Poststroke atrial fibrillation: Cause or consequence?

Abstract

Poststroke atrial fibrillation (AF) represents up to 1 of 4 overall AF cases in acute ischemic stroke. Current guidelines recommend oral anticoagulation for every ischemic stroke patient in whom AF is diagnosed. However, in some cases, AF detected after acute ischemic stroke may be short-lasting and perhaps a nonrecurrent autonomic and inflammatory epiphenomena of stroke. The autonomic regulation of cardiac rhythm constitutes an integrated relay system. The highest level of control is exerted by the cerebral cortex, particularly the insula. The onset of AF may be associated with an imbalance of sympathetic and parasympathetic activity, a common consequence of insular infarctions. This autonomic imbalance and an interruption in the cerebral regulation of the intrinsic cardiac autonomic system constitute the most likely mechanisms responsible for the autonomic pathway. The role of inflammation in the genesis of AF within the first few days after ischemic stroke may occur through inflammatory mediators stimulating the intrinsic autonomic system and by direct damage to atrial myocardium. To what extent poststroke AF is the cause or a consequence remains uncertain.