Abstract Background and purpose In acute coronary syndrome (ACS) patients, major cardiovascular events during follow-up were equally attributable to recurrence at the site of culprit lesions and to non-culprit lesions, and mostly occurred within one year. Recent studies showed that Proprotein convertase subtilisin kexin type 9 (PCSK9) inhibitor significantly reduces the risk of cardiovascular events. However, the rigorous effects of PCSK9 inhibitor in patients with ACS, especially for the stabilization of plaque in the non-culprit lesions has not been identified. The purpose of this study was to evaluate the efficacy of a PCSK9 inhibitor for the plaque stabilization in the non-culprit lesion of ACS patients. Methods We retrospectively analyzed the 10 ACS patients (STEMI:5 cases, NSTEMI:1 case, and UAP:4 cases) who had non-culprit lesions and were injected with a PCSK9 inhibitor. We analyzed 11 non-culprit lesions before and after PSCK9 injections by using a near-infrared intravascular ultrasonography (NIRS-IVUS). Results The follow up intervals were 229.4±82.9 days. Major cardiovascular events did not occur in all patients. The serum low-density lipoprotein (LDL) cholesterol levels were significantly decreased form 128±36.7 mg/dl to 26.7±7.4 mg/dl (P<0.01; Figure 1A). There were no significant changes in percent atheroma volume before and after PCSK9 injections. However, the max lipid core burden index (LCBI) were significantly improved from 392.5±155.8 to 209.4±116 (P<0.01; Figure 1B). Although the lesion characteristics did not change in the images, by IVUS, the LCBI of the lesion was significantly decreased after PCSK9 injections. This study suggested that NIRS-IVUS had the possibility of detection for the slight changes in the plaque characteristics, which could not be detected by only an IVUS. Conclusion This study suggested that the plaque morphology can be altered by the aggressive lipid lowering therapy by using a PCSK9 inhibitor, and NIRS-IVUS can detect these plaque stabilizations of non-culprit lesion in ACS patients. The authors have no financial conflicts of interest to disclose concerning the presentation. Figure 1 Funding Acknowledgement Type of funding source: None