Mechanisms
Lp(a) above 18.8 mg/dL independently predicts coronary plaque vulnerability on IVUS, 292-patient study (J Atheroscler Thromb 2026)
Original title: Lipoprotein(a) Is Associated with Coronary Plaque Vulnerability and Compensatory Vascular Enlargement: An Intravascular Ultrasound Study
Retrospective intravascular ultrasound (IVUS) study of 292 patients with coronary artery disease, comparing vulnerable (n=83) and stable (n=209) plaque groups. Median Lp(a) was higher in vulnerable plaques (14.56 vs 11.04 mg/dL, p=0.011), and Lp(a) above 18.8 mg/dL remained an independent predictor of plaque vulnerability after adjustment for age, sex, LDL-C, smoking, diabetes and hypertension (OR 1.76, 95% CI 1.00-3.07, p=0.049); LDL-C itself did not predict vulnerability. The high-Lp(a) group also had larger vessel area (EEM CSA 14.67±4.95 vs 13.22±4.20 mm2, p=0.016) and plaque area (11.07±4.61 vs 9.71±3.79 mm2, p=0.015), consistent with compensatory vascular enlargement. The authors argue this supports Lp(a) screening even when LDL-C is well controlled.
Original abstract
Aims: Lipoprotein(a) [Lp(a)] has emerged as a critical determinant of residual cardiovascular risk. However, its impact on plaque morphology remains underinvestigated. This study aimed to elucidate the relationship between the serum Lp(a) levels, coronary plaque vulnerability, and vascular remodeling characteristics by utilizing intravascular ultrasound (IVUS).
Methods: We retrospectively enrolled 292 consecutive patients with coronary artery disease who underwent IVUS. Target lesions were classified into vulnerable (n = 83) or stable (n = 209) plaque groups based on the IVUS criteria. Multivariate binary logistic regression was performed to identify independent predictors. The morphological parameters were further compared between the high (＞18.8 mg/dL) and low (≤ 18.8 mg/dL) Lp(a) groups.
Results: The vulnerable plaque group exhibited significantly higher median serum Lp(a) levels than the stable group (14.56 vs. 11.04 mg/dL, P = 0.011). After adjusting for age, sex, LDL-C, smoking, diabetes, and hypertension, Lp(a) ＞18.8 mg/dL remained an independent predictor of plaque vulnerability (OR = 1.76; 95% CI: 1.00-3.07; P = 0.049). Notably, the LDL-C levels did not predict vulnerability in this cohort. Furthermore, the high Lp(a) group demonstrated significantly larger vascular dimensions (EEM CSA: 14.67±4.95 vs. 13.22±4.20 mm2, P = 0.016) and plaque area (11.07±4.61 vs. 9.71±3.79 mm2, P = 0.015) than the low Lp(a) group, consistent with compensatory vascular enlargement, although the difference in the remodeling index did not reach statistical significance.
Conclusion: Elevated serum Lp(a) levels are independent predictors of coronary plaque vulnerability. The underlying mechanism involves Lp(a) promoting compensatory vascular enlargement, accompanied by an increased plaque volume. These findings underscore the necessity of Lp(a) screening to identify any residual risk, particularly in patients with effectively controlled low-density lipoprotein cholesterol (LDL-C).
Summary written by lp-a.org from the published abstract; figures as published. Page updated 17 August 2026. Methods.