Diastolic stiffening induced by acute myocardial infarction is reduced by early reperfusion.

Reperfusion early during myocardial infarction improves ejection fraction and this improvement may represent myocardial salvage in the injured segment. Alternatively, reperfusion of injured myocardium may cause intramyocardial hemorrhage with resultant increased stiffness causing a dyskinetic segment to become akinetic, thus improving ejection fraction without concomitant myocardial salvage. To evaluate this possibility, diastolic stiffness was assessed in a closed chest, anesthetized, normothermic dog model immediately after a 1 or 3 h occlusion of the left anterior descending coronary artery and during the 4 weeks after occlusion. Acute myocardial infarction in experimental dogs was accompanied by a fivefold increase in the chamber stiffness constant, a threefold increase in the myocardial stiffness constant and a significant increase in elastic stiffness and end-diastolic pressure. These changes occurred contemporaneously with a marked decline in ejection fraction. Early reperfusion (1 h occlusion) resulted in improvement of the ejection fraction accompanied by simultaneous resolution of the previously increased stiffness. Late reperfusion (3 h occlusion) resulted in permanent depression of ejection fraction with permanent elevation of stiffness. These results indicate that the improved systolic function observed after early reperfusion reflects a process other than increased stiffness, perhaps salvage of jeopardized myocardium.