The aim of this study was to assess the interaction between left ventricular and right ventricular systolic function after acute myocardial infarction (AMI). The study population comprises 27 normal subjects and 71 patients assessed at predischarge (12 +/- 7 days) after AMI and divided into two subgroups, 24 with inferior AMI and 47 with non inferior AMI. The three groups were comparable for sex, age, heart rate and blood pressure. Right ventricular function was evaluated by two-dimensional assessment of tricuspid annular plane systolic excursion (TAPSE) and by Doppler analysis of right ventricular outflow tract. Left ventricular systolic function was evaluated by two-dimensional determination of ejection fraction and wall motion score index, and by Doppler analysis of left ventricular outflow tract. The overall AMI population showed reduced TAPSE, velocity-time integral (both p < 0.05) and peak velocity (p < 0.005) of right ventricular outflow tract, prolongation of Q-S2 interval and increase of pre-ejection period/acceleration time ratio (both p < 0.05) in comparison with normals. These alterations were accompanied by a decrease of left ventricular ejection fraction and increase of wall motion score index. (p < 0.0001) The changes of right ventricular indexes were confirmed in patients with inferior AMI who had also lower left ventricular ejection fraction (46 +/- 9%). Functional parameters of the right ventricle were not significantly modified in patients with non inferior AMI who had greater left ventricular ejection fraction (53 +/- 8.6%). In the overall AMI population, and in particular in inferior AMI, we found univariate relations between time-velocity integrals of left ventricular and right ventricular outflow tract and between left ventricular ejection fraction and TAPSE. Only in inferior AMI creatinkinase peak was related to time-velocity integral of right ventricular outflow tract (r = -0.59, p < 0.01). In conclusion, the magnitude of right ventricular systolic impairment developing after left ventricular AMI depends on the degree of left ventricular dysfunction, likewise by changes of hemodynamic load imposed to the right ventricle. AMI location and, only in inferior AMI, infarct extension participate in determining this dysfunction.