Background Coronary artery disease (CAD) is increasing among young adults. We aimed to describe the cardiovascular risk factors and long‐term prognosis of premature CAD. Methods and Results Using the Duke Databank for Cardiovascular Disease, we evaluated 3655 patients admitted between 1995 and 2013 with a first diagnosis of obstructive CAD before the age of 50 years. Major adverse cardiovascular events (MACEs), defined as the composite of death, myocardial infarction, stroke, or revascularization, were ascertained for up to 10 years. Cox proportional hazard regression models were used to assess associations with the rate of first recurrent event, and negative binomial log‐linear regression was used for rate of multiple event recurrences. Past or current smoking was the most frequent cardiovascular factor (60.8%), followed by hypertension (52.8%) and family history of CAD (39.8%). Within a 10‐year follow‐up, 52.9% of patients had at least 1 MACE, 18.6% had at least 2 recurrent MACEs, and 7.9% had at least 3 recurrent MACEs, with death occurring in 20.9% of patients. Across follow‐up, 31.7% to 37.2% of patients continued smoking, 81.7% to 89.3% had low‐density lipoprotein cholesterol levels beyond the goal of 70 mg/dL, and 16% had new‐onset diabetes mellitus. Female sex, diabetes mellitus, chronic kidney disease, multivessel disease, and chronic inflammatory disease were factors associated with recurrent MACEs. Conclusions Premature CAD is an aggressive disease with frequent ischemic recurrences and premature death. Individuals with premature CAD have a high proportion of modifiable cardiovascular risk factors, but failure to control them is frequently observed.

OBJECTIVES: To investigate racial differences in elevated C-reactive protein (CRP) and the potential factors contributing to these differences in US older men and women. DESIGN: Nationally representative cohort study. SETTING: Health and Retirement Study, 2006 to 2014. PARTICIPANTS: Noninstitutionalized non-Hispanic black and white older adults living in the United States (n = 13 517). MEASUREMENTS: CRP was categorized as elevated (>3.0 mg/L) and nonelevated (≤3.0 mg/L) as the primary outcome. Measures for demographic background, socioeconomic status, psychosocial factors, health behaviors, and physiological health were examined as potential factors contributing to race differences in elevated CRP. RESULTS: Median CRP levels (interquartile range) were 1.67 (3.03) mg/L in whites and 2.62 (4.95) mg/L in blacks. Results from random effects logistic regression models showed that blacks had significantly greater odds of elevated CRP than whites (odds ratio = 2.58; 95% confidence interval [CI] = 2.20-3.02). Results also showed that racial difference in elevated CRP varied significantly by sex (predicted probability [PP] [white men] = 0.28 [95% CI = 0.27-0.30]; PP [black men] = 0.38 [95% CI = 0.35-0.41]; PP [white women] = 0.35 [95% CI = 0.34-0.36]; PP [black women] = 0.49 [95% CI = 0.47-0.52]) and remained significant after risk adjustment. In men, the racial differences in elevated CRP were attributable to a combination of socioeconomic (12.3%) and behavioral (16.5%) factors. In women, the racial differences in elevated CRP were primarily attributable to physiological factors (40.0%). CONCLUSION: In the US older adult population, blacks were significantly more likely to have elevated CRP than whites; and the factors contributing to these differences varied in men and women. J Am Geriatr Soc 68:362-369, 2020.

Background: While hypertriglyceridemia is a known risk factor for developing CVD, whether it poses residual risk in patients with type 2 diabetes mellitus (T2DM) and established CVD is under-studied. Methods: Using data from the Bypass Angioplasty Revascularization Investigation 2 Diabetes (BARI 2D) trial, we examined 2,307 patients with T2DM and CVD to determine the association of baseline fasting triglyceride (TG) levels with MACE (time to CV death, myocardial infarction (MI), or stroke) or CV death over a mean follow-up of 5.0 years. Results: At baseline, the mean fasting TG was 181 mg/dl with a median (Q1, Q3) of 148 (104, 219) mg/dl. Overall, 49.3% had TG≥ 150 mg/dl (N=1,167). Compared with those with TG<150 mg/dl, they were younger, more frequently Caucasian and with higher BMI. In unadjusted models, TGs were significantly associated with MACE and CV death (Table). This association did not remain after adjustment for multiple factors, including nonHDLc. Conclusions: In this analysis of patients with T2DM and known CVD, TGs were relatively high and were associated with CV outcomes, but not when other risk factors were taken into account. Thus, while TGs are clearly a marker of those with residual high risk for CV events in T2DM, whether they specifically need to be lowered awaits well conducted clinical trials. Disclosure N. Pagidipati: Research Support; Self; Amarin Corporation, Boehringer Ingelheim International GmbH, Novo Nordisk A/S, Regenerative Medical Solutions, Sanofi. A. Navar: Advisory Panel; Self; AstraZeneca, Novo Nordisk Inc. Research Support; Self; Janssen Pharmaceuticals, Inc. Other Relationship; Self; Amarin Corporation, Amgen Inc., Regeneron Pharmaceuticals, Sanofi. H. Mulder: None. D.M. Wojdyla: None. S. Philip: Employee; Self; Amarin Corporation. Stock/Shareholder; Self; Amarin Corporation. C.B. Granowitz: Employee; Self; Amarin Pharma Inc. Stock/Shareholder; Self; Amarin Pharma Inc. Funding Amarin Corporation