Abstract
Previous research suggests that elevated pulse pressure (PP) is a risk factor for atrial fibrillation (AF) independently of mean arterial pressure (MAP). PP may serve as an indirect measure of aortic stiffness (reduced distensibility), but whether directly measured aortic distensibility is related to risk for AF has not yet been studied. This analysis included 6,630 participants aged 45 to 84 years from the Multi-Ethnic Study of Atherosclerosis. At baseline, blood pressure and other relevant covariates were measured using standardized protocols. Magnetic resonance imaging-based aortic distensibility was measured in 3,441 participants. Incident AF was identified from hospitalization discharge codes and Medicare claims. Multivariate Cox models were used to estimate the association of blood pressure components and aortic distensibility with AF risk. During a mean follow-up of 7.8 years, 307 AF events (137 among those with aortic distensibility measurements) were identified. In multivariate-adjusted models simultaneously including MAP and PP, each 1-SD increase in PP was associated with a 29% increased risk of AF (95% confidence interval 5% to 59%, p = 0.02), with MAP not being associated with increased AF risk. Overall, aortic distensibility was not consistently associated with AF risk: after removing outliers, each 1-SD increase in aortic distensibility was associated with a 9% increased risk of AF (95% confidence interval -22% to 51%, p = 0.63). In conclusion, in this large community-based cohort, we found that PP, but not MAP or aortic distensibility, was a significant risk factor for AF, emphasizing the importance of PP when assessing the risk for developing AF. Our results cast doubt on the clinical utility of aortic distensibility as a predictor for the development of AF.
Original language | English (US) |
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Pages (from-to) | 587-592 |
Number of pages | 6 |
Journal | American Journal of Cardiology |
Volume | 114 |
Issue number | 4 |
DOIs | |
State | Published - Aug 15 2014 |
Bibliographical note
Funding Information:This research was supported by contracts N01-HC-95159 , N01-HC-95160 , N01-HC-95161 , N01-HC-95162 , N01-HC-95163 , N01-HC-95164 , N01-HC-95165 , N01-HC-95166 , N01-HC-95167 , N01-HC-95168 , and N01-HC-95169 from the National Heart, Lung, and Blood Institute, Bethesda, Maryland and by grants UL1-TR-000040 and UL1-RR-025005 from National Center for Research Resources, Bethesda, Maryland .
Funding Information:
Dr. Nazarian is a consultant to Biosense Webster and receives research grants from the National Institutes of Health (K23-HL-089333 and R01-HL-116280) and Biosense Webster .