ArticleJournal of atherosclerosis and thrombosis2022
A Resuscitated Case of Acute Myocardial Infarction with both Familial Hypercholesterolemia Phenotype Caused by Possibly Oligogenic Variants of the PCSK9 and ABCG5 Genes and Type I CD36 Deficiency.
Article in Journal of atherosclerosis and thrombosis, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 8 citations in OpenAlex.
- Association of PCSK9 inhibitors versus statins with cancer incidence: a target trial emulation.Cardio-oncology (London, England) · 2026Article
- Prognostic Value of the Selected Polymorphisms in theBiomedicines · 2023Article
- Review
- Genetic Heterogeneity of Familial Hypercholesterolemia: Repercussions for Molecular Diagnosis.International journal of molecular sciences · 2023Review
- Acute Coronary Syndrome Developed in a 17-year-old Boy with Sitosterolemia Comorbid with Takayasu Arteritis: A Rare Case Report and Review of the Literature.Internal medicine (Tokyo, Japan) · 2022Review
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A 56-year-old postmenopausal woman with out-of-hospital cardiac arrest caused by acute myocardial infraction was successfully resuscitated by intensive treatments and recovered without any neurological disability. She was diagnosed as having familial hypercholesterolemia (FH) based on a markedly elevated low-density lipoprotein cholesterol (LDL-C) level and family history of premature coronary artery disease. Genetic testing in her family members showed that a variant of the proprotein convertase subtilisin/kexin type 9 (PCSK9) gene (c.2004C＞A, p.S668R), which had been previously reported as having uncertain significance, was associated with FH, indicating that the variant is a potential candidate for the FH phenotype. Next-generation sequencing analysis for the proband also showed that there was a heterozygous mutation of the ATP-binding cassette sub-family G member 5 ( ABCG5) gene (c.1166G＞A, R389H), which has been reported to increase LDL-C level and the risk of cardiovascular disease. She was also diagnosed as having type 1 CD36 deficiency based on a lack of myocardial uptake of
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