Pulse Pressure and Risk of New-Onset Atrial Fibrillation
Gary F. Mitchell,* Ramachandran S. Vasan,†‡§ Michelle J. Keyes,¶ Helen Parise,¶ Thomas J. Wang,∥# Martin G. Larson,∥# Ralph B. D'Agostino, Sr,∥ William B. Kannel,§∥ Daniel Levy,∥** and Emelia J. Benjamin†‡§∥
(JAMA, 297:709-715, 2007)
*Cardiovascular Engineering Inc, Waltham, MA; †Evans Department of Medicine, ‡Whitaker Cardiovascular Institute and §Section of Preventive Medicine, Boston University School of Medicine, Boston, MA; ∥National Heart, Lung, and Blood Institute's Framingham Study, Framingham, MA; ¶Department of Mathematics and Statistics, Boston University, Boston, MA; #Cardiology Division, Massachusetts General Hospital, Boston, MA; and **National Heart, Lung and Blood Institute, Bethesda, MD.
Atrial fibrillation (AF) is responsible for considerable morbidity and mortality, which makes identification of modifiable risk factors a priority. Increased pulse pressure, which reflects aortic stiffness, increases cardiac load, and may increase the risk of AF. A prospective, community-based observational cohort in Framingham, MA, was studied to examine the relationship between pulse pressure and incident AF. The study included 5331 Framingham Heart Study participants 35 years and older who were initially free from AF (median age, 57 years; 55% women). Atrial fibrillation, the main outcome measure, developed in 698 (13.1%) participants at a median of 12 years after pulse pressure assessment. The cumulative 20-year incidence rates of AF 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 an increased risk for AF (adjusted hazard ratio [HR], 1.26 per 20-mm Hg increment; 95% confidence interval [CI], 1.12-1.43). By contrast, mean arterial pressure was not related to incident AF (adjusted HR, 0.96 per 10-mm Hg increment; 95% CI, 0.88-1.25). Systolic pressure was related to AF (HR, 1.14 per 20-mm Hg increment; 95% CI 1.04-1.25; 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), consistent with pulse pressure effect. Among patients who had 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). Pulse pressure is an important risk factor for incident AF in a community-based sample. More research is needed to ascertain whether interventions that reduce pulse pressure will limit the growing incidence of AF.