Statin-dependent coupling between circulating atherogenic lipoproteins and lesion-level plaque lipid burden assessed
Soojung Park1, Woohyeun Kim1, Hyungdon Kook1
1Division of Cardiology, Department of Internal medicine, College of Medicine, Hanyang University, Seoul, Republic of Korea.
Background:
The relationship between circulating lipid profiles and lesion-level plaque lipid burden in humans remains incompletely defined.
Objective:
We investigated the association between lipid profiles and plaque lipid burden assessed by near-infrared spectroscopy intravascular ultrasound (NIRS-IVUS), with stratification according to statin exposure.
Methods:
We analyzed 410 patients undergoing NIRS-IVUS-guided percutaneous coronary intervention. Associations between lipid profiles (total cholesterol, low-density lipoprotein cholesterol [LDL-C], non-high-density lipoprotein cholesterol [non-HDL-C], and triglycerides) and lesion-level plaque lipid burden, quantified by the maximum lipid core burden index within 4 mm (maxLCBI4 mm), were assessed using correlation analyses, multivariable linear regression, and logistic regression for lipid-rich plaque (defined as maxLCBI4 mm ≥324.7).
Results:
Circulating atherogenic lipoproteins, including LDL-C and non-HDL-C, were associated with plaque lipid burden in the overall cohort, with more pronounced and independent associations observed in statin-naïve patients (eg, LDL-C: β = 2.02 [1.24-2.81]). These lipid parameters were also independent predictors of lipid-rich plaque in statin-naïve individuals (eg, LDL-C per 10 mg/dL: odds ratio = 1.28 [1.15-1.42]). In contrast, no significant associations were observed in statin-treated patients.
Conclusion:
In statin-naïve patients, circulating atherogenic lipoproteins are associated with lesion-level plaque lipid burden, supporting a direct biological link between circulating lipid levels and local plaque lipid characteristics. This coupling is attenuated following statin exposure, suggesting that pharmacologic lipid lowering modifies the relationship between circulating lipid levels and plaque lipid biology.
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