Volume 106, Issue 1 pp. 633-643
ORIGINAL ARTICLE - CLINICAL SCIENCE

The Effect of Lipoprotein(a) Levels on Non-Culprit Atherosclerosis in Patients With Acute Coronary Syndrome Who Underwent Percutaneous Coronary Intervention: An Optical Coherence Tomography Study

Yi-fei Wang

Yi-fei Wang

Department of Cardiology, Nanjing First Hospital, Nanjing Medical University, Nanjing, China

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Tian Xu

Tian Xu

Department of Cardiology, Nanjing First Hospital, Nanjing Medical University, Nanjing, China

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Wei You

Wei You

Department of Cardiology, Nanjing First Hospital, Nanjing Medical University, Nanjing, China

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Jia-cong Nong

Jia-cong Nong

Department of Cardiology, The First Affiliated Hospital of Guangxi Medical University, Nanning, China

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Pei-na Meng

Pei-na Meng

Department of Cardiology, Nanjing First Hospital, Nanjing Medical University, Nanjing, China

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Xiang-qi Wu

Xiang-qi Wu

Department of Cardiology, Nanjing First Hospital, Nanjing Medical University, Nanjing, China

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Zhi-ming Wu

Zhi-ming Wu

Department of Cardiology, Nanjing First Hospital, Nanjing Medical University, Nanjing, China

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Feng-Wang

Corresponding Author

Feng-Wang

Department of Nuclear Medicine, Nanjing First Hospital, Nanjing Medical University, Nanjing, China

Correspondence: Feng-Wang ([email protected])

Fei Ye ([email protected])

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Fei Ye

Corresponding Author

Fei Ye

Department of Cardiology, Nanjing First Hospital, Nanjing Medical University, Nanjing, China

Correspondence: Feng-Wang ([email protected])

Fei Ye ([email protected])

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First published: 19 May 2025

Yi-fei Wang, Tian Xu, and Wei You are contributed equally to this study.

ABSTRACT

Background

The association between lipoprotein(a) [Lp(a)] levels and progression of non-culprit atherosclerosis (NSA) in patients with acute coronary syndrome (ACS) who underwent percutaneous coronary intervention (PCI) is unknown.

Methods

This study enrolled 177 patients with ACS who underwent OCT-guided PCI and follow-up OCT examinations of non-culprit lesions between 2013 and 2018. Lesion characteristics including fibrous tissue, calcium, lipid, and macrophage content were assessed using quantitative plaque analysis. High Lp(a) levels were defined as Lp(a) ≥ 30 mg/dL. The association between Lp(a) levels and NSA progression was investigated using linear effect models adjusted for clinical risk factors. A discordance analysis was also performed.

Results

At 1-year follow-up, individuals with Lp(a) levels ≥ 30 mg/dL had increased total atheroma volume and lipid component, and higher incidence of thin-cap fibroatheroma (TCFA) (p = 0.021; p = 0.006; p = 0.025, respectively). After adjusted, multivariable linear regression model revealed an association between Lp(a) and plaque progression in NSA (7.22 for each 1 SD increase, 95% CI: 0.96–13.48; p = 0.025) and increased lipid component (3.60 for each 1 SD increase, 95% CI: 0.63–6.56; p = 0.019). Discordance analyses showed that individuals with discordantly low Lp(a) levels had the lightest plaque progression and increase in lipid plaque burden (17.34 [10.22, 28.21] vs. 28.73 [14.88, 45.88] versus 25.73 [13.85, 45.70], p = 0.017).

Conclusion

Among patients with ACS, elevated Lp(a) levels were related to the progression of coronary plaques in non-culprit lesions, including increased total atheroma volume and lipid component, and a higher prevalence of TCFA at follow-up.

Conflicts of Interest

The authors declare no conflicts of interest.

Data Availability Statement

The data that support the findings of this study are available from the corresponding author upon reasonable request.

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