Atrial fibrillation (AF) is directly implicated in embolic stroke and suspected in a large proportion of cryptogenic stroke. The current stroke-prevention strategy in embolic and cryptogenic stroke starts with arrhythmia detection, followed by risk stratification and treatment for those deemed to be at increased risk. This approach is practical and widespread; however, more recent findings have questioned its validity. Arrhythmia detection is dependent on the length and fidelity of monitoring. Long-term monitoring using implanted recorders improves arrhythmia detection in patients with cryptogenic stroke. A large proportion of patients with cryptogenic stroke, however, were shown not to have any AF. Moreover, in patients with permanent pacemakers who also experienced thromboembolic events, AF did not always precede thromboembolisation. These results raise cause and effect questions about the role of AF, the arrhythmia, in thrombus formation and embolisation. Moreover, risk estimation scores; such as Congestive heart failure, Hypertension, Age, Diabetes and previous Stroke or Transient Ischaemic Attack, Vascular disease and female sex category (CHA2DS2-VASc), have a suboptimal predictive accuracy and the mechanism relating their individual components to thrombogenesis is unknown. Given these limitations, a more comprehensive and mechanistic evaluation of atrial disease is needed to better identify patients at risk for stroke and AF. Atrial fibrosis, quantified using late gadolinium enhancement cardiac MRI, is associated with reduced atrial function, stroke and the presence of left atrial thrombus in patients with AF. Biomarkers such as B-type natriuretic peptide, cardiac troponin have also been linked to increased thromboembolic risk and AF.
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