Apical Myocardial Stunning in a Large Size Porcine Model Assessed by Strain and Strain Rate Echocardiography

Abstract

Warm ischemia and subsequent reperfusion of the heart can induce a temporary dysfunction known as myocardial stunning. The aim of this study was to investigate the ability of tissue Doppler imaging (TDI) to quantify longitudinal myocardial stunning close to the apex, and perform a comparison with sonomicrometry using a well-established large size porcine model. In anesthetized pigs, postischemic myocardial stunning was induced by occluding LAD for 15 min followed by 90 min reperfusion (n = 7). Long-axis strain and strain rate was quantified by both TDI and sonomicrometry. During reperfusion, peak systolic strain measured by TDI decreased from -11.2% (+/-3.0) at baseline to -4.9% (+/-3.6), -3.4% (+/-2.9), and -4.3% (+/-5.0) at 30, 60, and 90 min, respectively (all P < 0.007). Postsystolic strain increased from -1.3% (+/-1.6) at baseline to -6.4% (+/-4.4), -4.8% (+/-4.0), and -5.2% (+/-2.7) by TDI in the reperfusion phase (all P < 0.048 except at 60 min of reperfusion (P = 0.081)). Postsystolic index increased from 0.10 (+/-0.13) at baseline to 0.56 (+/-0.24), 0.54 (+/-0.30), and 0.64 (+/-0.37) subsequently (all P < 0.012). [Correction added after online publication 30-May-2007: In the preceding sentence, the phrase 'Postsystolic index decreased from 0.10 (+/-0.13)' was changed to 'Postsystolic index increased from 0.10 (+/-0.13).'] Difference-mean and line of identity plots did not disclose any systematic error, but revealed substantial variation, indicating a mismatch between TDI and sonomicrometry. It is feasible to quantify postischemic myocardial stunning by TDI in a large size porcine model using longitudinal postsystolic shortening, and postsystolic index as indicators. TDI and sonomicrometry data reach the same end point, but the two techniques are not interchangeable when investigating myocardial stunning close to apex in reference to longitudinal strain and strain rate.