Early predictors of late dilation and remodeling after thrombolized anterior transmural myocardial infarction

Abstract

Background and hypothesis: Dilation of the left ventricle after myocardial infarction is associated with an adverse prognosis. There are no clinical studies on the role viable myocardium in the infarcted area assumes in relation to the development of late ventricular remodeling. The hypothesis of this study was to define the relation between remodeling and the presence of viable but akinetic myocardium in the infarct area and to identify early predictors of left ventricular (LV) dilation at 1 year.

Methods: In all, 92 consecutive patients with myocardial infarction were divided into two groups according to their ventricular volumes. Group I included 57 patients with normal volumes at discharge (9 +/- 3 days after acute infarction) and after 12 months or with LV dilation at discharge who had a normalization of their volumes over a 12-month period. Group II included 35 patients who, independent of their initial volumes, developed LV dilation during follow-up. Low-dose dobutamine infusion was utilized at discharge for echocardiographic evaluation of contractile recovery of viable myocardial segments.

Results: At the first control, patients in Group I presented an end-diastolic volume index (EDVI) of 100 +/- 7 ml/m2 which decreased to 68.8 +/- 6.5 ml/m2 12 months later (p < 0.0001), and an end-systolic volume index (ESVI) of 47.6 +/- 6.7 ml/m2 at the first control and 30.5 +/- 8.8 ml/m2 after 12 months (p < 0.001). Patients in Group II presented a mean EDVI of 116.2 +/- 8.1 ml/m2 at the first control and 138.8 +/- 8 ml/m2 12 months later (p < 0.001), and a mean ESVI of 68.8 +/- 6.5 ml/m2 at the first control and 79.5 +/- 5.4 after 12 months (p < 0.01). Ventricular mass index (VMI) in Group I increased from 106.4 +/- 11 to 122.3 +/- 15 g/m2 (p < 0.01), while in Group II it decreased from 101.1 +/- 10 to 98.7 +/- 8 g/m2 (p = NS). In Group I, mass-to-volume ratio was 1.15 +/- 0.1 g/ml at the first control and 1.67 +/- 0.1 g/ml 12 months later (p < 0.001), while in Group II it declined from 0.88 +/- 0.1 to 0.69 +/- 0.1 g/ml (p < 0.01). The multivariate analysis revealed that ejection fraction < or = 40%, restrictive filling pattern, wall motion score index > 2.5 in response to dobutamine infusion, and mass-to-volume ratio < or = 1 g/ml, all at discharge, as well as an occluded left anterior descending artery discriminate in favor of late LV dilation and remodeling.

Conclusions: Correct use of noninvasive strategies should result in early identification of postinfarct patients who are at risk of developing LV remodeling.