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Birminghan, UK
Dr. Lip is Professor of Cardiovascular Medicine, University Department of Medicine, City Hospital, Birmingham, UK.
Correspondence to: Gregory Y. H. Lip, MD, Haemostasis Thrombosis and Vascular Biology Unit, University Department of Medicine, City Hospital, Birmingham B18 7QH, UK; e-mail: g.y.h.lip{at}bham.ac.uk
Given the major mortality and morbidity associated with ischemic stroke in atrial fibrillation (AF) and how common this arrhythmia is in the general population, efforts have been directed toward refining stroke risk-stratification schemes in AF. The latter helps us target those at "high risk," so that oral anticoagulation (OAC), which has been proven to beneficially reduce stroke and thromboembolism, can be prescribed to the patients who need it most.1
There are numerous risk-stratification schema published2 that have many similarities but also some degrees of inconsistency. Patients with AF and cerebrovascular disease (prior stroke or transient ischemic attack) are well recognized to be at "very high" risk, and anticoagulation is recommended by all guidelines, with no ambiguity. However, a stroke risk factor for which some uncertainty remains is the presence (or absence) of other vascular disease (whether coronary artery disease [CAD] or peripheral artery disease [PAD]), despite the close association between AF and vascular disease. For example, the 2006 update of the expert consensus-based American College of Cardiology/American Heart Association/European Society of Cardiology guidelines on AF management refers to CAD as a "less validated or weaker risk factor."2 In the evidence-based UK National Institute for Health and Clinical Evidence guidelines for AF management, patients "aged 
75 years plus vascular disease (the latter defined as CAD or PAD)" were considered as "high risk," and OAC is recommended (http://www.nice.org.uk/page.aspx?o=cg36). In the AF investigators risk-stratification scheme, the presence of CAD was listed as a "moderate-high" risk factor.3
An explanation as to why a risk factor appears in some risk-stratification schema but not in others may be due to the fact that it may not have been investigated systematically in large studies, or has not been shown to have independent predictive value for stroke in cohorts of patients with AF (largely derived from trial populations) on multivariate analyses. The latter may not be too surprising because a common condition such as CAD or PAD commonly coexists with important stroke risk factors (such as age, hypertension, and diabetes), and statistical adjustment can never fully adjust for all biological and pathophysiologic processes. Indeed, myocardial infarction (MI) secondary to CAD can be associated with significant left ventricular dysfunction, itself an important risk factor for stroke.1
What does the evidence say? In some studies, CAD was a univariate predictor of stroke in otherwise low-risk patients.4 Other studies also considered a history of MI as a risk factor for stroke, and MI was a significant independent risk factor in two studies56 but not in the another study, which was essentially based in an elderly population in whom other comorbidities probably predominate.7 However, other studies did not find the presence of "ischemic heart disease," nor a history of angina to be a significant independent predictor of stroke on multivariate analysis.38 One problem here may be the definition of CAD used in different studies, given that many patients with a label of "angina" may not actually have CAD.
What about PAD? PAD was not systematically reported (nor investigated for) in many of the trial cohorts on which many risk-stratification schema are based. In one cohort of patients with PAD, the presence of AF was certainly associated with emergency admissions (adjusted odds ratio [OR], 11.64; 95% confidence interval [CI], 4.65 to 29.15; p < 0.001) and in-hospital mortality (OR, 2.53; 95% CI, 1.04 to 6.17; p < 0.05).9 Of note, complex aortic plaque on the descending aorta visualized by transesophageal echocardiography was an independent stroke risk factor,10 and ischemic stroke in AF could be associated with carotid artery disease.11 Thus, CAD and PAD should probably be regarded as part of the wide clinical spectrum of atherothrombotic vascular disease (that essentially includes carotid and cerebrovascular disease too!) that contributes to stroke risk, whether the subject is in AF or not.
In this issue of CHEST (see page 44), Siu et al12 report that transient AF complicating acute inferior MI was associated with an increased future risk of AF occurrence and ischemic stroke in patients with preserved left ventricular ejection fraction, despite the use of antiplatelet therapy. While this study is limited by its retrospective registry analysis and transient AF was observed in a relatively small proportion of patients (13.7%) during their hospitalization for MI, it adds to the ongoing debate on the relationship between ischemic stroke, AF, and CAD (and MI). Of note, all their patients were in sinus rhythm on discharge, but at 1-year follow-up the incidence of AF and ischemic stroke was much higher in patients with transient AF than those without. Indeed, a Cox regression analysis revealed the presence of transient AF (hazard ratio, 5.1) and age > 65 years (hazard ratio, 3.3) were independent predictors for the occurrence of ischemic stroke following acute MI.
There is a vast literature that AF during MI is an adverse feature for mortality and morbidity, but clearly the development of AF after MI may also contribute to stroke risk. While underlying left ventricular dysfunction (and other comorbidities) may confound this relationship, it is also possible that many post-MI patients have transient asymptomatic AF, which could have contributed to stroke and thromboembolism. Indeed, Wah et al12 did not systematically investigate all patients for AF burden, whether asymptomatic or not. Indeed, we should start considering that MI is part of the (very) wide clinical spectrum of atherothrombotic vascular disease (coronary, peripheral, carotid, and cerebrovascular disease) that ultimately increases stroke risk, whether the patient is in AF or not.
Footnotes
Dr. Lip has received funding for research, educational symposia, consultancy, and lecturing from different manufacturers of drugs used for the treatment of atrial fibrillation and thrombosis. He was clinical adviser to the Guideline Development Group writing the UK National Institute for Health and Clinical Excellence guidelines on atrial fibrillation management (www.nice.org.uk) and is on the writing group for the American College of Chest Physicians Consensus Guidelines on Antithrombotic Therapy for Atrial Fibrillation.
References
62 years of age with chronic atrial fibrillation. Am J Cardiol 1998;82,119-121[CrossRef][ISI][Medline]Related Article
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J. S. Taggar, T. Watson, and G. Y.H. Lip Can Patients With Atrial Fibrillation Be Optimally Risk Stratified for Stroke and Thromboembolism? Stroke, February 1, 2008; 39(2): e24 - e25. [Full Text] [PDF]
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