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The authors acknowledge the contributions of Dr. Shmuel S. Schwartzenberg, MD, who was a coauthor of this chapter in the previous edition.
Significant coronary artery stenosis results in impaired blood flow and reduced myocardial oxygen supply. When myocardial oxygen demand exceeds supply, myocardial ischemia develops. In addition, in the setting of a complete coronary artery occlusion, myocardial necrosis can occur. As a result of hypoxia, the myocardium shifts from aerobic oxidative phosphorylation to anaerobic metabolism. Consequently, both fatty acid and carbohydrate oxidation decrease, adenosine triphosphate production is impaired, and glycolysis is accelerated, which requires increased uptake of glucose by the heart. , The glucose taken up by the ischemic myocardium is not readily oxidized in the mitochondria but rather is converted to lactate, resulting in a fall in intracellular pH and a decrease in contractile work. Successful reperfusion of reversibly injured myocytes is associated with partial or complete restoration to the control state of many of the metabolic changes present in the ischemic myocytes and resumption of oxidative phosphorylation. ,
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