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 if S_IP and V_PS may serve as markers of global ES and their mechanism. In 6 anesthetized dogs we measured LV pressure and myocardial long axis function by TDI and sonomicrometry. Ischemia was induced by LAD occlusion. End-systole was defined by LV dP/dt_min. 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 (R_IC =0.996) and 6.8±10.7 ms (R_IC =0.89) for S_IP 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 by TDI were compared to ES defined by aortic valve closure. Time differences were -4±14 (R_IC=0.94) and -2±11 ms (R_IC=0.96), respectively. Conclusions: 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.