Time course of myocardial necrosis.

The time course of myocardial ischemia was studied in canine myocardium by electron microscopy. Ischemia of the myocardium produces ultrastructural alterations of mitochondria, nuclei, contractile apparatus, and the SR- and T-tubular system that are accompanied by loss of glycogen and intracellular edema. These changes are more pronounced with increasing severity of ischemia, and they allow the differentiation between different stages of reversible and of irreversible injury. Reperfusion of reversibly injured tissue leads to structural recovery; reperfusion of irreversibly injured tissue produces further deterioration. On the basis of ultrastructural data, it was found that in a dog, after 45 minutes of coronary artery occlusion, subendocardial infarction was present in 20% of all animals. Transmural infarction was present in 24% of all dogs after 90 minutes of coronary artery occlusion and in 53% after 24 hours. The individual variability in the speed of development of infarction is caused by the rate of oxygen consumption at the time of occlusion and by the amount of collateral flow. Intermittent ischemia is much better tolerated than permanent ischemia of the same duration. Species differences are evident. The course of development of myocardial necrosis, therefore, depends on time, rate of oxygen consumption, collateral flow, mode of ischemia, and on the species investigated.