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Left Atrial Thrombus and Cardioembolic Stroke in Chagas Cardiomyopathy Presenting with Atrial Flutter: A Case Report
Mauricio Sebastián Moreno-Bejarano1, Israel Silva-Patiño2, Andrea Cristina Aragón-Jácome2
1Centro de Salud, Ministerio de Salud Pública, Lasso 050102, Cotopaxi, Ecuador.
Insights
Chagas disease can cause stroke due to heart complications like atrial flutter and thrombus. Prompt diagnosis and treatment of Chagas cardiomyopathy are vital for preventing severe outcomes.
Area of Science:
- Cardiology
- Neurology
- Infectious Diseases
Background:
- Chagas disease, caused by *Trypanosoma cruzi*, is endemic in Latin America and spreading globally.
- Cardiac manifestations, including arrhythmias and thrombus formation, increase cardioembolic risk.
- Strokes secondary to Chagas cardiomyopathy are rare and challenging to manage.
Abstract:
Background: Chagas disease, caused by Trypanosoma cruzi, remains endemic throughout Latin America but is increasingly reported in urban areas due to migration and vector adaptation. The cardiac form is the most severe manifestation, associated with arrhythmia, mural thrombus formation, and a high risk of cardioembolic events. Stroke secondary to Chagas cardiomyopathy is uncommon and poses diagnostic and therapeutic challenges. Case Presentation: A 58-year-old woman with serologic evidence of T. cruzi infection presented with sudden-onset dyspnea, oppressive chest pain, and left-sided weakness. Neurological examination revealed left brachiocrural hemiparesis and mild dysarthria (NIHSS = 9). Non-contrast cranial CT showed an acute infarct in the right middle cerebral artery territory (ASPECTS = 7). Electrocardiography demonstrated typical atrial flutter with variable conduction, and transthoracic echocardiography revealed a markedly dilated left atrium containing a mural thrombus and a left ventricular ejection fraction of 45%. Intravenous thrombolysis with alteplase (0.9 mg/kg) was administered within 4.5 h of symptom onset. Pharmacologic rhythm control was achieved using intravenous and oral amiodarone, followed by oral anticoagulation with warfarin (target INR 2.0-3.0) after excluding hemorrhagic transformation. The patient showed rapid neurological improvement (NIHSS reduction from 9 to 2) and was discharged on day 10 with minimal residual deficit (mRS = 1), sinus rhythm, and stable hemodynamics. Conclusions: This case highlights the rare coexistence of Chagas cardiomyopathy, atrial flutter, and cardioembolic stroke due to left atrial thrombus. Early recognition, adherence to evidence-based guidelines, and multidisciplinary management were key to achieving a favorable outcome. Timely diagnosis and intervention remain crucial to preventing severe complications in patients with Chagas disease.
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