Mechanisms of improving regional and global ventricular function by preload alterations during acute ischemia in the canine left ventricle WILBUR

We examined the influence of left ventricular end-diastolic pressure (LVEDP) on the mechanical interaction between ischemic and nonischemic areas during acute myocardial ischemia. Circumferentially oriented ultrasonic segment gauges were implanted in the midwall of the anterior apex and posterior apex of the left ventricle in seven anesthetized dogs. Stroke volume was measured with a flow probe around the ascending aorta in five of these animals. We varied LVEDP with vena caval occlusion and dextran infusions to three matched levels (7, 12, and 19 mm Hg) before and 30 min after complete occlusion of the mid left anterior descending coronary artery. With acute ischemia, the anterior apex or ischemic zone demonstrated marked segmental lengthening during isovolumetric systole (end-diastole to aortic valve opening) and akinesis during the ejection phase (aortic valve opening to closure). In the posterior apex or nonischemic area, isovolumetric shortening increased and ejection phase shortening decreased during acute ischemia when compared with those under control conditions at the same LVEDP. Thus, a portion of the shortening generated by the nonischemic area was expended in stretching the ischemic zone during isovolumetric systole, thereby reducing the amount of ejection phase shortening. As LVEDP was increased, there was a parallel decrease in both the amount of isovolumetric lengthening in the ischemic zone and the isovolumetric shortening in the nonischemic area. As a result, acute ischemia produced less of a reduction in ejection phase shortening in the nonischemic area and in stroke volume at high as compared with low LVEDP. We conclude that the ischemic zone imposes a mechanical disadvantage on the nonischemic area, the magnitude of which is directly proportional to the amount of isovolumetric lengthening or bulge in the ischemic zone. An increase in LVEDP during acute ischemia improves regional and global ventricular function by both the Frank-Starling mechanism in the nonischemic (but not the ischemic) area and by reducing the mechanical disadvantage that the ischemic zone imposes on the nonischemic area. Circulation 72, No. 5, 1125-1134, 1985. IN PATIENTS with acute myocardial infarction, therapeutic alteration of the left ventricular filling pressure to an "optimal" level improves stroke volume while minimizing adverse hemodynamic effects. 1-Although much of this improvement is due to the FrankStarling mechanism in nonischemic areas, additional alterations in regional function may be involved. Accordingly, this study was designed to examine the effects of preload manipulation during acute ischemia on From the Cardiovascular Division, University of Califomia, San Diego, and the San Diego Veterans Administration Medical Center. Supported by the National Institutes of Health grant HL-28644 and by the Research Service of the Veterans Administration. Address for correspondence: Wilbur Y. W. Lew, M.D., Cardiovascular Division l l1A, VA Medical Center, 3350 La Jolla Village Dr., San Diego, CA 92161. Received Feb. 26, 1985; revision accepted Aug. 19, 1985. *Current address: Instituto Nacional de Cardiologia, Servicio de Medicina Nuclear, Juan Badiano No. 1, Tlalpan D.F. CP 14080, Mexico. regional function in the ischemic zone and on the mechanical interaction between ischemic and nonischemic areas. Recently, we postulated that a mechanical interaction between ischemic and nonischemic areas occurs during acute myocardial ischemia.7 After occlusion of a coronary artery, paradoxical lengthening during isovolumetric systole was observed in the ischemic zone. In nonischemic areas, end-diastolic segmental length increased due to the increase in left ventricular enddiastolic pressure (LVEDP), and total segmental shortening (from end-diastole to aortic valve closure) increased due to the Frank-Starling mechanism. However, all of the increase in nonischemic area shortening occurred during isovolumetric systole (from end-diastole to aortic valve opening), and developed coincident with the development of paradoxical isovoVol. 72, No. 5, November 1985 1125 by gest on A ril 0, 2017 http://ciajournals.org/ D ow nladed from