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Reversible left ventricular noncompaction caused by hypertensive hydrocephalus: a pediatric case report

BACKGROUND: Left ventricular noncompaction cardiomyopathy (LVNC) is characterized by prominent ventricular trabeculations on cardiovascular imaging. Acquired reversible LVNC has not been reported in pediatrics without a genetic background. CASE PRESENTATION: A 9-year-old girl with a ventriculoperito...

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Detalles Bibliográficos
Autores principales: Kato, Riko, Taneichi, Hiromichi, Takarada, Shinya, Okabe, Mako, Miyao, Nariaki, Nakaoka, Hideyuki, Ibuki, Keijiro, Ozawa, Sayaka, Adachi, Yuichi, Yoshimura, Naoki, Saito, Kazuyoshi, Ichida, Fukiko, Hirono, Keiichi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8080348/
https://www.ncbi.nlm.nih.gov/pubmed/33910553
http://dx.doi.org/10.1186/s12887-021-02680-6
Descripción
Sumario:BACKGROUND: Left ventricular noncompaction cardiomyopathy (LVNC) is characterized by prominent ventricular trabeculations on cardiovascular imaging. Acquired reversible LVNC has not been reported in pediatrics without a genetic background. CASE PRESENTATION: A 9-year-old girl with a ventriculoperitoneal (VP) shunt for neonatal posthemorrhagic hydrocephalus was referred due to exacerbation of hydrocephalus caused by VP shunt dysfunction. Transthoracic echocardiography (TTE) revealed depressed left ventricular (LV) systolic function and thick prominent trabeculae in the LV, predominantly in the apex, suggesting LVNC. Following treatment with extraventricular drainage for hydrocephalus, prominent trabeculation of the LV was diminished on TTE within 3 months. Genetic testing using next-generation sequencing was performed, and no significant variants were identified. CONCLUSIONS: We revealed for the first time a pediatric case of reversible LVNC without genetic predisposition. This case report provides valuable information on the pathogenesis of acquired LVNC and suggests that detailed evaluation is required to elucidate the diagnosis of this wide spectrum of etiologic–pathogenetic disorders. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12887-021-02680-6.