Serial changes in left and right ventricular systolic and diastolic dynamics during the first year after an index left ventricular Q wave myocardial infarction

Objectives. This study quantified serially biventricular emptying and filling after infarction and related these to changes in volume, muscle mass, wall stress and contractility. Background. There are limited dat on serial changes in ventricular dynamics after infarction. Methods. Forty patients had serial electron beam computed tomographic examinations during the first year after index Q wave infarction (21 anterior, 19 inferior), and global biventricular volumes, peak rates of emptying and filling and left ventricular muscle masses were quantified. Mean mid-left ventricular end-systolic wall stresses, rate-corrected velocities of circumferential shortening and two indexes of left ventricular contractility—the end-systolic wall stress/volume ratio and the end-systolic wall stress/rate-corrected velocity of circumferential shortening relation—were estimated in each instance. Results. Patients with anterior infarction had an increase in biventricular chamber volume of 15% to 35% by 1 year. Global biventricular peak rates of emptying and filling were decreased by 20% to 30% from hospital discharge to 6 weeks but thereafter remained unchanged. Despite significant increase in mean wall stresses, the end-systolic wall stress/volume ratio remained unchanged during the year. The rate-corrected velocities of circumferential shortening declined serially after anterior infarction but did so in proportion to the increase in mean wall stresses, consistent with no net change in left ventricular contractility. Patients with inferior infarction showed trend toward similar changes, but the magnitudes did not reach significance. Conclusions. Left (and right) ventricular global peak rates of emptying and filling during the first year after infarction can be altered in the absence of additional ischemic injury but are more consistent with responses to changes in left ventricular afterload than changes in intrinsic ventricular performance or contractility. Serial changes in left ventricular afterload after infarction are largely due to progressive chamber enlargement and limited development of compensatory hypertrophy during the first year. Intrinsic global left ventricular contractile performance was not altered by postinfarction cardiac remodeling in the patients examined