Laurie Brunette and Asher Kimchi M.D.
Atrial fibrillation is associated with an increased risk of
mortality and stroke, and every one in four people will develop
AF at some point in their lifetime. Already recognized clinical
risk factors for AF include advancing age, increased systolic
blood pressure, diabetes, hypertension, heart failure, valvular
disease, myocardial infarction, and obesity. Echocardiographic
risk factors for AF include left atrial enlargement, increased
left ventricular wall thickness, and impaired left ventricular
systolic function. Gary F. Mitchell, MD et al from the
Cardiovascular Engineering Inc. in Waltham, MA investigated
whether pulse pressure, a reflection of aortic stiffness, could
be a potentially easily modifiable risk factor for AF. Their
study, published in the February 21, 2007 issue of The
Journal of the American Medical Association, found that
pulse pressure is in fact an important risk factor for incident
AF in a community-based sample.
included 5331 participants (55% women) of the Framingham Heart
Study who were aged 35 years and older with no past or current
findings of AF or atrial flutter on electrocardiogram. At each
examination (every 2-8 years, censored at 20 years), a medical
history, physical examination, and electrocardiography were
administered. A standardized 2-dimensional guided M-mode
echocardiogram was also performed at the baseline examination.
in 698 participants (13.1%), a median of 12 years after pulse
pressure assessment. 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;
P<.001). Mean arterial pressure was found to be unrelated to
new-onset 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); but with the
addition of diastolic pressure, 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). This is consistent with a
pulse pressure effect. 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;
arterial stiffness, as evidenced by elevated pulse pressure,
represents a potentially modifiable risk factor for AF. Mitchell
et al has shown that pulse pressure is the single blood pressure
component most predictive of future development of AF.
Interventions known to reduce pulse pressure, such as blockade
of the renin-angiotensin system, have been shown to reduce the
incidence of new or recurrent AF. Further research is needed to
determine whether other interventions aimed at reducing pulse
pressure or preventing the increase in pulse pressure with
advancing age effectively reduce the incidence of AF.
Ramachandran S. Vasan, MD; Michelle J. Keyes, MA; Helen Parise,
ScD; Thomas J. Wang, MD; Martin G. Larson, ScD; Ralph B.
D’Agostine, Sr, PhD; William B. Kannel, MD,
MPH; Daniel Levy, MD; Emelia J. Benjamin, MD, ScM.