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Cardioembolic stroke in a young male with cor triatriatum sinister: a case report
Richard S Amara1, Rakhee Lalla2, Jean Jeudy3
1Department of Cardiology, University of Maryland Medical Center, 22 South Greene Street, Baltimore, MD 21201, USA.
Insights
Cor triatriatum sinister (CTS), a rare heart defect, can cause stroke even without typical blood clots. This case highlights the hidden risks of CTS and protein C deficiency in stroke.
Area of Science:
- Cardiology
- Neurology
- Congenital Heart Disease
Background:
- Cor triatriatum sinister (CTS) is a rare congenital cardiac anomaly where a membrane divides the left atrium.
- CTS is linked to cardioembolic stroke via blood flow stagnation, atrial fibrillation, or septal defects.
Observation:
- A 35-year-old presented with stroke symptoms, revealing CTS with an atrial septal defect (ASD) and potential protein C deficiency.
- Imaging confirmed the CTS membrane, and the patient underwent successful mechanical thrombectomy.
Findings:
- This is the 13th reported case of CTS associated with stroke.
- Unlike previous cases, this patient had no blood stasis or atrial fibrillation, underscoring the subtle risks of CTS.
- Protein C deficiency further elevated the thromboembolic risk.
Implications:
- Highlights the importance of considering CTS in cryptogenic stroke evaluations.
- Emphasizes the need for comprehensive workups to identify co-existing conditions like protein C deficiency.
- Underscores the role of multidisciplinary management in complex thromboembolic cases involving congenital heart defects.
Background:
Cor triatriatum sinister (CTS) is a rare congenital cardiac anomaly defined by a fibromuscular membrane which bisects the left atrium. Cor triatriatum sinister has been associated with cardioembolic stroke through mechanisms including stagnation of blood flow within the left atrium, an association with atrial fibrillation (AF), and/or an accompanying atrial septal defect (ASD) or patent foramen ovale. We describe a case highlighting the role that CTS may play in cardioembolic stroke, provide high-quality computed tomography angiography and two- and three-dimensional echocardiography of the CTS membrane, and outline management strategies for this uncommon clinical scenario.
Case Summary:
A 35-year-old man with no prior medical history presented with acute onset weakness and aphasia. He was found to have an embolic stroke with left M1 and A1 occlusions and received tissue plasminogen activator followed by mechanical thrombectomy with successful recanalization. A thorough stroke workup revealed CTS with an associated ASD as well as potential protein C deficiency. He was managed with indefinite anticoagulation with apixaban.
Discussion:
This is the 13th reported case of CTS associated with stroke. In most previous cases evidence of blood stasis or frank thrombus was associated with the CTS membrane, and/or existing AF was noted. In this case, none of these were identified, particularly highlighting the surreptitious risk of CTS. In addition, the presence of potential protein C deficiency in this case compounded the risk for thromboembolism and factored into multidisciplinary management decisions.
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