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.

BACKGROUND

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.

CASE SUMMARY: 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 LCBI4mm 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.

DISCUSSION: 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.