Objective: To assess the relative influence of contractile reserve and inducible ischaemia on subsequent left ventricular volume changes after myocardial infarction. Design: Left ventricular end diastolic and end systolic index volumes were calculated prospectively at discharge and at six months in 143 patients referred for early postinfarction dobutamine stress echocardiography. On the basis of their responses to this test, patients were divided into three groups: scar (n = 48; group 1); contractile reserve (n = 36; group 2); inducible ischaemia (n = 59; group 3). Results: At six months, the left ventricular end diastolic index volume decreased in group 2 (mean (SD), −3.9 (9.4) ml/m 2 ) and increased in both group 1 (+2.8 (10.6) ml/m 2 , p = 0.009 v group 2) and group 3 (+7.5 (11.4) ml/m 2 , p < 0.0001 v group 2). The end systolic index volume decreased in group 2 (−4.9 (7.3) ml/m 2 ) and increased in both group 1 (+1.3 (8.3) ml/m 2 , p = 0.0015 v group 2) and group 3 (+2.8 (8.9) ml/m 2 , p = 0.0002 v group 2). In multivariate analysis, the contractile reserve (hazard ratio 0.19, 95% confidence interval (CI) 0.14 to 0.47), inducible ischaemia (5.86, 95% CI 1.54 to 29.7), and end systolic index volume at discharge (1.04, 95% CI 0.99 to 1.11) were independent predictors of an increase in end diastolic index volume of > 15 ml/m 2 at six months. Conclusions: Contractile reserve and inducible ischaemia, as detected by early dobutamine stress echocardiography, identify patients with differences in long term left ventricular remodelling after acute myocardial infarction.T he development of left ventricular dilatation following myocardial infarction is the main finding in the complex process named ventricular remodelling, and it is one of the major determinants of a poor outcome.1 In previous studies, left ventricular remodelling occurred in patients with a larger infarct size 2 3 and with persistent occlusion of the infarct related artery. [4][5][6] Moreover, the transmural extent of necrosis and the presence of surviving myocardium within the infarct area were found, respectively, to be directly and inversely related to the early infarct zone expansion process. [7][8][9] The presence of viable myocytes-generally located in the outer layers of the ventricular wall and in the peripheral areas of the infarct area-may therefore contribute to preventing left ventricular enlargement by limiting infarct expansion.Few studies have investigated the influence of postinfarction contractile reserve on left ventricular volume changes. The favourable effect of infarct zone viability on left ventricular enlargement, as detected by early dobutamine stress echocardiography (DSE), has been shown in a population with successful primary coronary angioplasty, 10 and the relative role of contractile reserve, inducible ischaemia, and their combination on left ventricular postinfarct dilatation has recently been investigated.11 However, definitive data on patients with their first uncomplicated myocardial infarction treated by a conservativ...