We read with interest the recent report by Carraba et al on the effect of age on left ventricular remodeling (LVR) and heart failure (HF) in patients treated by primary angioplasty for myocardial infarction (MI). The study demonstrated that despite very few differences in LVR, elderly patients had a much greater risk of HF at long-term follow-up. As noted by the authors, their study was, however, performed in a selected population as patients receiving lytic treatment or patients with clinical signs of HF during the first week after MI were excluded.

By analyzing the data of a prospective study, we recently reported on the effect of aging on cardiac remodeling and hospitalization for HF after MI. The patients were included irrespective of the type of reperfusion therapy (thrombolysis in 53%; primary angioplasty in 29%; or no reperfusion in 17%). Patients with early signs of HF were not excluded (Killip class ≥2 in 27%). Echocardiographic studies were performed in 266 patients at hospital discharge, at 3 months, and at 1 year after MI. Left ventricular end-diastolic and end-systolic volumes, analyzed in an Echographic Core Laboratory, did not differ according to age for all points studied. When LVR was defined as a >20% increase in left ventricular end-diastolic volume between baseline and 1 year after MI, it had occurred in 31%, 26%, 34%, and 34% of patients who were <48, 48 to 57, 58 to 71, and >71 years, respectively (p = 0.43). The 3-year hospitalization rate for HF was 1.9%, 1.5%, 11.0%, and 20.3% in patients <48, 48 to 57, 58 to 71, and >71 years, respectively (p = 0.0001).

When taken together, the results of the 2 studies demonstrate that the more frequent progression to HF observed after MI in elderly patients is not related to an increased risk of LVR. These results are concordant with those of the Perindopril and Remodeling in Elderly with Acute Myocardial Infarction (PREAMI) study in which 1,252 elderly post-MI patients were randomized to angiotensin-converting enzyme inhibitor or placebo and in which the reduction in LVR observed in the angiotensin-converting enzyme inhibition arm did not translate into a better clinical outcome.

The explanations for the greater risk of HF in elderly patients after MI remain highly hypothetical. The decreased recovery of systolic function in elderly patients reported by Carraba et al was not observed in our study. As reported by Carraba et al, we found greater left atrial volumes in older patients, suggesting that diastolic dysfunction might play some role in the greater risk of HF. In our study, the prevalence of moderate/severe mitral regurgitation was also greater in older patients.

In conclusion, it is likely that specific mechanisms underlie the transition to HF in elderly patients after MI. Because most cases of HF after MI are occurring in this high-risk population, we believe that this should be the focus of additional research.