Characterization of residual lipid-rich plaques despite achieving LDL-C <1.8mmol/l with a statin in patients with coronary artery disease: insights from the REASSURE-NIRS registry

Abstract

Abstract Introduction Recent studies have demonstrated favourable modification of lipidic plaque materials under achieving LDL-C <1.8mmol/l with a statin, which potentially accounts for its clinical benefit. However, coronary events still occur even under optimal LDL-C management. This may suggest the presence of residual lipid-rich coronary plaque despite on-treatment LDL-C <1.8mmol/l. Given that near-infrared spectroscopy (NIRS) enables quantitative evaluation of lipidic plaque in vivo, we employed this imaging modality to investigate characteristics and drivers of residual lipid-rich plaques in statin-treated patients with coronary artery disease (CAD) who achieved LDL-C <1.8mmol/l. Purpose To clarify the frequency, clinical demographics and factors associated with residual lipid-rich plaques under LDL-C <1.8mmol/l. Methods The REASSURE-NIRS registry is an on-going multi-center registry to enroll CAD subjects receiving NIRS/intravascular ultrasound-guided PCI. The current analysis included 133 statin-treated stable CAD patients with on-treatment LDL-C <1.8mmol/l from August 2015 to December 2020. The maximum 4-mm lipid core burden index (maxLCBI4mm) at culprit lesions was measured by NIRS imaging prior to PCI. Clinical characteristics were compared in patients with and without maxLCBI4mm ≥400 at culprit lesions. Results In the current study, 45% (=58/128) of study subjects exhibited maxLCBI4mm ≥400 at culprit lesions under on-treatment LDL-C <1.8 mmol/l. They were more likely to be female, whereas there were no differences in age and the frequency of risk factors. Most of study subjects received moderate to high-intensity statin (p=0.79), and over one-fourth of them were treated with ezetimibe (p=0.56). Under these lipid-lowering therapies, LDL-C level was significantly higher in patients with maxLCBI4mm ≥400 (Table). Additionally, a lower frequency of LDL-C <1.4mmol/l was observed in those exhibiting maxLCBI4mm ≥400 (31.0 vs. 45.7%), but this comparison failed to meet statistical significance (p=0.09). Despite LDL-C control with a statin, deterioration of coronary flow after PCI with stent implantation more frequently occurred in patients with maxLCBI4mm ≥400 (Table). Multivariate analysis demonstrated that an independent factor associated with maxLCBI4mm ≥400 was LDL-C level (OR=1.05; 95% CI=1.00–1.10, p=0.03), but not other lipid and clinical parameters. Conclusion Almost half of CAD subjects who achieved LDL-C level <1.8mmol/l still exhibited the accumulation of lipidic plaque materials within vessel wall. Given that LDL-C level was associated with this residual lipid-rich plaque features, our findings support current ESC-guideline recommended LDL-C goal (<1.4mmol/l) to optimize the secondary prevention in stable CAD patients. Funding Acknowledgement Type of funding sources: None.