Atrial Fibrillation and Stroke

Atrial fibrillation (AF) is a well-known independent risk factor for stroke, resulting in an approximately 3- to 5-fold excess risk [1]. In patients with type 2 diabetes mellitus, AF confers an up to 8-fold risk for stroke, according to the UKPDS data [2]. Its incidence increases with advancing age, affecting 6–10% of people aged >75 years [3]. Presence of impaired left ventricular function [4, 5], thoracic aortic plaques [6]and extracranial carotid disease [7]significantly raises the risk of stroke in patients with AF.AF is the most common chronic arrhythmia associated with an adverse prognosis. The worsened survival seen with AF does not reflect the increased mortality of the cardiovascular conditions with which it is associated: from the Framingham Heart Study [8]we know that AF is associated with a 1.5- to 1.9-fold mortality risk after adjustment for the preexisting cardiovascular conditions with which AF is related, and the decreased survival is present in men and women, across a wide range of ages. Studies aimed at identifying major factors predicting mortality after stroke include AF both for early death [9]and within 30 days and 1 year [10].There are conflicting data concerning the prognostic importance, rate of embolic complications, and survival in subjects affected by lone AF (LAF), i.e. AF unassociated with other evidence of organic heart disease. Recently, it has been claimed [11]that LAF occurring after 60 years of age is a risk marker for a substantial increase in cardiovascular events; another recent report [12]focuses on the different risk due to paroxysmal versus chronic LAF in young patients.Since AF is a modifiable risk factor, it should be thoroughly assessed and treated in both primary and secondary prevention setting. Risk stratification and subsequent therapeutic measures (table 1) have been clearly pointed out [4]; according to the results of a recent meta-analysis which has included all published randomized trials testing antithrombotic agents to prevent stroke in patients with AF [13], adjusted-dose warfarin (six trials, 2,900 participants) reduced stroke by 62% (95% confidence interval, CI, 48–72%); absolute risk reductions were 2.7% per year for primary prevention and 8.4% per year for secondary prevention. Aspirin (six trials, 3,119 participants) reduced stroke by 22% (CI, 2–38%); absolute risk reductions were 1.5% per year for primary prevention and 2.5% per year for secondary prevention. Adjusted-dose warfarin (five trials, 2,837 participants) was more efficacious than aspirin (relative risk reduction, 36%, CI, 14–52%), and the benefit of antithrombotic therapy was not offset by the occurrence of major hemorrhages.Although the striking evidence for efficacy of antithrombotic therapy, with special emphasis on oral anticoagulants, the underuse of antithrombotic treatment is even more impressive [14, 15]. The reasons why anticoagulation trials have not actually influenced the clinical practice are not completely understood; a possible explanation might be the insufficient information of the patient, which should be achieved by means of decision aids to be used in clinical settings [16].AF is an independent determinant of low cognitive function [17]: elderly subjects with AF had lower cognitive function independent of socioeconomic factors, blood pressure, diabetes or previous stroke. In the Rotterdam Study, stroke-free women with AF had a higher risk of dementia and cognitive impairment without dementia [18]. These evidences emphasize the importance to adequately assess and treat AF as effective preventive measure with respect to both stroke and dementia, the leading causes of disability in the elderly.A better understanding of the reasons for undertreatment, an improved information and education of patients on this topic, maximum effort for improving management and care of stroke patients and stroke-related diseases, represent the ideal tools assisting in the prevention of disability in daily clinical practice.