Circulation, Vol 72, 1125-1134, Copyright © 1985 by American Heart Association
WY Lew and E Ban-Hayashi
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.
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Mechanisms of improving regional and global ventricular function by preload alterations during acute ischemia in the canine left ventricle
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