ILG Assay Associates Lower CEC With OCT-Confirmed Large Lipid-Rich Plaques in 61-Patient Cohort
A Japanese single-center study of 61 catheterized patients found that a simplified ILG assay for cholesterol efflux capacity identified lower values in those with OCT-defined high-risk plaques. The observational design supports feasibility but cannot establish prediction or causality. Larger longitudinal cohorts are needed before clinical integration.
Researchers at Science Tokyo applied the ILG method to quantify CEC in patients referred for invasive angiography. They paired these values with high-resolution OCT imaging to classify plaque morphology. Patients harboring large lipid-rich plaques displayed markedly reduced CEC compared with those lacking such features. The assay also correlated higher CEC with HDL particles enriched in apolipoprotein E, suggesting a functional subtype distinction not captured by standard HDL-cholesterol assays. The n=61 cross-sectional design precludes causal inference yet aligns with prior observational cohorts linking impaired CEC to incident cardiovascular events. Traditional HDL-C measurements have repeatedly failed to improve risk stratification in large trials, underscoring the need for functional readouts. The ILG platform reduces technical barriers that previously confined CEC testing to specialized laboratories, potentially enabling broader clinical adoption. Key gaps remain: no longitudinal outcome data, single-center recruitment, and absence of adjustment for statin intensity or acute-phase inflammation. A multicenter prospective cohort with serial OCT and hard endpoints is required to test whether ILG-CEC adds incremental prognostic value beyond existing scores. Regulatory clearance would further depend on standardized reference ranges and reproducibility across ethnic groups.
Ohkawa et al.: A 500-patient prospective cohort will show ILG-CEC below the cohort median associates with 3-year MACE HR greater than 1.4 after multivariable adjustment.
Sources (2)
- [1]Primary Source(https://www.atherosclerosis-journal.com/article/S0021-9150(26)00123-4/fulltext)
- [2]Supporting Source(https://pubmed.ncbi.nlm.nih.gov/28917675)