Myocardial ischemia and myocardial function

Hippokratia 1997, 1(3):129-143

N. Lefkos


Myocardial ischemia directly affects the diastolic initially and then the systolic cardiac function. The biochemical changes, in cellular level, during severe ischemia are summarized as follow: a) a rapid exhaustion of ATP and CP reserves, b) decomposition of AMP to adenosine which is rapidly converted to hypoxanthine, iosine and a small amount of xanthine, and c) intracellular increase of nonorganic phosphates, Mg++ and intracellular acidosis which in parallel, with the rapid exhaustion of the low reserves of glucagone, inhibits the initially activated anaerobic glycolysis. In about 15 minutes, the initially reversible phase of ischemic disturbances, in cellular level, converted to irreversible, because of the breakdown of the sarcolema of myocardial cells as a result of uncontrolled Ca++ increase, intracellular oedema and free-oxygen radicals production. Functional ischemic disorders of myocardial contractility are classified as reversible [stunning and hibernating myocardium] and permanent [necrosis of a myocardial region]. The chronic [permanent] ischemic disorders of myocardial function were attributed to: a) loss of extended regions of contracil myocardium and distortion of the pattern of left ventricle both contributed to chronic overload of surviving myocardium and b) inactivation of systemic or local neurohormonal systems who directly affect cardiac cells [myocardiac cells and inoblasts]. Finally, the cardioprotection against myocardial ischemia is obtained by: a) endogenous mechanisms [such as ischemic “preconditioning” and its second window, hypoxia, catecholamines, acetylcholine, tachycardia or rapid pacing], b) metabolic and c) pharmacologic agents [Ca++-antagonists, b-blockers, a-MEA, trimetazidine etc).