EDITORIAL COMMENT
Atrial fibrillation—more evidence that it’s here to stay*
John H. McAnulty, MD, FACC*,*
* Division of Cardiology, Oregon Health Sciences University, Department of Cardiology, Portland, Oregon, USA
* Reprint requests and correspondence: Dr. John H. McAnulty, Oregon Health Sciences University, Cardiology, 3181 SW Sam Jackson Park Road, Mail code MPV-62, Portland, Oregon 97201-3011, USA.
mcanultj{at}ohsu.edu
Wondering how to fit in yet another person with atrial fibrillation (AF)—given the complexity of decision making and the time required to appropriately involve patients in the treatment plans—makes it seem only obvious that the prevalence of this rhythm must be increasing. In support of the thought that there "must be more," is the work by Tsang et al. (1) published in this issue of the Journal. In this longitudinal case-control study, the prevalence of a previously documented AF was assessed in 1,871 individuals presenting with an ischemic stroke, and in age- and gender-matched controls. In both groups, the prevalence increased during each decade of calendar time from 1960 to 1989, independent of age, gender, or ischemic stroke status. As with any good work, this study raises questions. Among these are the following four:
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Is it true?
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In the article by Tsang et al. (1), the authors acknowledge that "analyzing multiple concurrent trends is a highly complex process." Case and control ascertainment was through assessment of coded diagnoses in a central diagnostic index. This raises the question of whether coding approaches, diligence, and interpretation were the same in the early decade of this trial compared with the last decade. If it is assumed that the coding was consistent, another concern is that AF was not considered to be present until documented on an electrocardiogram. Was the likelihood of finding the index electrocardiogram the same in all three time periods? The questions are not enough to doubt the validity of the findings.
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Is it true outside of Rochester, Minnesota?
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As acknowledged by Tsang et al. (1), the population of Rochester, Minnesota is predominantly white and, by definition, lives in a North Midwestern U.S. community. Mr. Garrison Keiller may well be able to innovatively add to the list of the many obvious ways this group of individuals differs from those in other parts of the country and world. As the authors note, cautious interpretation of the applicability of these findings is appropriate. In support of the observation of an increasing prevalence of AF is that it is in agreement with findings from other studies of other, also limited, populations.
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Assuming it is true, why?
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There certainly have been changes over time in residents having health care contact in Rochester, Minnesota. Tsang et al. (1) acknowledge that with their assessment, "cause and effect interpretations are not possible." Changes in co-morbidity would seem to be one obvious explanation. Analysis in this study revealed increases over time in myocardial infarction and congestive heart failure in stroke patients and older controls, whereas diabetes mellitus and coronary bypass surgery increases were found only in controls. Although this supports the possibility of an increase in embolic rather than vascular disease as an explanation for strokes in the later decade, it does not clearly explain the change in prevalence of AF.
Health care itself may be playing a role. Medications are always a potential cause of AF, and they certainly have changed. Additionally, in any age group, individuals are more likely to survive co-morbid conditions and thus have the "opportunity" to develop AF.
Any reader can consider his or her own list of potential explanations, including changes in habits, activity, and diet. A possible change in the intake of fatty acids is of interest. Diets rich in long chain polyunsaturated fatty acids are associated with a decrease in the risk of sudden cardiac death, and increased trans-fatty acid intake is associated with an increased risk (2,3). If sudden cardiac death is most often due to arrhythmias, it could be hypothesized that a change in intake of these fatty acids could alter the prevalence of AF as well as ventricular arrhythmias. There is no definitive evidence for either of these, although one study has suggested less AF with increased fish intake (4). The influence of fatty acid intake is of interest to this writer and his colleagues, but hypotheses related to other variables could and should be considered in the same way.
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What are the implications of increased AF?
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The increased morbidity and mortality due to AF are reasons to look for and correct the likely reasons "why" there is an increase in this arrhythmia. Until the "why" is better understood, the increased prevalence is a reason to plan for the future. If, as Tsang et al. (1) predict, there is a 2.5-fold increase in the prevalence of AF in the next 50 years, attention to management of the prevention of thromboembolic events will be increasingly important. We have the chance to optimize anticoagulation management systems and to better define patient groups who can be managed with self-monitoring of the International Normalized Ratio at home. The projections of more AF should be a stimulus to define alternatives to warfarin or aspirin and to further define the best anti-fibrillation therapy for those who will not accept the symptoms of the rate controlled rhythm.
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Footnotes
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* Editorials published in the Journal of the American College of Cardiology reflect the views of the authors and do not necessarily represent the views of JACC or the American College of Cardiology. 
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References
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- Tsang TSM, Petty GW, Barnes ME, et al. The prevalence of atrial fibrillation in incident stroke cases and matched population controls in Rochester, Minnesota: changes over three decades. J Am Coll Cardiol 2003;42:93–100
- Albert CM, Campos H, Stampfer MJ, et al. Blood levels of long-chain n-3 fatty acids and the risk of sudden death. N Engl J Med. 2002;346:1113–1118[Abstract/Free Full Text]
- Lemaitre RN, King IB, Raghunathan TE. Cell membrane trans-fatty acids and the risk of primary cardiac arrest. Circulation. 2002;105:697–701[Abstract/Free Full Text]
- Siclari C, Iannucci G, DiMaio F, et al. Long chain n-3 fatty acids can prevent paroxysmal atrial fibrillation. Circulation. 2002;106(Suppl II):II635
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Is it true?
Is it true outside...