Transmural myocardial perfusion.
The predilection for subendocardial underperfusion and ischemia is great and must be considered in the management of any patient, especially if there is coronary artery disease or ventricular hypertrophy. Although the mechanisms of subendocardial ischemia remain to be fully defined, they are clearly associated with the transmural distribution of intramyocardial systolic pressures. Even though almost all the myocardium is perfused in diastole, a reduction of diastolic perfusion pressure or duration will result in subendocardial ischemia. The factors that produce subendocardial ischemia are all associated with a reduction or loss of coronary flow reserve, and as our ability to measure flow reserve in humans improves, it is likely that we will be able to select medical or surgical therapy that will minimize or abolish subendocardial ischemia. For example, it will someday become possible to choose a time for valve replacement in an asymptomatic patient to obtain maximal protection of the myocardium or to select the right combination of therapies for the immediate post-operative period so that as much myocardium as possible will be spared. The more we learn to understand the mechanisms of subendocardial ischemia, the sooner will we be able to achieve these desired ends.
D000818:Animals; D001024:Aortic Valve Stenosis / Q000503:physiopathology; D006332:Cardiomegaly / Q000503:physiopathology; D002417:Cattle; D003326:Coronary Circulation; D003327:Coronary Disease / Q000503:physiopathology*; D004285:Dogs; D006321:Heart / Q000503:physiopathology; D006352:Heart Ventricles; D006439:Hemodynamics; D006706:Homeostasis; D006801:Humans; D009200:Myocardial Contraction; D009203:Myocardial Infarction / Q000503:physiopathology; D009206:Myocardium / Q000378:metabolism; D010101:Oxygen Consumption; D010496:Pericardium / Q000503:physiopathology; D005082:Physical Exertion; D013610:Tachycardia / Q000503:physiopathology