| Literature DB >> 31762833 |
Kota Motozato1, Daisuke Sueta1, Kenji Sakamoto1, Suguru Nagamatsu1, Takayoshi Yamashita1, Ryota Sato1, Tatsuro Mitsuse1, Yusuke Kanemaru1, Kyoji Takaoka2, Koichiro Fujisue1, Seiji Takashio1, Yuichiro Arima1, Eiichiro Yamamoto1, Koichi Kaikita1, Kenichi Tsujita1.
Abstract
The low-density lipoprotein-cholesterol (LDL-C) level of a 60-year-old woman diagnosed with acute coronary syndrome (ACS) was 212 mg/dL. She was suspected of having familial hypercholesterolemia, therefore, administration of a proprotein convertase subtilisin-kexin type 9 (PCSK9) antibody in addition to atorvastatin plus ezetimibe was initiated, reducing her LDL-C level to 42 mg/dL. Nine months after initial ACS, the PCSK9 antibody was discontinued. Six months after the iturruption, she relapsed with ACS, and neoatherosclerosis progression was confirmed via intravascular ultrasound. Then, the PCSK9 antibody was reintroduced. Disruption of a PCSK9 may be associated with the progression and destabilization of neoatherosclerosis. <Learning objective: Administration of a proprotein convertase subtilisin-kexin type 9 (PCSK9) antibody in addition to statin decreases low-density lipoprotein-cholesterol level and is effective in suppressing cardiovascular events, the effect on neoatherosclerosis after coronary artery stent deployment is not clear. We experienced an interesting reccurent ACS case with familial hypercholesterolemia, and reported the possibility that PCSK9 antibody disruption might contribute to destabilization of neoatherosclerosis after coronary stenting utilizing intravascular ultrasound.>.Entities:
Keywords: Lipid management; Neoatherosclerosis; PCSK9 antibody
Year: 2019 PMID: 31762833 PMCID: PMC6859554 DOI: 10.1016/j.jccase.2019.08.007
Source DB: PubMed Journal: J Cardiol Cases ISSN: 1878-5409