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Highlights the paradox that patients with atrial fibrillation-related stroke are largely excluded from modern anti-inflammatory cardiovascular trials despite evidence linking inflammation to AF pathophysiology and thromboembolism.
Understanding why patients with atrial fibrillation (AF) continue to face a substantial risk of stroke recurrence despite appropriate anticoagulation remains one of the most persistent challenges in secondary prevention.1, 2 Inflammation has long been implicated in the pathophysiology of AF, and converging mechanistic, genetic, and epidemiologic evidence has strengthened the view that inflammatory signaling contributes not only to arrhythmia initiation and progression but also to thromboembolism and long-term vascular vulnerability.3 Yet, paradoxically, patients with AF-related stroke have been largely excluded from modern anti-inflammatory cardiovascular trials, which have focused on non-cardioembolic strokes.4
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Acampa et al. (2026) studied this question.
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