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Left Ventricular Noncompaction Cardiomyopathy as a Potential Cause of Bilateral Posterior Cerebral Artery Stroke – a Rare and Unique Clinical Occurrence

Patient: Male, 63-year-old Final Diagnosis: Occurrence of bilateral PCA infarcts with LVNC cardiomyopathy Symptoms: Acute vision loss in both eyes • dysarthria Medication: — Clinical Procedure: Emergency endovascular thrombectomy Specialty: Neurology OBJECTIVE: Rare co-existence of disease or pathol...

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Detalles Bibliográficos
Autores principales: Elnazeir, Marwa, Nobel, Lisa, Narayanan, Siddharth, Darmoch, Fahed, Massari, Francesco, Fitzgibbons, Timothy, Carandang, Raphael A., Jun-O’Connell, Adalia
Formato: Online Artículo Texto
Lenguaje:English
Publicado: International Scientific Literature, Inc. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8235723/
https://www.ncbi.nlm.nih.gov/pubmed/34157014
http://dx.doi.org/10.12659/AJCR.931103
Descripción
Sumario:Patient: Male, 63-year-old Final Diagnosis: Occurrence of bilateral PCA infarcts with LVNC cardiomyopathy Symptoms: Acute vision loss in both eyes • dysarthria Medication: — Clinical Procedure: Emergency endovascular thrombectomy Specialty: Neurology OBJECTIVE: Rare co-existence of disease or pathology BACKGROUND: Bilateral posterior cerebral artery (PCA) occlusions are exceedingly rare, and are considered a devastating phenomenon that presents as cortical blindness. Predominant causes of PCA infarcts include cardiac and arterial embolisms. Left ventricular noncompaction (LVNC) cardiomyopathy is also an extremely rare cardiopathology. Several reports describe stroke as a potential manifestation of LVNC, but bilateral PCA infarcts are likely also caused by underlying LVNC cardiomyopathy, although this has not yet been reported. CASE REPORT: A 63-year-old man presented to the emergency department of an outside hospital with acute vision loss in both eyes and dysarthria. His neurological examination necessitated an emergent stroke evaluation. His electrocardiogram and telemetry at admission did not reveal arrhythmia. He underwent an emergency endovascular thrombectomy at our facility. During the post-intervention stroke workup, a transthoracic echocardiogram with contrast showed left ventricle dilation, with an ejection fraction (EF) of 29%. Subsequent cardiac magnetic resonance imaging confirmed the presence of LVNC cardiomyopathy. He was started on therapeutic anticoagulation (apixaban) and remained stable neurologically during the 3-month followup, with some residual visual field deficits. His cardiac outcome also improved (stress test was unremarkable for any cardiac ischemia, and an echocardiogram showing improved EF of 40%). CONCLUSIONS: Our report is distinct, as it presents 2 exceedingly rare events in a patient: the occurrence of simultaneous bilateral PCA infarcts and LVNC cardiomyopathy. Prompt and accurate diagnosis was pivotal to the successful management of both conditions. Prospective studies are warranted to further knowledge of LVNC pathophysiology and the occurrence of stroke in such patients so that comprehensive management plans can be devised.