LV Remodeling Following Acute Myocardial Infarction AMI

The clinical association of cardiomegaly, congestive heart failure, and decreased survival has been documented extensively (29). Over half a century ago, Waris et al. (30) studied 125 patients who had sustained their first MI. Patients exhibiting cardiac enlargement on chest radiography demonstrated a significantly increased 5-yr mortality. A high proportion of the survivors with an enlarged heart developed New York Heart Association

Fig. 1. Cumulative mortality from all causes in the study groups. The number of patients at risk at the beginning of each year is shown at the bottom. Therapy with captopril (within 3-16 d after MI) significantly reduced mortality from all causes compared with the placebo group. The reduction in risk was 19% (95% CI: 3-32%; p = 0.019). Data from ref. 34.

Fig. 1. Cumulative mortality from all causes in the study groups. The number of patients at risk at the beginning of each year is shown at the bottom. Therapy with captopril (within 3-16 d after MI) significantly reduced mortality from all causes compared with the placebo group. The reduction in risk was 19% (95% CI: 3-32%; p = 0.019). Data from ref. 34.

class III angina or congestive heart failure during follow-up. White et al. and St. John Sutton et al. (31,32) have demonstrated that after MI, LV volumes predict clinical outcome. This has been further evidenced from higher brain natriuretic peptide (BNP) concentrations early after first MI, which is associated with adverse LV remodeling characteristics. This partially explains why BNP is a strong predictor of outcome after MI (33). Thus, the early clinical impression regarding the importance of cardiac enlargement following MI was correct and provided an impetus for defining mechanisms responsible for the observed topographic alterations, as well as and therapeutic modalities to limit them.

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