Regional Relaxation Abnormalities in Coronary Artery Disease

Abstract

Global left ventricular diastolic dysfunction may be detected in chronic coronary artery disease patients with normal systolic function. M-mode echocardiography was used to investigate the regional left ventricular wall thickening/thinning dynamics that might be responsible for abnormal left ventricular filling in patients with normal or mildly decreased left ventricular ejection fraction. Regional thinning was evaluated in 22 patients with coronary artery disease; comparison regional thickening and thinning indices were derived from 8 angiographically normal control subjects. Regional peak left ventricular posterior wall thinning and early fractional filling decreased from 99 to 65.3 mm/s and from 0.73 to 0.65, respectively, in segments with decreased thickening. By contrast, in posterior wall segments with normal contractility, peak thinning and early fractional filling remained unchanged at 98.2 mm/s and 0.71, respectively. During atrial systole, the peak rate of posterior wall thinning increased in normal and decreased thickening segments from 30.2 to 47.2 and to 44.2 mm/s, respectively. The increase in fractional thinning with atrial systole was only significant, however, in areas with decreased thickening (from 0.15 to 0.25). Thus, in coronary disease patients the results show: (1) areas with decreased systolic function may show disproportionate diastolic dysfunction; (2) ‘compensatory’ early diastolic changes in wall thinning are not demonstrated by areas with normal systolic function, and (3) atrial systole assumes increased importance in maintaining left ventricular diastolic function. These findings suggest that the mechanism for the increased sensitivity of measures of global diastolic function for detecting coronary artery disease may result from a decrease in early relaxation in segments with systolic dysfunction and an inadequate compensatory hyperrelaxation of segments with normal systolic function. Active atrial contraction becomes a major compensatory mechanism for maintaining ventricular filling with diastolic dysfunction.