We appreciate the comments of Drs. Shishehbor and Litaker. We agree that socioeconomic status is a multidimensional construct of which income serves as only 1 of many social measures. Although such limitations were acknowledged in our paper, our study did adjust for individual education, employment status, ethnicity, and social support. Adjustment for such variables partially accounted for some of the heterogeneous features of socioeconomic status. Furthermore, the inclusion of more elaborative social measures, although intriguing, would not have mitigated the importance of exploring the causal pathway factors that mediate income–mortality associations—associations that have been consistently observed in the literature and require explanation (1).

We acknowledge that the exclusion of very high-risk patients (that is, those receiving mechanical ventilation or those who died before enrollment) may have introduced bias and attenuated the association between socioeconomic status and mortality. Unfortunately, the exclusion was unavoidable because income was ascertained by using self-administered surveys. Enrollment into the SESAMI (Socio-Economic and Acute Myocardial Infarction) study required patient consent, which also probably contributed to selection bias (2). Consequently, the magnitude of association between income and mortality after acute myocardial infarction might have been less than otherwise expected had we been able to examine a more representative "real-world" population.

Nonetheless, the extent to which such limitations altered our results remains speculative. For example, available evidence suggests that wealth-health gradients are more likely to narrow, not widen, among elderly patients than among younger subgroups—subgroups that disproportionately make up higher-risk "real-world" populations (1, 3). Of importance, the objective of our study was not to measure the true magnitude of association between income and mortality after acute myocardial infarction but to quantify the extent to which income-mortality associations were explained by traditional atherogenic or vascular factors, noncardiac comorbid conditions, and health service use. On the basis of our results and those of others (4), there is no reason to believe that age and cardiovascular risk factors would not have exerted similar explanatory effects on income-mortality associations if higher-risk populations had been examined.

To what extent, if any, can disparities between socioeconomic status and mortality rates be modified through intensive secondary prevention strategies? Are socially disadvantaged patients predestined to die after acute myocardial infarction (regardless of intensive secondary prevention initiatives) because of their baseline cardiovascular risk profiles at the time of presentation? These remain the pertinent questions for future study. Social–epidemiologic and health service research must now explore the impact of secondary preventive interventions to determine whether outcomes can be improved effectively and efficiently among high-risk populations in the real world.