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Background Black patients tend to develop coronary artery disease at a younger age than other groups. Previous data on racial disparities in outcomes of myocardial infarction (MI) have been inconsistent and limited to older populations. Our objective was to investigate racial differences in the outcome of MI among young and middle‐aged patients and the role played by socioeconomic, psychosocial, and clinical differences. Methods and Results We studied 313 participants (65% non‐Hispanic Black) <61 years old hospitalized for confirmed type 1 MI at Emory‐affiliated hospitals and followed them for 5 years. We used Cox proportional‐hazard models to estimate the association of race with a composite end point of recurrent MI, stroke, heart failure, or cardiovascular death after adjusting for demographic, socioeceonomic status, psychological, and clinical risk factors. The mean age was 50 years, and 50% were women. Compared with non‐Black patients, Black patients had lower socioeconomic status and more clinical and psychosocial risk factors but less angiographic coronary artery disease. The 5‐year incidence of cardiovascular events was higher in Black (35%) compared to non‐Black patients (19%): hazard ratio (HR) 2.1, 95% CI, 1.3 to 3.6. Adjustment for socioeconomic status weakened the association (HR 1.3, 95% CI, 0.8–2.4) more than adjustment for clinical and psychological risk factors. A lower income explained 46% of the race‐related disparity in outcome. Conclusions Among young and middle‐aged adult survivors of an MI, Black patients have a 2‐fold higher risk of adverse outcomes, which is largely driven by upstream socioeconomic factors rather than downstream psychological and clinical risk factors.

Objective: In patients with stable coronary artery disease (CAD), the risk of major adverse cardiovascular events (MACE) remains elevated despite treatment. The role of microvascular dysfunction on MACE beyond traditional risk indicators and inflammation is not well established. We examined whether peripheral microvascular dysfunction is associated with MACE in patients with CAD. Approach and Results: Microvascular function was measured with the Reactive Hyperemia Index (RHI) using digital peripheral arterial tonometry in 546 patients with CAD, who were followed 7 years for incident MACE. The primary end point included cardiovascular death or myocardial infarction; the secondary end point included cardiovascular death, myocardial infarction, or heart failure hospitalization. Hazard models for competing risk were used to estimate the association between RHI and MACE adjusting for age, sex, race, traditional risk factors, medications, and CAD severity. We also examined the association of baseline interleukin-6, C-reactive protein, monocyte chemoattractant protein-1, and matrix metallopeptidase-9 with RHI. Mean age was 62±9 years. Mean RHI was 2.1±0.63. After adjustment, for each 1-SD decrease in RHI, there was a 40% increase in the primary end point (hazard ratio, 1.4 [95% CI, 1.1–1.9], P =0.01) and a similar increase in the secondary end point (HR, 1.3 [95% CI, 1.1–1.7], P =0.006). Inflammatory biomarker levels were associated with greater RHI impairment ( P <0.05) but did not affect the relationship between RHI and MACE. Conclusions: Peripheral microvascular dysfunction is associated with increased risk of MACE in patients with stable CAD, implicating the role of microvascular disease in the pathogenesis of adverse outcomes in patients with CAD.