Program

Lecture Abstract：
Can atrial cardiomyopathy (AtCM) or subclinical device-detected atrial fibrillation (AF) justify anticoagulation in the absence of clinical AF? This talk traces AtCM from a 1972 descriptive curiosity to a staged, measurable entity under the 2024 EHRA/HRS/APHRS/LAHRS consensus and the 2025 HFA/ESC diagnostic criteria, which require electrical dysfunction plus atrial enlargement, contractile impairment, or fibrosis. Epidemiologic data tie AtCM to ischemic stroke independent of AF, but the direct test—ARCADIA—showed no benefit of apixaban over aspirin, suggesting the problem lies in biomarker selection rather than the underlying biology; its MRI substudy hints that a true cardioembolic signal may have been masked by non-cardioembolic recurrences. For device-detected subclinical AF, stroke risk rises sharply once episodes exceed roughly 24 hours, and NOAH-AFNET 6 and ARTESiA together show a narrow but real net benefit of anticoagulation, concentrated among patients with vascular disease. These findings converge in the APHRS 4S-DDAF algorithm, a four-step bedside pathway—confirming the tracing, episode duration, symptoms, prior stroke, and CHA₂DS₂-VASc score—that turns an ambiguous diagnosis into an actionable anticoagulation decision.