doi: 10.1161/01.STR.0000015783.61960.FB
(Stroke. 2002;33:1179.)
© 2002 American Heart Association, Inc.
Letters to the Editor |
Prevalence and Risk Factors of Silent Brain Infarcts in the Population
Haemostasis, Thrombosis and Vascular Biology Unit, University Department of Medicine, City Hospital, Birmingham, United Kingdom
To the Editor:
We read with interest the study reported by Vermeer et al on the prevalence and risk factors for silent brain infarcts in the Rotterdam scan study.1
We were, however, very surprised that the authors neither commented on nor investigated the presence of associated atrial fibrillation (AF) as a risk factor in this study population. As we already know, AF is an independent risk factor for stroke,2 and many other investigators have firmly established the presence of silent cerebral infarction (SCI) in patients with atrial fibrillation.3,4 For example, the Veteran Affairs Stroke Prevention in Nonrheumatic Atrial Fibrillation Investigators reported that 14.7% of neurologically normal male patients with nonvalvular AF had evidence of cerebral infarction on CT scanning.3 As with Vermeer et al,1 they too reported that an increasing age and a history of hypertension was associated with silent cerebral infarction at entry into the study. Angina was also a risk factor for SCI and was the only independent predictor for later development of symptomatic stroke. Nevertheless, SCI was not an independent predictor of subsequent (symptomatic) stroke in this AF population, although it must be noted that half of the study population were receiving warfarin as part of an intervention study.
Another study from Japan reported a much higher prevalence of SCI in lone AF patients examined with MRI: of 79 patients with lone AF (57 male, 22 female) on no anticoagulant therapy, silent cerebral infarcts were detected in 88% of patients. This high prevalence of SCI increased with age, and, importantly, there was no difference between those patients with paroxysmal and continuous AF.4 These observations are in contrast to a Danish report, which shows a low prevalence of SCI on CT in 30 patients with paroxysmal AF.5 We accept that there are no population studies to indicate whether AF is an independent risk factor for SCI, although the evidence above would suggest that a strong association between SCI and AF may exist.
Vermeer et al1 suggest that the odds ratio of both silent and symptomatic SCI increases with age, at 8% per year—but this could best be explained by an important risk factor from stroke that also increases with age, as is the case with AF.6 Another area of interest would be the relationship of SCI to cognitive function in the affected patients. Indeed, in the Rotterdam study population, an association between dementia and AF has been noted, and SCI would seem to be a likely mechanism.7
References
1.
Vermeer SE, Koudstaal PJ, Oudkerk M, Hofman A, Breteler MMB. Prevalence and risk factors of silent brain infarcts in the population based Rotterdam scan study. Stroke. 2002; 33: 21–25.
2.
Wolf PA, Abbott RD, Kannel WB. Atrial fibrillation as an independent risk factor for stroke: the Framingham Study. Stroke. 1991; 22: 983–988.
3.
Ezekowitz MD, James KE, Nazarian SM, Davenport J, Broderick JP, Gupta SR, Thadani V, Meyer ML, Bridgers SL. Silent cerebral infarction in patients with nonrheumatic atrial fibrillation. Circulation. 1995; 92: 2178–2182.
4. Koretsune Y, Hori M, Kamada T. High prevalence of silent cerebral infarction in patients with lone atrial fibrillation. J Am Coll Cardiol. 1995; 25: 179A.Abstract.
5. Petersen P, Pedersen F, Johnsen A, Madsen EB, Brun B, Boysen G, Godtfredsen J. Cerebral computed tomography in paroxysmal atrial fibrillation. Acta Neurol Scand. 1989; 79: 482–486.[Medline] [Order article via Infotrieve]
6. Kannel WB, Abbot RD, Savage DD, McNamara PM. Epidemiological features of chronic atrial fibrillation: the Framingham Study. N Engl J Med. 1982; 306: 1018–1022.[Abstract]
7.
Ott AO, Breteler MMB, de Bruyne MC, van Harskamp F, Grobbee DE, Hoffman A. Atrial fibrillation and dementia in a population-based study: the Rotterdam Study. Stroke. 1997; 28: 316–321
Departments of Epidemiology & Biostatistics and Neurology
Department of Epidemiology & Biostatistics
Department of Neurology, Erasmus Medical Center, Rotterdam, the Netherlands
Response
Drs Freestone and Lip suggest that the rise in prevalence of silent brain infarcts with increasing age could be well explained by atrial fibrillation (AF), which also increases with age. We agree that it is indeed very interesting to examine the relationship between AF and silent brain infarcts in the general population. The high prevalence of silent brain infarcts in AF patients,1 who often suffer from small- and large-vessel disease as well,2 is insufficient proof of a direct relationship between AF and silent brain infarcts, of which the majority are lacunes.3 This relationship has not been examined in the general population. In patients with lacunar stroke, however, atrial fibrillation is rarely the causative factor.4 In our population-based study, a 12-lead ECG was recorded in all participants a few weeks before MRI scanning from 1995 to 1996. The presence of atrial fibrillation was diagnosed with a computer program, Modular ECG Analysis System (MEANS).5 In total, 32 participants had AF, of whom 22 had no infarcts on MRI, 8 had silent brain infarcts, and 2 had symptomatic infarcts. AF was not associated with the presence of silent brain infarcts (age- and sex-adjusted odds ratio 1.0, 95% CI 0.4 to 2.3). However, the number of participants with AF in our study was lower than expected in an elderly population.6 The use of MEANS to detect AF might have led to a misclassification of participants with AF. Moreover, we will certainly miss people with paroxysmal atrial fibrillation, especially because we recorded for only 10 seconds. If anything, this misclassification will have resulted in an underestimation of the association. Nevertheless, the absence of a relationship in our study and our finding that the vast majority of silent lesions were lacunes make it unlikely that AF is a contributing factor in the age-related increase in the prevalence of silent brain infarcts in the general population.
References
1.
Silent brain infarction in nonrheumatic atrial fibrillation: EAFT Study Group: European Atrial Fibrillation Trial. Neurology. 1996; 46: 159–165.
2.
Allessie MA, Boyden PA, Camm AJ, Kléber AG, Lab MJ, Legato MJ, Rosen MR, Schwartz PJ, Spooner PM, van Wagoner DR, Waldo AL. Pathophysiology and prevention of atrial fibrillation. Circulation. 2001; 103: 769–777.
3. Vermeer SE, Koudstaal PJ, Oudkerk M, Hofman A, Breteler MMB. Prevalence and risk factors of silent brain infarcts in the population-based Rotterdam Scan Study. Stroke. 2002; 33: 21–25.
4.
Boiten J, Lodder J. Lacunar infarcts. Pathogenesis and validity of the clinical syndromes. Stroke. 1991; 22: 1374–1378.
5. de Bruyne MC, Kors JA, Hoes AW, Kruijssen DACM, Deckers JW, Grosfeld M, van Herpen G, Grobbee DE, van Bemmel JH. Diagnostic interpretation of electrocardiograms in population-based research: computer program research physicians, or cardiologists? J Clin Epidemiol. 1997; 50: 947–952.[CrossRef][Medline] [Order article via Infotrieve]
6. Kannel WB, Wolf PA, Benjamin EJ, Levy D. Prevalence, incidence, prognosis, and predisposing conditions for atrial fibrillation: population-based estimates. Am J Cardiol. 1998; 82: 2N–9N.[CrossRef][Medline] [Order article via Infotrieve]
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