Stepwise regression of non-culprit lipid-rich plaque observed using serial near-infrared spectroscopy–intravascular ultrasound and optical coherence tomographic measurements after aggressive cholesterol-lowering treatment: a case report

Lipid-rich plaques (LRP) in the non-culprit lesions (NCL) in patients with the acute coronary syndrome may trigger lesion-related, adverse cardiovascular events. Aggressive lipid-lowering therapy may stabilize LRP; however, the times of stabilization remain undefined.

A 60-year-old man presented with unstable angina. Coronary angiography revealed a severely stenotic lesion (culprit lesion) in the left descending artery, and another non-obstructive lesion in the distal left main trunk artery. Near-infrared spectroscopy (NIRS) imaging showed LRP with a maximum lipid core burden index (LCBI)_4mm of 422. Optical coherence tomographic (OCT) imaging showed the vulnerable plaque as a thin cap fibroatheroma with a thickness of 50 µm. We prescribed aggressive lipid-lowering treatment with a proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitor, and serially observed this lesion for 24 months. The NIRS imaging showed that the LCBI gradually decreased over time (max LCBI_4mm of 422, 417, 318, 265, and 106 conducted at index percutaneous coronary intervention, 3, 8, 12, and 24 months, respectively). As plaque regression and stabilization of high-risk LRP were observed, we promptly discontinued treatment with the PCSK9i inhibitor.

During the long-term, 24-month, follow-up using serial NIRS–IVUS imaging, we observed the gradual decrease in LCBI over time, due to aggressive lipid-lowering therapy. Compared with the lowering of low-density lipoprotein cholesterol, the stabilization of vulnerable plaques may require longer times of about 2 years. Evaluation of NCL-related adverse cardiac events by serial intravascular imaging over time, using NIRS–IVUS or OCT, may be warranted in such cases.