Coronary Artery Plaque Regression by a PCSK9 Antibody and Rosuvastatin in Double-heterozygous Familial Hypercholesterolemia with an <i>LDL Receptor</i> Mutation and a <i>PCSK9</i> V4I Mutation
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- Shirahama Ryo
- Department of Cardiovascular Medicine, Arao City Hospital, Japan
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- Ono Takamichi
- Department of Cardiovascular Medicine, Arao City Hospital, Japan
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- Nagamatsu Suguru
- Department of Cardiovascular Medicine, Graduate School of Medical Sciences, Kumamoto University, Japan
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- Sueta Daisuke
- Department of Cardiovascular Medicine, Graduate School of Medical Sciences, Kumamoto University, Japan
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- Takashio Seiji
- Department of Cardiovascular Medicine, Graduate School of Medical Sciences, Kumamoto University, Japan
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- Chitose Tadasuke
- Department of Cardiovascular Medicine, Arao City Hospital, Japan
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- Fujisue Koichiro
- Department of Cardiovascular Medicine, Graduate School of Medical Sciences, Kumamoto University, Japan
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- Sakamoto Kenji
- Department of Cardiovascular Medicine, Graduate School of Medical Sciences, Kumamoto University, Japan
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- Yamamoto Eiichiro
- Department of Cardiovascular Medicine, Graduate School of Medical Sciences, Kumamoto University, Japan
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- Izumiya Yasuhiro
- Department of Cardiovascular Medicine, Graduate School of Medical Sciences, Kumamoto University, Japan
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- Kaikita Koichi
- Department of Cardiovascular Medicine, Graduate School of Medical Sciences, Kumamoto University, Japan
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- Hokimoto Seiji
- Department of Cardiovascular Medicine, Graduate School of Medical Sciences, Kumamoto University, Japan
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- Hori Mika
- Department of Molecular Innovation in Lipidology, National Cerebral and Cardiovascular Center Research Institute, Japan
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- Harada-Shiba Mariko
- Department of Molecular Innovation in Lipidology, National Cerebral and Cardiovascular Center Research Institute, Japan
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- Kajiwara Ichiro
- Department of Cardiovascular Medicine, Arao City Hospital, Japan
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- Ogawa Hisao
- National Cerebral and Cardiovascular Center, Japan
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- Tsujita Kenichi
- Department of Cardiovascular Medicine, Graduate School of Medical Sciences, Kumamoto University, Japan
抄録
<p>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. </p>
収録刊行物
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- Internal Medicine
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Internal Medicine 57 (24), 3551-3557, 2018-12-15
一般社団法人 日本内科学会
