Background: Left atrial (LA) volume and function provides prognostic value in post-infarction patients. However, quantitative assessment of LA function remains limited with no accepted golden standard. Aim: To evaluate the existence and determinants of LA volume and mechanical remodeling following ST-elevation myocardial infarction (STEMI) using tissue Doppler imaging (TDI). Methodology: A total of 30 patients (median age: 48 years; 27 males; 8 with diabetes mellitus) in sinus rhythm with STEMI were prospectively enrolled. All patients had echocardiography within 24 hours of index STEMI and in FU (median: 9 months; range: 6-12). LA maximal, minimal, and volume at onset of P wave on surface ECG were calculated using biplane area-length method and were indexed to body surface area. LA total, active, and passive emptying volumes and fractions were calculated. Using pulsed-TDI, both peak velocity and duration of regional atrial contraction (A’) in all basal segments of LA walls (septal, lateral, anterior, inferior, posterior) were measured and then averaged. LA electromechanical function (the average of time intervals from the onset of P wave on surface ECG to the beginning; peak; and end of A’ wave) was assessed. Systolic and diastolic TDI velocities of lateral mitral annulus were measured. LA systolic dysfunction was defined as reduction of A’ velocity by ≥ 0.14 cm/s during FU while LA volume remodeling was defined as change in LA maximum volume index > 4 ml/m2 during FU (values represent the median change among the whole study population). Results: During FU, there was significant increase in the three indexed LA volumes (p<0.05) with significant increase in both total (10 to 12.5 ml/m2, p=0.016) and passive (5.3 to 7.4 ml/m2, p =0.001) emptying volumes and no significant change in active emptying volume. All emptying fractions showed no significant changes between baseline and FU. Increased LV diastolic dimension (p=0.026) and decreased lateral mitral annular systolic velocity (p=0.04) were the only factors associated with LA volume remodeling.. Compared to baseline, A’ wave at FU showed reduced velocity (from 10.5 to 8.3 cm/s, p= 0.03) and prolonged duration (from 117 to 124 msec, p= 0.02). Among several clinical and echocardiographic variables, only mitral annular systolic velocity was reduced in patients with LA dysfunction (6.7 cm/s) compared to patients without (9.6 cm/s; p =0.006). Mitral annular systolic velocity correlated significantly with A’ velocity at baseline (r=0.51, p =0.01) but not at FU. All indices of LA electromechanical function showed no significant changes between baseline and FU. Conclusion: Following STEMI, LA systolic function - as assessed by TDI - could be abnormal, even in condition with a normal LA function when assessed by phasic volume changes. Worsening of LA systolic function is associated with deterioration of longitudinal left ventricular systolic function. No LA electromechanical abnormalities were detected among post STEMI patients.