Key result
Atrial fibrillation leads to stasis-precipitated thrombi, with emboli to the brain accounting for about 80 percent of symptomatic emboli.
This article provides a historical and pathophysiological overview of stroke prevention in atrial fibrillation.
Highlights appendage stasis as stroke mechanism in AF; leaves open targeted prevention beyond anticoagulation.
Atrial fibrillation is a common cardiac arrhythmia whose most serious clinical consequence is stroke. Described in pathological studies in the 1940s, uncoordinated atrial contractions result in sluggish blood flow and the formation of thrombus in the atrial appendage: “The immobility of the auricular walls makes them defenceless against thrombotic deposits, as a horse should be against flies without his cutaneous muscles”1 (see Figure). The stasis-precipitated thrombi lead to emboli that are distributed according to cardiac output, but emboli to the brain account for about 80 percent of symptomatic emboli. Because they are larger on average than emboli of valvular origin, . . .
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Robert G. Hart (2003) conducted a review in Atrial fibrillation. Atrial fibrillation leads to stasis-precipitated thrombi, with emboli to the brain accounting for about 80 percent of symptomatic emboli.