Acute myocardial ischemia has been associated with abnormal filling patterns in the left ventricular (LV) apex. We hypothesized that this may in part be due to postsystolic shortening of ischemic apical segments, which leads to reversal of early diastolic apical flow. Fourteen open-chest anesthetized dogs were instrumented with micromanometers in the LV apex and left atrium and myocardial sonomicrometers in the anterior apical LV wall. Intraventricular filling by color Doppler and wall motion by strain Doppler echocardiography (SDE) were assessed from an apical view. Measurements were taken before and after 5 min of left anterior descending coronary artery (LAD) occlusion. In four dogs, we measured the pressure difference between the LV apex and outflow tract. At baseline, peak early diastolic flow velocities in the distal one-third of the LV were directed toward apex (9.2 Ϯ 1.6 cm/s). After LAD occlusion, the velocities reversed (Ϫ2.3 Ϯ 0.4 cm/s, P Ͻ 0.01), indicating that blood was ejected from the apex toward the base during early filling. This interpretation was confirmed by wall motion analysis, which showed postsystolic shortening of apical myocardial segments. The postsystolic shortening represented 9.7 Ϯ 1.7% (P Ͻ 0.01) and 14.2 Ϯ 2.4% (P Ͻ 0.01) of end-diastolic segment length by SDE and sonomicrometry, respectively. Consistent with the velocity changes, we found reversal of the early diastolic pressure gradient from the LV apex to outflow tract. In the present model, acute LAD occlusion resulted in reversal of early diastolic apical flow, and this was attributed to postsystolic shortening of dyskinetic apical segments. The clinical diagnostic importance of this finding remains to be determined. strain-Doppler echocardiography; two-dimensional color Doppler; myocardial ischemia; diastolic filling ASSESSMENT OF LEFT VENTRICULAR (LV) intracavitary filling by Doppler echocardiography is one of several noninvasive approaches for studying LV diastolic function. In the normal LV, the initial intraventricular filling wave propagates rapidly toward the apex, and, as demonstrated by color M-mode Doppler, there is near simultaneous onset of filling velocities along the entire LV inflow tract (7). However, in patients with reduced LV ejection fraction or impaired diastolic function, the early diastolic apical filling may be markedly delayed, and this can be measured as slowing of mitral-to-apical flow propagation (1, 13). This has been attributed to a decrease in rate of LV relaxation, which causes a decrease in the driving pressure for mitral-to-apical flow (1, 12, 13), to loss of "apical suction" (12), and enhanced vortex formations due to changes in LV and mitral valve geometry (10).There is, however, very limited insight into how regional wall motion interacts with intraventricular flow. A common finding in ischemic myocardium is postsystolic (postejection) shortening and consequently delayed onset of diastolic lengthening (8,16,17). Therefore, in the ischemic ventricle, there may be substantial regional async...