OBJECTIVE: To evaluate whether the presence of viable myocardium, detected by low dose dobutamine echocardiography, limits the likelihood of left ventricular dilatation in patients with acute myocardial infarction. PATIENTS: 107 patients were studied by low dose dobutamine echocardiography at (mean (SD)) 3 (1) days after acute myocardial infarction. Cross sectional echocardiography was repeated three months later. Patients were divided in two groups based on the presence (n = 47) or absence (n = 60) of myocardial viability. RESULTS: Baseline characteristics were comparable between the two groups, except for infarct location. Left ventricular end diastolic volume index (EDVI) was stable in patients with viability, but end systolic volume index (ESVI) decreased significantly (p = 0.006). Patients without viability had a significant increase in both EDVI (p < 0.0001) and ESVI (p = 0.0007). Subgroup analysis in patients with small and large infarcts (peak creatine kinase < or = 1000 v > 1000 IU/l) showed that ventricular dilatation occurred only in patients with large infarcts without viability. This resulted in larger ESVI values at three months in that group compared with patients with large infarcts plus viability (p < 0.05). Multivariate regression analysis identified myocardial viability as an independent predictor of left ventricular dilatation, along with wall motion score index on low dose dobutamine echocardiography and the number of pathological Q waves. CONCLUSIONS: The presence of viability early after acute myocardial infarction is associated with preservation of left ventricular size, whereas the absence of viability results in ventricular dilatation, particularly in large infarcts.
OBJECTIVE: To evaluate whether the presence of viable myocardium, detected by low dose dobutamine echocardiography, limits the likelihood of left ventricular dilatation in patients with acute myocardial infarction. PATIENTS: 107 patients were studied by low dose dobutamine echocardiography at (mean (SD)) 3 (1) days after acute myocardial infarction. Cross sectional echocardiography was repeated three months later. Patients were divided in two groups based on the presence (n = 47) or absence (n = 60) of myocardial viability. RESULTS: Baseline characteristics were comparable between the two groups, except for infarct location. Left ventricular end diastolic volume index (EDVI) was stable in patients with viability, but end systolic volume index (ESVI) decreased significantly (p = 0.006). Patients without viability had a significant increase in both EDVI (p < 0.0001) and ESVI (p = 0.0007). Subgroup analysis in patients with small and large infarcts (peak creatine kinase < or = 1000 v > 1000 IU/l) showed that ventricular dilatation occurred only in patients with large infarcts without viability. This resulted in larger ESVI values at three months in that group compared with patients with large infarcts plus viability (p < 0.05). Multivariate regression analysis identified myocardial viability as an independent predictor of left ventricular dilatation, along with wall motion score index on low dose dobutamine echocardiography and the number of pathological Q waves. CONCLUSIONS: The presence of viability early after acute myocardial infarction is associated with preservation of left ventricular size, whereas the absence of viability results in ventricular dilatation, particularly in large infarcts.
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