論文ID: CJ-18-0983
A 70-year-old woman with hypertension and dyslipidemia underwent drug-eluting stent implantation in the mid-left anterior descending artery (LAD) due to acute coronary syndrome (ACS). Optical coherence tomography (OCT) during the index procedure showed lipid-rich plaque in non-culprit lesions of the proximal LAD and mid-right coronary artery (Figure B,E). Near-infrared spectroscopy-intravascular ultrasound (NIRS-IVUS) showed plaque with high lipid burden in both sites (Figure C,F). Intensive lipid-lowering therapy with combined strong statin and proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitor was started after the index procedure. Scheduled 10-month follow-up OCT and NIRS-IVUS showed increase in minimum fibrous cap thickness and decrease in lipid arc and maximum lipid core burden index at 4 mm (max LCBI4 mm) at both sites (Figure B’,C’,E’,F’).
(A) Coronary angiography after drug-eluting stent implantation showed intermediate stenosis in the proximal left anterior descending coronary artery (LAD; white arrow). (B) Optical coherence tomography (OCT; ILUMIEN OPTIS, St. Jude Medical, St. Paul, MN, USA) showed lipid rich plaque (minimum fibrous cap thickness, 80 μm; lipid arc, 152°) at the site. (C) Near-infrared spectroscopy-intravascular ultrasound (NIRS-IVUS; TVC Imaging System, Infraredx, Burlington, MA, USA) and chemogram showed plaque with high lipid burden (max lipid core burden index at 4 mm [max LCBI4 mm], 336) at the same site. We selected the coronary plaques that had the highest max LCBI4 mm in each coronary vessel at index procedure as the analyzed legion in a prospective manner, according to a previous report.1 Intensive lipid-lowering therapy with combined rosuvastatin (10 mg/day) and evolocumab (140 mg every 2 weeks) was started after the index procedure. Low-density lipoprotein cholesterol fell from 121 to 60 mg/dL, and was maintained at <70 mg/dL after that. (A’) Scheduled 10-month follow-up angiography showed no in-stent restenosis and no progression of angiographic lesion severity in the proximal LAD (white arrow). (B’) OCT and (C’) NIRS-IVUS showed increase in minimum fibrous cap thickness (from 80 to 130 μm) and decrease in lipid arc (152 to 124°) and in maxLCBI4 mm (from 336 to 59). (D) Coronary angiography showed intermediate stenosis in the mid-right coronary artery (RCA; white arrow). (E) OCT showed lipid-rich plaque (minimum fibrous cap thickness, 60 μm; lipid arc, 169°) with macrophage accumulations at the site. (F) NIRS-IVUS and chemogram showed plaque with high lipid burden (maxLCBI4 mm, 415) at the same site. (D’) Scheduled 10-month follow-up angiography showed no progression of the lesion severity in the mid-RCA (white arrow). (E’) OCT and (F’) NIRS-IVUS showed increase in minimum fibrous cap thickness (from 60 to 160 μm) and decrease in lipid arc (from 169 to 126°), macrophage accumulation, and in maxLCBI4 mm (from 415 to 173).
Lipid-rich plaque assessed on OCT and IVUS is a high risk for ACS.1 High low-density lipoprotein cholesterol (LDL-C) is one of the most important therapeutic targets for the stabilization of high-risk plaque. PCSK9 inhibitors dramatically decrease LDL-C, and prevent progression of atherosclerosis and atherosclerotic cardiovascular events in patients with coronary artery disease. Intensive lipid-lowering therapy with combined strong statin and PCSK9 inhibitor may have the potential for stabilization of high-risk plaque on OCT and NIRS-IVUS.
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T.K. has received lecture fees from Abbott Vascular. T.A. has received lecture fees from Abbott Vascular and research grants from Abbott Vascular and Nipro. The other authors declare no conflicts of interest.