論文ID: CJ-25-0451
A 57-year-old man presented with acute anterior myocardial infarction. After percutaneous coronary intervention (PCI) for the left anterior descending artery, he was started on rosuvastatin (10 mg) and ezetimibe (10 mg) because his low-density lipoprotein cholesterol (LDL-C) level was 180 mg/dL (Figure A). Two months later, PCI was repeated to address residual lesions of the left circumflex artery (LCX) (Figure B). Optical coherence tomography (OCT) revealed a thin-cap fibroatheroma in the mid-LCX (Figure C). Given his persistently high level of LDL-C (100 mg/dL), alirocumab (75 mg bi-weekly) was added, reducing the LDL-C to between 8 and 42 mg/dL. After 12 months, OCT showed increased fibrous cap thickness and decreased lipid arc (Figure D), but the patient requested alirocumab be discontinued after 13 months of treatment. His LDL-C level gradually increased, leading to rosuvastatin titration to 20 mg, stabilizing LDL-C around 100 mg/dL. OCT performed 4 years later, showed complete change to fibrous plaque (Figure E).
Low-density lipoprotein cholesterol (LDL-C) and plaque regression. (A) LDL-C levels and treatments. (B) Left circumflex artery (LCX) after stenting (line). (C–E) (Top) Magnified mid-LCX (inset in B). (Bottom) Optical coherence tomography of intermediate stenosis (arrowheads), at baseline (C), 1 year (D), and 4 years (E). Dashed circle, lipid arc; arrows, minimum fibrous cap thickness.
Intensive LDL-C lowering is crucial for plaque stabilization.1,2 Even transiently achieving very low LDL-C levels with statins plus alirocumab reduces the longer-term cardiovascular risk.3 Statins plus evolocumab, even for a short duration, have a mid-term benefit on plaque stabilization.4 This case suggests there is a longer-term legacy effect of transient intensive LDL-C lowering with alirocumab on plaque stabilization.
K.M. has received lecture fees from Novartis Pharma K.K. and is a member of Circulation Journal’s Editorial Team. The other authors report nothing to disclose.