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Ischemia-induced depressed systolic thickening is transiently augmented by remote coronary occlusion
J A Gascho1, G L Copenhaver, W R Davidson
1Milton S. Hershey Medical Center, Pennsylvania State University, Hershey 17033.
Insights
Remote coronary occlusion can temporarily boost myocardial thickening during ischemia. This effect, observed in canine hearts, may be linked to systolic unloading, not increased blood flow.
Area of Science:
- Cardiovascular Physiology
- Myocardial Ischemia Research
- Coronary Circulation Dynamics
Background:
- Ischemia-induced myocardial dysfunction is a critical clinical concern.
- Understanding compensatory mechanisms in the heart is vital for therapeutic development.
- Previous studies have explored regional myocardial responses to coronary occlusion.
Purpose of the Study:
- To investigate whether remote coronary occlusion can enhance myocardial thickening impaired by ischemia.
- To elucidate the mechanisms underlying the transient augmentation of myocardial function during combined coronary insults.
- To assess the role of blood flow and the Frank-Starling mechanism in this phenomenon.
Main Methods:
- Utilized an anesthetized open-chest canine model.
- Measured posterior wall function using pulsed Doppler crystal.
- Induced left anterior descending coronary artery occlusion during reduced circumflex coronary artery flow.
- Quantified blood flow using microspheres and assessed cardiac function via echocardiography.
Main Results:
- Left anterior descending occlusion caused a significant, transient increase in posterior wall thickening fraction (3.7% to 5.9%).
- This augmentation diminished within 135 seconds.
- Increased posterior blood flow or a Frank-Starling mechanism did not explain the observed transient thickening.
- Systolic unloading was proposed as a potential etiological factor.
Conclusions:
- Remote coronary occlusion can transiently augment ischemia-impaired myocardial thickening.
- The observed effect is likely mediated by systolic unloading rather than increased perfusion.
- This finding offers insights into the complex interplay of regional myocardial responses during ischemic events.
Abstract:
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.