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

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.

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.

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).

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 predominantely by factors related to the severity of ischemia and, to a smaller extent, by changes in wall thickness.