Altered load dependence of postischemic myocardium.
Intermittent myocardial ischemia can produce areas of postischemic ("stunned") myocardium in the heart of the human with coronary artery disease. These areas are no longer ischemic, but have diminished contractile performance. Although the effects of loading conditions on systolic contraction of normal, ischemic, and failing myocardium have been investigated in great detail, the way in which load affects contraction of postischemic myocardium is not known. The aim of this study was to determine in anesthetized dogs how loading conditions affect the systolic function of a region of myocardium after 10 min of ischemia and 1 h of reperfusion. Sets of piezoelectric crystals were implanted in a test zone and in a remote zone of myocardium. Measurements of systolic wall thickening were made during nine combinations of left atrial pressure (3, 6, and 9 cmH2O) and mean arterial pressure (70, 90, and 110 mmHg). One set of measurements was made under baseline conditions, and a second set was made after 10 min of coronary occlusion and 1 h of reperfusion. Ischemia and reperfusion reduced wall thickening in the test zone 36 +/- 3% and diminished the response to increases in preload. In contrast, the response of the test zone to changes in afterload was unchanged. An interaction between the test zone (in which depressed contraction was observed) and the surrounding myocardium (in which enhanced function was observed) produced the appearance of a regional wall motion abnormality as afterload increased. These results emphasize that the load dependence of postischemic myocardium differs from that of normal myocardium and must be taken into account in clinical studies in which regional contraction is used to monitor the heart for ischemia.
Buffington
C W
CW
Department of Anesthesiology and Critical Care Medicine, University of Pittsburgh, Pennsylvania.
Coyle
R J
RJ
D000818:Animals; D002304:Cardiac Pacing, Artificial; D003250:Constriction; D003327:Coronary Disease / Q000209:etiology / Q000503:physiopathology*; D003331:Coronary Vessels; D004285:Dogs; D006352:Heart Ventricles / Q000503:physiopathology; D006439:Hemodynamics; D008954:Models, Biological; D009200:Myocardial Contraction / Q000502:physiology*; D015425:Myocardial Reperfusion