Ischemia‐Induced depressed systolic thickening is transiently augmented by remote coronary occlusion

To determine if ischemia‐induced depressed myocardial thickening can be augmented by remote coronary occlusion, posterior wall function (pulsed Doppler crystal) was measured before and after left anterior descending coronary artery occlusion in the presence of reduced circumflex coronary artery flow (of sufficient severity to reduce resting function) in an anesthetized open‐chest canine preparation in which the circumflex was pump‐perfused with carotid arterial blood. Left anterior descending coronary occlusion elicited an immediate significant increase in posterior bed thickening fraction (TF%) (3.7 ± 1.5 to 5.9 ± 1.3%), but by 135 sec TF% had again deteriorated. The transient increase in thickening was not caused by increased flow to the posterior bed (microspheres, n = 3), nor was it related to a Frank‐Starling mechanism (echocardiography, n = 3). Despite an ischemic‐induced reduction in systolic shortening, systolic thickening can be transiently augmented by remote coronary occlusion. The etiology may be related to systolic unloading.