{'fraction_non_alphanumeric': 0.017232890201871, 'fraction_numerical': 0.01772525849335303, 'mean_word_length': 5.410094637223975, 'pattern_counts': {'":': 0, '<': 2, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Role of atrial fibrillation burden in assessing thromboembolic risk.

Stroke represents the most devastating complication of atrial fibrillation (AF). Our understanding of the pathophysiology of thromboembolism in patients with AF remains incomplete, and as such, our assessment and management of this risk is imperfect. Current guidelines regard the risk of thromboembolism as independent of the frequency or duration of AF.1 Paradoxically, standard practice in the pericardioversion period considers thromboembolic risk to accrue after 48 hours of AF.1 This recommendation, however, is based on limited data, including an observational study of 357 patients which demonstrated that the risk of thromboembolic events was <1% in patients with AF lasting <48 hours who cardioverted without prolonged anticoagulation therapy or a transesophageal echocardiogram.2 No strong randomized control trial data exist to specifically support a 48-hour safety cut-off, and recent data suggest that the duration of AF associated with a significantly increased risk of stroke may in fact be less.3–8 The emergence of technology to allow absolute quantification of the frequency and duration, or burden, of AF offers the opportunity to refine our assessment and management of thromboembolic risk associated with AF.

It has been 200 years since William Wood described a ball thrombus in the left atrium of a patient with mitral stenosis9 and 170 years since Virchow identified the critical components required for thrombus formation.10 It took until 1930 for Harvey and Levine to first declare that “auricular fibrillation definitely increases the incidence of auricular thrombosis” in an autopsy series of patients with mural thrombi.11 Uncertainty as to whether nonrheumatic AF resulted in stroke continued for the next 40 plus years until Wolfe and colleagues, in their landmark analysis using the Framingham population data, identified a 5.6-fold increased risk of stroke in patients with chronic nonvalvular AF.12 With time it would become …