A higher non‐HDL‐C/HDL‐C ratio was associated with an increased risk of progression of nonculprit coronary lesion in patients with acute coronary syndrome undergoing percutaneous coronary intervention

Abstract

AbstractBackgroundThe ratio of nonhigh‐density lipoprotein cholesterol (non‐HDL‐C) to high‐density lipoprotein cholesterol (HDL‐C) has been shown associated with various metabolic diseases and atherosclerosis in primary prevention. However, there is limited evidence on the relationship between the non‐HDL‐C/HDL‐C ratio and progression of nonculprit coronary lesion (NCCL) after percutaneous coronary intervention (PCI).HypothesisOur study aimed to investigate the potential association between the non‐HDL‐C/HDL‐C ratio and NCCL progression in patients with acute coronary syndrome (ACS) undergoing PCI.MethodsWe conducted a retrospective analysis of ACS patients who underwent coronary angiography twice at a single center from 2016 to 2022. Lipid measurements, demographic, clinical, and other laboratory data were collected from electronic medical records. NCCLs were evaluated using quantitative coronary angiography. The primary outcome was the progression of NCCL. Patients were categorized based on NCCL progression and tertiles of the non‐HDL‐C/HDL‐C ratio. Associations were analyzed using univariate and multivariate logistic regression analysis.ResultsThe study included 329 ACS patients who underwent PCI, with a median follow‐up angiography of 1.09 years. We found NCCL progression in 95 (28.9%) patients with acceptable low‐density lipoprotein cholesterol control (median: 1.81 mmol/L). Patients in the top tertile of the non‐HDL‐C/HDL‐C ratio had a higher risk of NCCL progression. After adjusting for potential confounding factors, the non‐HDL‐C/HDL‐C ratio remained a significant predictor for NCCL progression (adjusted odds ratio: 1.45; 95% confidence interval: 1.14–1.86; p < 0.05).ConclusionsThe non‐HDL‐C/HDL‐C ratio predicts NCCL progression in ACS patients following PCI, providing a valuable tool for risk assessment and enhancing secondary prevention of atherosclerotic cardiovascular disease.