Key result
Cardiac myxoma excision resolves recurrent embolic strokes presenting as cognitive decline in antiphospholipid syndrome.
This case highlights the necessity of comprehensive structural cardiac evaluation (e.g., TEE) in young patients with embolic strokes, even when a prothrombotic condition like APS is already identified.
Challenges reliance on APS diagnosis alone in young embolic stroke; leaves open utility of routine TEE to detect coexistent myxoma.
A woman in her 40s presented with progressive cognitive decline, expressive language difficulty and episodic confusion. Her initial symptoms were misattributed to psychiatric illness, and later to small vessel ischaemia, delaying appropriate evaluation. Over 2 years, serial MRIs revealed multiple new cortical infarcts. Stroke workup confirmed antiphospholipid syndrome (APS) yet continued concern for a persistent embolic source prompted trans-oesophageal echocardiography, which revealed a mass on the posterior mitral leaflet. Surgical excision confirmed a benign cardiac myxoma with no further embolic events on follow-up. This case illustrates how neuro-embolic events can manifest as non-specific psychiatric or cognitive symptoms, and how early assumptions may delay appropriate diagnosis. Even after diagnosing a prothrombotic condition like APS, clinicians must look for structural cardiac lesions that may coexist and amplify embolic risk. Comprehensive aetiological assessment is essential in embolic stroke of undetermined source, especially in younger patients with atypical presentations.
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George et al. (2026) studied this question. Delayed diagnosis of cardiac myxoma with antiphospholipid syndrome caused recurrent embolic strokes presenting as cognitive decline, resolved after tumor removal.
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