The present study introduces a new clinical method to define left ventricular (LV) end systole (ES) during tissue Doppler imaging (TDI). Preliminary experiments showed a sharp inflection point in strain traces (S(IP)) from ischemic borderzones, which coincided with onset of a postsystolic shortening wave (V(PS)) in the velocity trace. In a single-vessel disease model, we investigated whether S(IP) and V(PS) may serve as markers of global ES and their mechanism. In six anesthetized dogs we measured LV pressure and myocardial long-axis function by using TDI and sonomicrometry. Ischemia was induced by left anterior descending coronary artery occlusion. ES was defined by the minimum first derivative of LV pressure. TDI and sonomicrometry demonstrated a sharp S(IP) and V(PS) at ES in the ischemic borderzone (defined as moderately ischemic myocardium by pressure-dimension loop analysis). Time differences relative to ES ( +/- SD) were -0.1 +/- 2.3 (intraclass correlation coefficient R(IC) = 0.996) and 6.8 +/- 10.7 ms (R(IC) = 0.89) for S(IP) as shown by sonomicrometry and TDI, respectively. There was a strong inverse relationship between postsystolic shortening in the borderzone and simultaneous lengthening of nonischemic myocardium. In 30 patients with acute myocardial infarction, S(IP) and V(PS) evaluated by TDI were compared with ES defined by aortic valve closure. Time differences were -4 +/- 14 (R(IC) = 0.94) and -2 +/- 11 ms (R(IC) = 0.96), respectively. In the ischemic borderzone, S(IP) and V(PS) identified global ES with high accuracy. The force balance or "tug of war" between borderzone and nonischemic myocardium is a likely underlying mechanism for these markers. The method may be used as an "all in one heart beat" approach for TDI analysis in acute myocardial ischemia.