Details

Autor(en) / Beteiligte

• Dewland, Thomas A., MD
• Vittinghoff, Eric, PhD, MPH
• Harris, Tamara B., MD, PhD
• Magnani, Jared W., MD, MSc
• Liu, Yongmei, MD, PhD
• Hsu, Fang-Chi, PhD
• Satterfield, Suzanne, MD, DrPH
• Wassel, Christina, PhD
• Marcus, Gregory M., MD, MAS

Titel

Inflammation as a Mediator of the Association Between Race and Atrial Fibrillation

Ist Teil von

• JACC. Clinical electrophysiology, 2015-08, Vol.1 (4), p.248-255

Ort / Verlag

Elsevier Inc

Erscheinungsjahr

2015

Quelle

Alma/SFX Local Collection

Beschreibungen/Notizen

• Abstract Objectives This study sought to determine the degree to which racial differences in atrial fibrillation (AF) risk are explained by differences in inflammation and adiposity. Background Despite having a lower prevalence of established AF risk factors, whites exhibit substantially higher rates of this arrhythmia than blacks. The mechanism underlying this observation is not known. Both inflammation and obesity are risk factors for AF, and adipose tissue is a known contributor to systemic inflammation. Methods Baseline serum inflammatory biomarker concentrations and abdominal adiposity (assessed by computed tomography) were quantified in a subset of black and white participants without prevalent AF in the Health ABC (Health, Aging, and Body Composition) study. Participants were prospectively followed for the diagnosis of AF, using study electrocardiography and Medicare claims data. Cox proportional hazards models were used to determine the adjusted relative hazard of incident AF between races before and after biomarker adjustment. Results Among 2,768 participants (43% black), 721 participants developed incident AF over a median follow-up of 10.9 years. White race was associated with a heightened adjusted risk of incident AF (HR: 1.55; 95% confidence interval [CI]: 1.30 to 1.84, p < 0.001). Abdominal adiposity was not associated with AF when added to the adjusted model. Among the biomarkers studied, adiponectin, tumor necrosis factor (TNF)-α, TNF-α soluble receptor (SR) I, and TNF-α SR II concentrations were each higher among whites and independently associated with a greater risk of incident AF. Together, these inflammatory cytokines mediated 42% (95% CI: 15% to 119%, p = 0.004) of the adjusted association between race and AF. Conclusions Systemic inflammatory pathways significantly mediate the heightened risk of AF among whites. The higher level of systemic inflammation and concomitant increased AF risk in whites is not explained by racial differences in abdominal adiposity or the presence of other proinflammatory cardiovascular comorbidities.