Newer concepts in the pathophysiology of ischemic heart disease.
A model of myocardial ischemia based on the balance of oxygen demand and supply is presented. Ischemia is invariably the result of a limited coronary blood flow (supply), but increased oxygen consumption is often cited as a factor causing an imbalance of demand and supply. The role of contractility in ischemia, however, has been overemphasized, and inotropic agents such as glycosides and isoproterenol frequently have effects on supply that overshadow their effects on myocardial oxygen consumption. With deep ischemia leading to infarction, supply also tends to overshadow demand in determining the extent of transmural necrosis. Moreover, the anatomic pattern of supply precisely delineates both the region at risk following coronary occlusion and the ultimate extent of the infarction. These views are presented in anatomic models of myocardial ischemia and infarction.
D000818:Animals; D002301:Cardiac Glycosides / Q000627:therapeutic use; D003097:Collateral Circulation; D003326:Coronary Circulation; D003327:Coronary Disease / Q000188:drug therapy / Q000503:physiopathology*; D004285:Dogs; D006339:Heart Rate; D006801:Humans; D007545:Isoproterenol / Q000627:therapeutic use; D008833:Microcirculation; D008954:Models, Biological; D009200:Myocardial Contraction; D009203:Myocardial Infarction / Q000473:pathology; D009206:Myocardium / Q000378:metabolism; D010042:Ouabain / Q000627:therapeutic use; D010101:Oxygen Consumption
D002301:Cardiac Glycosides; D010042:Ouabain; D007545:Isoproterenol