Relaxation and Diastolic Distensibility of the Regionally Ischemic Left Ventricle

Abstract

Normal left ventricular contraction and relaxation are dependent upon an appropriate balance between myocardial oxygen supply and demand. In the clinical setting, myocardial ischemia is commonly associated with left ventricular dysfunction. It has been observed by many investigators that a transient, reversible rise in left ventricular diastolic pressure commonly accompanies angina pectoris [1–4]. This increase in diastolic pressure could be due simply to an increase in diastolic volume, resulting from contractile failure of ischemic myocardium and an increased residual volume. Alternatively, the increased diastolic pressure might reflect decreased diastolic distensibility of the left ventricular chamber, with a higher diastolic pressure being needed to achieve the same degree of end-diastolic sarcomere stretch. These potential mechanisms for the increased diastolic pressure that characterizes angina pectoria are illustrated in Figure 20-1. The rise in diastolic pressure seen in patients with angina pectoris has been studied extensively by clinical investigators [5–14], and there is now widespread agreement that the phenomenon results from both decreased left ventricular diastolic distensibility and impaired contractile function. As shown by Sasayama and coworkers [9], the left ventricular diastolic pressure-volume relationship curve shifts upward and slightly to the right during angina pectoris. This shift apparently represents a direct upward shift of the pressure-segment length relationship for ischemic myocardium and a rightward or Frank-Starling shift for the remaining nonischemic myocardium (Figure 20-2).