(Circulation. 1995;92:2178-2182.)
© 1995 American Heart Association, Inc.
Articles |
Silent Cerebral Infarction in Patients With Nonrheumatic Atrial Fibrillation
From the VA Medical Center, West Haven, Conn, and Department of Medicine, Yale University (M.D.E.); the VA Medical Center, Portland, Ore, and Department of Public Health and Preventive Medicine, Oregon Health Sciences University (K.E.J.); the VA Medical Center, Little Rock, Ark, and Department of Neurology, University of Arkansas (S.M.N.); the VA Medical Center, Minneapolis, Minn, and Department of Neurology, University of Minnesota (J.D.); the Department of Neurology, University of Cincinnati, Cincinnati, Ohio (J.P.B.); the VA Medical Center, Hines, Ill, and Department of Neurology, Loyola University (S.R.G.); the Department of Neurology, Dartmouth-Hitchcock Medical Center, Lebanon, NH (V.T.); Yale University, New Haven, Conn (M.L.M.); and Yale–New Haven Medical Center, New Haven, Conn (S.L.B.).
Correspondence to Kenneth E. James, PhD, Health Services Research and Development (152), VA Medical Center, 3710 SW US Veterans Hospital Rd, Portland, OR 97201. E-mail james@hsrd.gov
Background Cerebral infarction in patients with atrial fibrillation may vary from being clinically silent to catastrophic. The prevalence of silent cerebral infarction and its effect as a risk factor for symptomatic stroke are important considerations for the evaluation of patients with atrial fibrillation.
Methods and Results This Veterans Affairs cooperative study was a double-blind controlled trial designed primarily to determine the efficacy of warfarin for the prevention of stroke in neurologically normal patients with nonrheumatic atrial fibrillation. It also was designed to evaluate patients with silent cerebral infarction. Computed tomography scans of the head were performed at entry, at the time of any subsequent stroke, and at termination of follow-up on all patients who completed the study without a neurological event. Of 516 evaluable scans performed at entry, 76 (14.7%) had evidence of one or more silent cerebral infarcts. Age (P=.011), a history of hypertension (P=.003), active angina (P=.012), and elevated mean systolic blood pressure (P<.001) were associated with the presence of this finding. Silent cerebral infarction occurred during the study at rates of 1.01% and 1.57% per year for the placebo and warfarin treatment groups, respectively (NS). Silent cerebral infarction at entry was not an independent predictor of later symptomatic stroke, but active angina was a significant predictor; 15% of the placebo-assigned patients with angina developed a stroke compared with 5% of the placebo-assigned patients without angina.
Conclusions Silent cerebral infarction is frequently seen in asymptomatic patients with atrial fibrillation. Age, history of hypertension, active angina, and elevated mean systolic blood pressure were associated with silent infarction at entry. The sample size was too small to determine whether warfarin had an effect on the incidence of silent infarction during the trial. Active angina at baseline was the only significant independent predictor for the later development of symptomatic stroke.
Key Words: cerebral infarction • atrial fibrillation • tomography
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