Objective

To test whether the association between depressive symptoms and cardiovascular disease (CVD) mortality is stronger among Blacks than Whites.

Design, setting and participants

2,638 Black and 15,132 White participants from a prospective, observational study of community-dwelling Health and Retirement Study participants (a nationally representative sample of U.S. adults aged > or = 50). Average follow-up was 9.2 years.

Outcome measure

Cause of death (per ICD codes) and month of death were identified from National Death Index linkages.

Methods

The associations between elevated depressive symptoms and mortality from stroke, ischemic heart disease (IHD), or total CVD were assessed using Cox proportional hazards models to estimate adjusted hazard ratios (HRs). We used interaction terms for race by depressive symptoms to assess effect modification (multiplicative scale).

Results

For both Whites and Blacks, depressive symptoms were associated with a significantly elevated hazard of total CVD mortality (Whites: HR=1.46; 95% CI: 1.33, 1.61; Blacks: HR=1.42, 95% CI: 1.10, 1.83). Adjusting for health and socioeconomic covariates, Whites with elevated depressive symptoms had a 13% excess hazard of CVD mortality (HR=1.13, 95% CI: 1.03, 1.25) compared to Whites without elevated depressive symptoms. The HR in Blacks was similar, although the confidence interval included the null (HR=1.12, 95% CI: .86, 1.46). The hazard associated with elevated depressive symptoms did not differ significantly by race (P>.15 for all comparisons). Patterns were similar in analyses restricted to respondents age > or =65.

Conclusion

Clinicians should consider the depressive state of either Black or White patients as a potential CVD mortality risk factor.

Although depressive symptoms have been linked to stroke, most research has been in relatively ethnically homogeneous, predominantly white, samples. Using the United States based Health and Retirement Study, we compared the relationships between elevated depressive symptoms and incident first stroke for Hispanic, black, or white/other participants (N = 18,648) and estimated the corresponding Population Attributable Fractions. The prevalence of elevated depressive symptoms was higher in blacks (27%) and Hispanics (33%) than whites/others (18%). Elevated depressive symptoms prospectively predicted stroke risk in the whites/other group (HR = 1.53; 95% CI: 1.36-1.73) and among blacks (HR = 1.31; 95% CI: 1.05-1.65). The HR was similar but only marginally statistically significant among Hispanics (HR = 1.33; 95% CI: 0.92-1.91). The Population Attributable Fraction, indicating the percent of first strokes that would be prevented if the incident stroke rate in those with elevated depressive symptoms was the same as the rate for those without depressive symptoms, was 8.3% for whites/others, 7.8% for blacks, and 10.3% for Hispanics.

Background and purpose

Depression is associated with stroke, but the effects of changes in depressive symptoms on stroke risk are not well understood. This study examined whether depressive symptom changes across 2 successive annual assessments were associated with incident stroke the following year.

Methods

We used visit data from 4319 participants of the Cardiovascular Health Study who were stroke free at baseline to examine whether changes in depressive symptoms classified across 2 consecutive annual assessments predicted incident first stroke during the subsequent year. Depressive symptoms were assessed using the 10-item Center for Epidemiologic Studies Depression scale (high versus low at ≥10). Survival models were inverse probability weighted to adjust for demographics, health behaviors, medical conditions, past depressive symptoms, censoring, and survival.

Results

During follow-up, 334 strokes occurred. Relative to stable low scores of depressive symptoms, improved depression symptoms were associated with almost no excess risk of stroke (adjusted hazards ratio, 1.02; 95% confidence interval, 0.66-1.58). New-onset symptoms were nonsignificantly associated with elevated stroke risk (adjusted hazards ratio, 1.44; 95% confidence interval, 0.97-2.14), whereas persistently high depressive symptoms were associated with elevated adjusted hazard of all-cause stroke (adjusted hazards ratio, 1.65; 95% confidence interval, 1.06-2.56). No evidence for effect modification by race, age, or sex was found.

Conclusions

Persistently high symptoms of depression predicted elevated hazard of stroke. Participants with improved depressive symptoms had no elevation in stroke risk. Such findings suggest that strategies to reduce depressive symptoms may ameliorate stroke risk.

The QT interval (QT) is heritable and its prolongation is a risk factor for ventricular tachyarrhythmias and sudden death. Most genetic studies of QT have examined European ancestral populations; however, the increased genetic diversity in African Americans provides opportunities to narrow association signals and identify population-specific variants. We therefore evaluated 6,670 SNPs spanning eleven previously identified QT loci in 8,644 African American participants from two Population Architecture using Genomics and Epidemiology (PAGE) studies: the Atherosclerosis Risk in Communities study and Women's Health Initiative Clinical Trial. Of the fifteen known independent QT variants at the eleven previously identified loci, six were significantly associated with QT in African American populations (P≤1.20×10(-4)): ATP1B1, PLN1, KCNQ1, NDRG4, and two NOS1AP independent signals. We also identified three population-specific signals significantly associated with QT in African Americans (P≤1.37×10(-5)): one at NOS1AP and two at ATP1B1. Linkage disequilibrium (LD) patterns in African Americans assisted in narrowing the region likely to contain the functional variants for several loci. For example, African American LD patterns showed that 0 SNPs were in LD with NOS1AP signal rs12143842, compared with European LD patterns that indicated 87 SNPs, which spanned 114.2 Kb, were in LD with rs12143842. Finally, bioinformatic-based characterization of the nine African American signals pointed to functional candidates located exclusively within non-coding regions, including predicted binding sites for transcription factors such as TBX5, which has been implicated in cardiac structure and conductance. In this detailed evaluation of QT loci, we identified several African Americans SNPs that better define the association with QT and successfully narrowed intervals surrounding established loci. These results demonstrate that the same loci influence variation in QT across multiple populations, that novel signals exist in African Americans, and that the SNPs identified as strong candidates for functional evaluation implicate gene regulatory dysfunction in QT prolongation.