Temporal changes and histologic relation of postsystolic thickening in an animal model of acute ischemia and reperfusion.

BACKGROUND: We investigated the incidence and temporal changes of postsystolic thickening (PST) during myocardial ischemia and reperfusion to determine factors associated with PST. METHODS: The inferoposterior wall infarction was induced by coronary artery ligation (L) in 22 male cats. Epicardial echocardiographic examination including 2-dimensional, M-mode, and pulsed wave myocardial Doppler imaging of inferoposterior wall was performed at short-axis view before L, and regularly repeated during L until PST was not detected by myocardial Doppler image. Reperfusion (R) was done immediately after PST disappeared, and epicardial echocardiographic examination was repeated for 1 hour. Transmural extent of myocardial necrosis was morphometrically analyzed with triphenyltetrazolium chloride staining. RESULTS: PST measured by myocardial Doppler image was well correlated with that by M-mode (r = 0.63, P <.001). Immediately after L, all 22 cats showed akinesia in 2-dimensional imaging; among them PST was present in 13 cats (59%) and absent in the other 9 cats. The extent of ischemia by perimetric measurement with 2-dimensional imaging was smaller in cats with PST compared with those without (32 +/- 10% vs 47 +/- 5%, P <.001). In 13 cats with PST, the occlusion time until disappearance of PST (90-270 minutes, 160 +/- 70) and transmural extent of myocardial necrosis (0%-72%, 22 +/- 24) were quite variable. After R, PST promptly reappeared in all 13 cats. PST persisted until 1 hour after R in 5 cats, whereas it disappeared in 8 cats as systolic thickening became predominant; occlusion time was significantly longer (220 +/- 40 vs 120 +/- 40 minutes, P <.005) and transmural extent of myocardial necrosis was larger (43 +/- 17% vs 8 +/- 15%, P <.005) in cats with persistent PST until 1 hour after R. CONCLUSION: In acute ischemia and R, we observed variable patterns of PST genesis and maintenance, and different factors were related with these phenomena in each stage. PST could be used not only as a marker of acute ischemia but also as a marker of successful myocardial R, and further study is necessary to test whether PST represents different status of myocardial mechanics according to the extent of myocardial ischemia and necrosis in the clinical setting.