Abstract
Background Left ventricular (LV) remodeling after acute myocardial infarction has still to be clarified in the thrombolytic era. Methods To evaluate timing and the magnitude and pattern of postinfarct LV remodeling, a subset of 614 patients enrolled in the Gruppo Italiano per lo Studio della Sopravvivenza nell’Infarto Miocardico-3 Echo Substudy underwent serial 2-dimensional echocardiograms at 24 to 48 hours from symptom onset (S1), at hospital discharge (S2), at 6 weeks (S3), and at 6 months (S4) after acute myocardial infarction. Results During the study period the end-diastolic volume index (EDVi) increased (P <.001) and wall motion abnormalities (%WMA) decreased (P <.001), whereas ejection fraction (EF) remained unchanged. Nineteen percent of patients showed a > 20% increase in EDVi at S2 compared with S1 (severe early dilation), and 16% of patients showed a > 20% dilation at S4 compared with S2 (severe late dilation). Independent predictors of severe in-hospital LV dilation were relatively small EDVi (odds ratio [OR] 0.961, 95% confidence interval [CI] 0.947-0.974, P =.0001) and relatively large %WMA (OR 1.030, 95% CI 1.013-1.048, P =.0005). Similarly, smaller predischarge EDVi (OR 0.975, 95% CI 0.963-0.987, P =.0001), greater %WMA (OR 1.026, 95% CI 1.008-1.045, P =.0042), and moderate to severe mitral regurgitation (OR 2.261, 95% CI 1.031-4.958, P = 0.0417) independently predicted severe late dilation. Importantly, 92% of the patients with severe early dilation did not have further dilation at S4, and 91% of patients with severe late dilation did not have in-hospital dilation. EF was unchanged over time in patients with early dilation, whereas it significantly decreased in those with late dilation. Conclusions Although in-hospital LV enlargement is not predictive of subsequent dilation and dysfunction, late remodeling is associated with progressive deterioration of global ventricular function over time: patients with extensive %WMA and not significantly enlarged ventricular volume before discharge are at higher risk for progressive dilation and dysfunction. (Am Heart J 2001;141:131-8.)
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