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The effect of different mechanisms of myocardial ischemia on left ventricular function
R E Carlson1, K M Kavanaugh, A J Buda
1Department of Internal Medicine, University of Michigan Medical School, Ann Arbor 48109-0366.
Insights
Supply-type ischemia from coronary occlusion causes more severe left ventricular dysfunction than demand-type ischemia. This study compared both ischemia types in dogs, finding greater impairment with reduced blood flow.
Area of Science:
- Cardiovascular Physiology
- Ischemic Heart Disease Research
- Animal Models in Cardiac Studies
Background:
- Myocardial ischemia, a condition of insufficient blood flow to the heart muscle, can arise from reduced supply or increased demand.
- Understanding the distinct impacts of supply- versus demand-induced ischemia is crucial for diagnosing and treating heart conditions.
Purpose of the Study:
- To comparatively assess the extent and severity of left ventricular dysfunction caused by supply-type versus demand-type myocardial ischemia.
- To elucidate the differential effects of coronary occlusion and pharmacologically induced increased myocardial oxygen demand on cardiac function.
Main Methods:
- Utilized anesthetized, open-chest dogs for experimental investigation.
- Employed two-dimensional echocardiography to evaluate left ventricular function.
- Employed tracer microspheres to quantify regional myocardial blood flow, specifically in the left circumflex artery (LCx) territory.
Main Results:
- Supply-type ischemia (LCx occlusion) led to a significant decrease in mean arterial pressure, while demand-type ischemia (dobutamine infusion post-stenosis) increased heart rate and mean arterial pressure.
- Subendocardial blood flow in the LCx region was drastically reduced in the supply-type ischemia group compared to the demand-type ischemia group.
- Left ventricular dysfunction, assessed by echocardiography, was significantly more extensive and severe in the supply-type ischemia group than in the demand-type ischemia group.
Conclusions:
- Coronary occlusion-induced supply-type ischemia results in a more profound and widespread impairment of left ventricular function compared to demand-type ischemia.
- Pharmacological induction of increased myocardial oxygen demand, even with a compromised coronary artery, causes less severe cardiac dysfunction than complete flow limitation.
Abstract:
Myocardial ischemia may be produced by limitation of blood flow as in abrupt coronary occlusion, termed supply-type ischemia, or by increasing myocardial oxygen demand in the setting of restricted flow, termed demand-type ischemia. To examine the comparative extent and severity of the dysfunction related to both forms of ischemia, we studied anesthetized, open-chest dogs by means of two-dimensional echocardiography and tracer microspheres. Supply-type ischemia was produced by total occlusion of the LCx (n = 7); demand-type ischemia was induced by infusion of dobutamine after creation of a critical LCx stenosis (n = 6). At the time of the production of ischemia, the group with demand-type ischemia had significant increases in both heart rate (p less than 0.05) and mean arterial pressure (p less than 0.05), whereas the group with supply-type ischemia had a decrease in mean arterial pressure (p less than 0.05). Subendocardial blood flow in the LCx region was severely depressed in supply-type ischemia (0.09 +/- 0.04 ml/min/gm) compared to demand-type ischemia (1.04 +/- 0.07 ml/min/gm; p less than 0.01). Although both groups of animals had an abnormality of left ventricular function during ischemia, as determined by two-dimensional echocardiography, the extent of the dysfunction in the group with supply-type ischemia was greater (146 +/- 12 degrees) compared to the group with demand-type ischemia (99 +/- 9 degrees; p less than 0.01). Similarly, the degree of left ventricular dysfunction in the group with supply-type ischemia was greater than that for the group with demand-type ischemia (p less than 0.05). Thus these data suggest that supply-type ischemia produced by coronary occlusion results in a greater extent and degree of left ventricular functional abnormality than pharmacologically induced demand-type ischemia.