Physiological early diastolic intraventricular pressure gradient is lost during acute myocardial ischemia

A consistent pattern of intraventricular regional pressure gradients exists under physiological conditions during the rapid filling phase of diastole in the normal dog left ventricle. We hypothesized that this pressure gradient pattern is caused, in part, by early diastolic recoil of the left ventricular walls in conjunction with release of elastic potential energy stored during systole, generating suction and thus contributing to diastolic filling. If so, any condition that interferes with normal regional systolic function might be expected to modify the pattern of the normal early diastolic intraventricular pressure gradients. Accordingly, the present study was designed to determine whether acutely induced regional systolic left ventricular mechanical dysfunction is accompanied by changes in the pattern of the early diastolic intraventricular pressure gradients. Acute myocardial ischemia was induced by balloon occlusion of the left anterior descending coronary artery (LAD) in nine anesthetized closed-chest dogs. The maximum early diastolic intraventricular pressure gradient (MIVP) was measured between the mid-left ventricle and apex with a dual-sensor micromanometer (3-cm spacing between the sensors) before and 20 minutes after LAD occlusion. Ejection fraction (EF) and number of dyskinetic chords (DChords) were measured from left ventricular contrast ventriculograms. Twenty minutes after LAD occlusion, the nine dogs evidenced significant changes in EF (56±10% to 37±8%), DChords (0±0 to 17±16 chords), left ventricular minimum pressure (-1.7±0.5 to 0.0±1.5 mm Hg), left ventricular end-diastolic pressure (4.2±1.2 to 5.9±2.2 mm Hg), and heart rate (90±17 to 103±18 beats/min). These changes were accompanied by a marked decline in MIVP (1.2±0.5 to 0.6±0.6 mm Hg). All changes are significant at the 0.05 level. Throughout both baseline and occlusion conditions, a significant linear relation between MIVP and EF was found for the nine dogs (r=0.76, p<0.001). For baseline data alone, the relation between MIVP and EF was also strong (r=0.81, p<0.008). After LAD occlusion, MIVP and EF did not correlate significantly (r=0.53, p=NS), whereas MIVP and the DChords did (r=0.80, p<0.010). These results strongly suggest that the left ventricular early diastolic apical intraventricular pressure gradient is causally related to left ventricular systolic function, and that in the setting of a severe regional wall motion abnormality, factors operate that are not explained by single-plane angiography and single-site pressure measurement. We conclude that systolic dysfunction, engendered by extensive anterior myocardial ischemia, is associated with the attenuation, loss, or even reversal of the MIVP during the rapid filling phase of diastole. We speculate that these changes are probably related to the loss of myocardium available to store and release energy in the form of elastic recoil, and to changes known to occur in the pattern of blood flow during systole, especially in ventricles exhibiting extensive regions of dyskinesis.