afterload is attributable to regional dyssynchrony, we analyzed in dogs simultaneous left ventricular contrast ventriculography and pressure before and during angiotensin II infusion. Regional shortening was measured by a centerline method and a video-intensity method that served to define asynchronous motion. During angiotensin II, peak left ventricular pressure increased 35 +/- 6 mmHg, and the isovolumic pressure time constant (tau) was prolonged from 32.7 +/- 4.1 to 39.2 +/- 7.6 ms (P < 0.01). During increased afterload, early diastolic asynchrony, confined to the apical (5 of 7) and inferior regions (2 of 7), was detected in all dogs. Early systolic asynchrony was detected in the apical (5 of 7) and inferior (1 of 7) regions in six dogs. At control, systolic excursion was lower in the anteroapical than in the anterobasal region (P < 0.05). During angiotensin II, excursion of all regions was reduced, with the apical region lower than other regions (P < 0.01). In the normal dog heart, impaired relaxation with augmented afterload is coincident with asynchronous wall motion, especially in the apical-inferior region. Temporal dispersion of regional contraction may explain delayed left ventricular relaxation associated with increased afterload.