The Atrium and Embolic Stroke: Myopathy Not Atrial Fibrillation as the Requisite Determinant?

Abstract

Atrial fibrillation (AF) is well-recognized in the pathophysiology of left atrial thrombogenesis and resultant cardioembolic stroke. Subclinical AF is believed to account for a significant proportion of embolic stroke. However, recent randomized control trials failed to demonstrate a significant benefit for oral anticoagulation, in an unselected population with embolic stroke of undetermined source. This has reinvigorated the focus on finding robust markers to identify patients at risk of cardioembolic stroke. Several nonfibrillatory atrial electrical markers, along with structural and biochemical abnormalities, have been associated with ischemic stroke, independently of AF. An increasingly complex relationship exists among vascular risk factors, atrial remodeling, and thrombogenesis. Identifying robust markers of an underlying atrial myopathy may allow for early identification of patients at risk for cardioembolic stroke. This review outlines the inconsistencies in the evidence for AF as the prerequisite for left atrial thrombogenesis and embolic stroke. It will highlight the current evidence and controversies for adverse atrial remodeling, independent from rhythm, as a plausible mechanism for left atrial thrombogenesis and ischemic stroke.

Keywords: ESUS; atrium; myopathy; stroke; thrombogenesis.