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Lipoprotein(a) and coronary inflammation: Joint predictors of residual risk in post-percutaneous coronary intervention coronary artery disease.

June 6, 2026pubmed logopapers

Authors

Ye Z,Liu C,Xie E,Song C,Zhang R,Wang HY,Shi S,Zhao Z,Dou K

Affiliations (4)

  • Department of Cardiology, Fuwai Hospital, National Center for Cardiovascular Diseases, National Clinical Research Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China (Ye, Xie, Song, Zhang, Wang, Shi, Zhao, and Dou); State Key Laboratory of Cardiovascular Disease, Beijing, China (Ye, Xie, Song, Zhang, Wang, Shi, Zhao, and Dou); Cardiometabolic Medicine Center, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China (Ye, Xie, Song, Zhang, Wang, Shi, Zhao, and Dou).
  • Department of Radiology, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China (Liu).
  • Department of Cardiology, Fuwai Hospital, National Center for Cardiovascular Diseases, National Clinical Research Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China (Ye, Xie, Song, Zhang, Wang, Shi, Zhao, and Dou); State Key Laboratory of Cardiovascular Disease, Beijing, China (Ye, Xie, Song, Zhang, Wang, Shi, Zhao, and Dou); Cardiometabolic Medicine Center, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China (Ye, Xie, Song, Zhang, Wang, Shi, Zhao, and Dou). Electronic address: [email protected].
  • Department of Cardiology, Fuwai Hospital, National Center for Cardiovascular Diseases, National Clinical Research Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China (Ye, Xie, Song, Zhang, Wang, Shi, Zhao, and Dou); State Key Laboratory of Cardiovascular Disease, Beijing, China (Ye, Xie, Song, Zhang, Wang, Shi, Zhao, and Dou); Cardiometabolic Medicine Center, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China (Ye, Xie, Song, Zhang, Wang, Shi, Zhao, and Dou). Electronic address: [email protected].

Abstract

The interaction of elevated lipoprotein(a) [Lp(a)] with local coronary inflammation remains unclear. We investigated whether pericoronary inflammation modulates Lp(a)'s prognostic impact on major adverse cardiovascular events (MACE) after percutaneous coronary intervention (PCI). Patients with coronary artery disease undergoing PCI were included with coronary computed tomography angiography within 3 months before coronary angiography. Pericoronary fat attenuation index (FAI) was quantified for pericoronary inflammation evaluation. Four machine learning models with SHapley Additive exPlanations (SHAP) ranked FAI features. Lp(a) was categorized using a 30 mg/dL cut-off per Chinese lipid guidelines. Associations with MACE (all-cause mortality, nonfatal myocardial infarction, unplanned revascularization, and stroke) were assessed via multivariable Cox regression, restricted cubic splines (RCS), and subgroups. Over a median 3-year follow-up, 181 (9.0%) patients experienced MACE. High Lp(a) and elevated FAI independently predicted MACE (hazard ratio [HR] 1.29, 95% CI 1.05-1.76 for high Lp(a); HR 2.06, 95% CI 1.51-2.81 for high FAI-Left anterior descending artery [LAD]). Extreme gradient boosting (area under the curve [AUC] 0.936) ranked FAI-LAD highest (SHAP 1.57). RCS revealed nonlinear associations, with MACE risk escalating sharply above FAI-LAD -77.00 HU. High Lp(a) markedly increased MACE risk in the high FAI-LAD group (HR 2.69, 95% CI 1.75-4.10) but the risk increase was attenuated in the low-FAI-LAD group (HR 1.10, 95% CI 0.65-1.87). Combining Lp(a) and FAI-LAD improved prognostic accuracy (AUC 0.713) over conventional risk factors (AUC 0.599) or either alone (DeLong P < .05). Subgroup analyses showed interactions with age and diabetes (P < .05). Lp(a) elevates post-PCI risk mainly in high pericoronary inflammation settings. Integrating Lp(a) and FAI refines risk stratification, supporting targeted Lp(a)-lowering in inflamed subgroups.

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