Atrial fibrillation is responsible for almost half of all strokes with a cardioembolic source. In this article, the authors discuss the causal association of atrial fibrillation in stroke, the role of anticoagulation in stroke prevention, and the risk stratification strategies that currently exist to help select, at the bedside, those patients who benefit the most from anticoagulation and those with the highest risk of hemorrhagic complications from such therapy.
Historical note and terminology
As early as 1628, Harvey had observed undulation in the right atrium of a dying animal heart (McMichael 1982); in 1874, Vulpian reported uncoordinated twitching of the atrium, "fremissement fibrillaire" after application of an electrical current (Vulpian 1874). Nothnagel published 3 arterial pulse curves showing irregular heart rates in the mid-1800s and called the arrhythmia "delirium cordis" (Nothnagel 1876), which was defined by the complete irregularity of heartbeats continuously changing in "height and tension." However, the association between these atrial fibrillary contractions and the irregular pulse was not made formally until 1907 (Cushny and Edmunds 1907).
In 1940, Karl Paul Link synthesized dicumarol, a substance found in spoiled sweet clover known to cause a hemorrhagic disease in cattle, and in 1947 for the first time its use was advocated for the prevention of cardiac emboli in patients with rheumatic atrial fibrillation (Wright and Foley 1947). However, the risk of stroke in patients with chronic atrial fibrillation unassociated with valvular or rheumatic disease was generally believed to be too low to require medication. It was not until 1978 when the results of the Framingham Study clearly demonstrated an increase in stroke incidence in patients with chronic nonrheumatic atrial fibrillation (Wolf et al 1978).
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