Distinctive changes in end-diastolic wall thickness and postsystolic thickening in viable and infarcted myocardium

Objectives In this study, we sought to compare the magnitude of changes in end-diastolic wall thickness (WT_ed) and postsystolic thickening (PST) in a swine model of stunning and reperfused acute myocardial infarction, and to explore the relationship between WT_ed and PST. Methods Twenty-six pigs were subjected to left anterior descending coronary artery occlusion followed by reperfusion to induce stunning (n = 6), nontransmural (n = 8), or transmural (n = 12) myocardial infarction. Myocardial wall thickness was measured using intracardiac echocardiography. Transmural extent of necrosis (TEN) was quantified by triphenyltetrazolium chloride technique. Results During the first minutes of reperfusion, a marked increase in WT_ed occurred in the myocardial walls with nontransmural and transmural infarct (42% and 102%, respectively) but less in those with stunning (19%). PST persisted at reperfusion in walls with stunning and nontransmural infarct (23% and 26%, respectively). In transmurally infarcted walls, PST progressively decreased either during occlusion (5/12 pigs) or shortly after reperfusion (7/12 pigs). PST at reperfusion was virtually absent when TEN was >70%. Both PST and the increase in WT_ed at reperfusion correlated well with TEN (P < .0001 for both). Changes in PST at reperfusion were weakly correlated with changes in WT_ed. Conclusions A marked increase in WT_ed after reperfusion and absence of PST indicate transmural myocardial infarction. Presence of PST at reperfusion indicates viable tissue in more than 30% of wall thickness. The results suggest that amplitude of PST is modulated predominately by factors related to the severity of ischemia and, to a smaller extent, by changes in wall thickness.