Chronic Chagas heart disease presented as comma-shaped stroke

A previously healthy 52-year-old woman from Minas Gerais was admitted with subacute left-sided motor and sensory hemiparesis and dysarthria. A head computed tomography scan revealed a large infarct in the right lenticulostriate artery territory. Intracranial and cervical vessel studies showed occlusion of the left MCA segment M1 with preserved cortical vascularization. Brain magnetic resonance imaging revealed similar findings. An electrocardiogram identified atrial fibrillation and right bundle branch block. A 24-hour Holter monitor detected nonsustained ventricular tachycardia. Transthoracic echocardiogram revealed dilated cardiomyopathy with diffuse hypokinesis and an ejection fraction of 36%. The thrombophilia screen was negative. Given the dilated cardiomyopathy in the absence of cardiovascular risk factors or a history of alcoholism, Chagas disease was suspected and confirmed by two serological tests. Large deep striatocapsular infarctions account for 1-6% of ischemic strokes. The basal ganglia and parts of the caudate nucleus, internal capsule, putamen, and globus pallidus are supplied by the lenticulostriate arteries, the artery of Heubner, and the anterior choroidal artery. Large striatocapsular infarctions, previously termed giant or super lacunae, occur due to MCA trunk occlusion affecting all lenticulostriate arteries, typically caused by cardioembolism or atheroembolism. The cortex is often spared due to collateral artery formation, resulting in comma-shaped infarctions. Clinical manifestations include motor and/or sensory hemiparesis and may include dystonia, involuntary movements, aphasia, and hemineglect. Bladin and Verkovic described two mechanisms for preserving cortical perfusion: thrombotic occlusion at the carotid T-junction with cortical blood supply via anastomoses, and embolism at the carotid T-junction obstructing lateral striate arteries while allowing some cortical perfusion. The patient presented with this unusual form of stroke, likely due to chronic Chagas cardiomyopathy, previously asymptomatic. Full anticoagulation and heart rate control were initiated as secondary prophylaxis. Electrical cardioversion was considered after resolving contraindications. The possibility of etiological treatment for Chagas disease was discussed, which is reserved for the chronic indeterminate form in adults under 50 years old. Identifying stroke etiology and understanding the involved pathophysiology, especially in rare presentations, is crucial for establishing secondary prophylaxis and treating the underlying disease. Advanced vessel imaging studies were particularly useful for understanding the pathophysiological and anatomical mechanisms.