4.2 Article

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

Journal

INTERNAL MEDICINE
Volume 57, Issue 24, Pages 3551-3557

Publisher

JAPAN SOC INTERNAL MEDICINE
DOI: 10.2169/internalmedicine.1060-18

Keywords

Double-heterozygous familial hypercholesterolemia; PCSK9 inhibitor; plaque regression

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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/PCSK 9 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.

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