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Gary F. Mitchell, MD; Ramachandran S. Vasan, MD; Michelle J. Keyes, MA; Helen Parise, ScD; Thomas J. Wang, MD; Martin G. Larson, ScD; Ralph B. D’Agostino, Sr, PhD; William B. Kannel, MD, MPH; Daniel Levy, MD; Emelia J. Benjamin, MD, ScM

JAMA. 2007;297:709-715.

Context  Atrial fibrillation (AF) is responsible for considerable morbidity and mortality, making identification of modifiable risk factors a priority. Increased pulse pressure, a reflection of aortic stiffness, increases cardiac load and may increase AF risk.

Objective  To examine relations between pulse pressure and incident AF.

Design, Setting, and Participants  Prospective, community-based observational cohort in Framingham, Mass, including 5331 Framingham Heart Study participants aged 35 years and older and initially free from AF (median age, 57 years; 55% women).

Main Outcome Measures  Incident AF.

Results  AF developed in 698 participants (13.1%) a median of 12 years after pulse pressure assessment. Cumulative 20-year AF incidence rates were 5.6% for pulse pressure of 40 mm Hg or less (25th percentile) and 23.3% for pulse pressure greater than 61 mm Hg (75th percentile). In models adjusted for age, sex, baseline and time-dependent change in mean arterial pressure, and clinical risk factors for AF (body mass index, smoking, valvular disease, diabetes, electrocardiographic left ventricular hypertrophy, hypertension treatment, and prevalent myocardial infarction or heart failure), pulse pressure was associated with increased risk for AF (adjusted hazard ratio [HR], 1.26 per 20-mm Hg increment; 95% confidence interval [CI], 1.12-1.43; P<.001). In contrast, mean arterial pressure was unrelated to incident AF (adjusted HR, 0.96 per 10-mm Hg increment; 95% CI, 0.88-1.05; P = .39). Systolic pressure was related to AF (HR, 1.14 per 20-mm Hg increment; 95% CI, 1.04-1.25; P = .006); however, if diastolic pressure was added, model fit improved and the diastolic relation was inverse (adjusted HR, 0.87 per 10-mm Hg increment; 95% CI, 0.78-0.96; P = .01), consistent with a pulse pressure effect. Among patients with interpretable echocardiographic images, the association between pulse pressure and AF persisted in models that adjusted for baseline left atrial dimension, left ventricular mass, and left ventricular fractional shortening (adjusted HR, 1.23; 95% CI, 1.09-1.39; P = .001).

Conclusion  Pulse pressure is an important risk factor for incident AF in a community-based sample. Further research is needed to determine whether interventions that reduce pulse pressure will limit the growing incidence of AF.

Author Affiliations: Cardiovascular Engineering Inc, Waltham, Mass (Dr Mitchell); Evans Department of Medicine (Drs Vasan and Benjamin), Whitaker Cardiovascular Institute (Drs Vasan and Benjamin), and Section of Preventive Medicine, Boston University School of Medicine, Boston, Mass (Drs Vasan, Kannel, and Benjamin); Department of Mathematics and Statistics, Boston University (Ms Keyes, Drs Parise and Larson), Cardiology Division, Massachusetts General Hospital, Boston (Dr Wang); National Heart, Lung, and Blood Institute's Framingham Study, Framingham, Mass (Drs Vasan, Wang, Larson, D’Agostino, Kannel, Levy, and Benjamin); National Heart, Lung, and Blood Institute, Bethesda, Md (Dr Levy).

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