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Intern Med. 2018;57(24):3551-3557. doi: 10.2169/internalmedicine.1060-18. Epub 2018 Dec 15.

Coronary Artery Plaque Regression by a PCSK9 Antibody and Rosuvastatin in Double-heterozygous Familial Hypercholesterolemia with an LDL Receptor Mutation and a PCSK9 V4I Mutation.

Author information

1
Department of Cardiovascular Medicine, Arao City Hospital, Japan.
2
Department of Cardiovascular Medicine, Graduate School of Medical Sciences, Kumamoto University, Japan.
3
Department of Molecular Innovation in Lipidology, National Cerebral and Cardiovascular Center Research Institute, Japan.
4
National Cerebral and Cardiovascular Center, Japan.

Abstract

The low-density lipoprotein-cholesterol (LDL-C) level of a 38-year-old man diagnosed with acute coronary syndrome was 257 mg/dL. The administration of a proprotein convertase subtilisin-kexin type 9 (PCSK9) antibody in addition to rosuvastatin plus ezetimibe was initiated, reducing his LDL-C level to 37 mg/dL. A genetic analysis revealed both an LDL receptor (LDLR) mutation and a PCSK9 V4I mutation. Nine months after revascularization, intravascular ultrasound revealed plaque regression in the coronary arteries. LDLR/PCSK9 mutation carriers are prone to coronary artery disease. Intensive LDL-C lowering by including PCSK9 antibody was associated with coronary plaque regression, suggesting the expectation of prognosis improvement.

KEYWORDS:

Double-heterozygous familial hypercholesterolemia; PCSK9 inhibitor; plaque regression

PMID:
30555118
PMCID:
PMC6355420
DOI:
10.2169/internalmedicine.1060-18
[Indexed for MEDLINE]
Free PMC Article

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