Newer concepts in the pathophysiology of ischemic heart disease.
Thus the thrust of these studies suggests that blood flow is the overwhelming factor in determining the consequences of the imbalance of oxygen supply and demand. Moreover, the factors that determine the requirements for tissue survival in the presence of deep ischemia are not the same as those shown for the normal myocardium in figure 1. In deep ischemia, contraction ceases, and metabolism shifts from aerobic to anaerobic pathways. Survival rather than contractile function then becomes the agenda. Not only does supply tend to overshadow demand in determining extent of transmural necrosis, but the anatomical pattern of supply precisely delineates the region at risk following a coronary occlusion as well as the ultimate extent of infarction. These views are summarized in the model presented in figures 12 and 13. The anatomic distribution of the ligated artery determines the lateral limits of the ischemic region (Fig. 12) and thus the lateral extension of necrosis (Fig. 13). The extension of the necrosis across the heart wall depends largely on the status of perfusion within the ischemic region. Extension of an infarct, should it occur, has to be explained by other mechanisms. These might include: (i) vascular obstruction in adjacent vascular systems that were not involved in the first occlusion, (ii) relative ischemia in the normal tissue surrounding the ischemic tissue due to an increased wall stress at the demarcation between contracting and noncontracting tissue, or (9) interruption of vessels supplying large interdigitations of normal tissue within the originally ischemic tissue due to changes associated with the process of infarction of ischemia. Alternatively, much that is called extension of infarction may involve more of the wall transmurally without lateral extension. Additional features of the development of myocardial infarction in figures 12 and 13 include: (i) the development of collateral vessel function resulting in an increased capacity to supply the ischemic area, and (ii) a redistribution of collateral blood flow from necrotic to surviving myocardium within the ischemic area. Thus, as coronary collaterals develop, collateral blood flow becomes increasingly heterogeneous within the ischemic area. Following a coronary occlusion, blood flow is reduced more in the subendocardium, and infarction occurs. Resistance to flow in infarcting tissue increase and causes a redistribution of flow to adjacent surviving layers of myocardium that life toward the epicardium. The process continues and combined with the enlargement of collateral vessels results in a sufficient flow to the epicardial layers so that they may survive.
D000818:Animals; D003326:Coronary Circulation / Q000187:drug effects; D003327:Coronary Disease / Q000201:enzymology / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D003402:Creatine Kinase / Q000378:metabolism; D004285:Dogs; D006339:Heart Rate / Q000187:drug effects; D006801:Humans; D007545:Isoproterenol / Q000494:pharmacology; D009200:Myocardial Contraction / Q000187:drug effects; D009203:Myocardial Infarction / Q000473:pathology; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D010101:Oxygen Consumption
D003402:Creatine Kinase; D007545:Isoproterenol