72 research outputs found

    Does the Association Between Depressive Symptoms and Cardiovascular Mortality Risk Vary By Race? Evidence from the Health and Retirement Study

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    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 communitydwelling Health and Retirement Study participants (a nationally representative sample of U.S. adults age 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: 0.86, 1.46). The hazard associated with elevated depressive symptoms did not differ significantly by race (p>0.15 for all comparisons). Patterns were similar in analyses restricted to respondents age 65+. Conclusions—Clinicians should consider the depressive state of either black or white patients as a potential CVD mortality risk factor

    Advancing Research on the Complex Interrelations Between Atrial Fibrillation and Heart Failure A Report From a US National Heart, Lung, and Blood Institute Virtual Workshop

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    The interrelationships between atrial fibrillation (AF) and heart failure (HF) are complex and poorly understood, yet the number of patients with AF and HF continues to increase worldwide. Thus, there is a need for initiatives that prioritize research on the intersection between AF and HF. This article summarizes the proceedings of a virtual workshop convened by the US National Heart, Lung, and Blood Institute to identify important research opportunities in AF and HF. Key knowledge gaps were reviewed and research priorities were proposed for characterizing the pathophysiological overlap and deleterious interactions between AF and HF; preventing HF in people with AF; preventing AF in individuals with HF; and addressing symptom burden and health status outcomes in AF and HF. These research priorities will hopefully help inform, encourage, and stimulate innovative, cost-efficient, and transformative studies to enhance the outcomes of patients with AF and HF

    Genetic analyses of the QT interval and its components in over 250K individuals identifies new loci and pathways affecting ventricular depolarization and repolarization

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    Genetic analyses of the electrocardiographic QT interval and its components identify additional loci and pathways

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    The QT interval is an electrocardiographic measure representing the sum of ventricular depolarization and repolarization, estimated by QRS duration and JT interval, respectively. QT interval abnormalities are associated with potentially fatal ventricular arrhythmia. Using genome-wide multi-ancestry analyses (>250,000 individuals) we identify 177, 156 and 121 independent loci for QT, JT and QRS, respectively, including a male-specific X-chromosome locus. Using gene-based rare-variant methods, we identify associations with Mendelian disease genes. Enrichments are observed in established pathways for QT and JT, and previously unreported genes indicated in insulin-receptor signalling and cardiac energy metabolism. In contrast for QRS, connective tissue components and processes for cell growth and extracellular matrix interactions are significantly enriched. We demonstrate polygenic risk score associations with atrial fibrillation, conduction disease and sudden cardiac death. Prioritization of druggable genes highlight potential therapeutic targets for arrhythmia. Together, these results substantially advance our understanding of the genetic architecture of ventricular depolarization and repolarization

    Assessment and the Competencies: A Faculty Development Game

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