Parental Atrial Fibrillation as a Risk Factor for Atrial Fibrillation in Offspring
- Caroline S. Fox, MD, MPH;
- Helen Parise, ScD;
- Ralph B. D'Agostino, Sr, PhD;
- Donald M. Lloyd-Jones, MD, ScM;
- Ramachandran S. Vasan, MD;
- Thomas J. Wang, MD;
- Daniel Levy, MD;
- Philip A. Wolf, MD;
- Emelia J. Benjamin, MD, ScM
- Author Affiliations: National Heart, Lung, and Blood Institute Framingham Heart Study, Framingham, Mass (Drs Fox, Parise, D'Agostino, Lloyd-Jones, Vasan, Wang, Levy, Wolf, and Benjamin); Department of Endocrinology, Diabetes, and Hypertension, Brigham and Women's Hospital, Harvard Medical School, Boston, Mass (Dr Fox); National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Md (Drs Fox and Levy); Department of Mathematics, Boston University (Drs Parise and D'Agostino); Cardiology Section, Department of Medicine (Drs Vasan, Levy, and Benjamin), Preventive Medicine Section (Drs Vasan, Levy, Wolf, and Benjamin), and Department of Neurology (Dr Wolf), Boston University School of Medicine, Boston; Cardiology Division, Department of Medicine, Massachusetts General Hospital, Boston (Dr Wang); Department of Preventive Medicine and Division of Cardiology, Feinberg School of Medicine, Northwestern University, Chicago, Ill (Dr Lloyd-Jones).
Abstract
Context Atrial fibrillation (AF) is the most common cardiac dysrhythmia in the United States. Whereas rare cases of familial AF have been reported, it is unknown if AF among unselected individuals is a heritable condition.
Objective To determine whether parental AF increases the risk for the development of offspring AF.
Design, Setting, and Participants Prospective cohort study (1983-2002) within the Framingham Heart Study, a population-based epidemiologic study. Participants were 2243 offspring (1165 women, 1078 men) at least 30 years of age and free of AF whose parents had both been evaluated in the original cohort.
Main Outcome Measures Development of new-onset AF in the offspring was prospectively examined in association with previously documented parental AF.
Results Among 2243 offspring participants, 681 (30%) had at least 1 parent with documented AF; 70 offspring participants (23 women; mean age, 62 [range, 40-81] years) developed AF in follow-up. Compared with no parental AF, AF in at least 1 parent increased the risk of offspring AF (multivariable-adjusted odds ratio [OR], 1.85; 95% confidence interval [CI], 1.12-3.06; P = .02). These results were stronger when age was limited to younger than 75 years in both parents and offspring (multivariable-adjusted OR, 3.23; 95% CI, 1.87-5.58; P<.001) and when the sample was further limited to those without antecedent myocardial infarction, heart failure, or valve disease (multivariable-adjusted OR, 3.17; 95% CI, 1.71-5.86; P<.001).
Conclusions Parental AF increases the future risk for offspring AF, an observation supporting a genetic susceptibility to developing this dysrhythmia. Further research into the genetic factors predisposing to AF is warranted.
