ArticleThe American journal of case reports2021
Left Ventricular Noncompaction Cardiomyopathy as a Potential Cause of Bilateral Posterior Cerebral Artery Stroke - a Rare and Unique Clinical Occurrence.
Article in The American journal of case reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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2 citing papers in PubMed, 3 citations in OpenAlex.
- Left Ventricular Noncompaction Cardiomyopathy in an Elderly Patient: A Case Report and Literature Review.Cureus · 2023Article
- Simultaneous acute cardio-cerebral infarction associated with isolated left ventricle non-compaction cardiomyopathy.Annals of medicine and surgery (2012) · 2022Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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