ArticleFrontiers in cardiovascular medicine2025
Association between antiphospholipid antibodies, rheumatic-immune inflammation, and coronary in-stent restenosis.
Article in Frontiers in cardiovascular medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Antiphospholipid antibodies (aPL) and systemic rheumatic-immune inflammation (RII) may be associated with angiographic in-stent restenosis (ISR) after drug-eluting stent (DES) implantation. We prospectively evaluated these associations in a large Chinese cohort of DES recipients. Methods: In this prospective cohort, we enrolled 2,503 consecutive adults who received at least one new-generation DES between May 2022 and January 2024. Preprocedural blood samples were assessed for antiphospholipid antibodies (anticardiolipin IgG/IgM, anti-β2-glycoprotein I IgG/IgM, and lupus anticoagulant) and inflammatory biomarkers [RII; high-sensitivity C-reactive protein (hs-CRP), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), erythrocyte sedimentation rate (ESR), complement C3/C4, rheumatoid factor, and anti-cyclic citrullinated peptide (anti-CCP) antibodies]. At 12 months, invasive coronary angiography or coronary CT angiography (CCTA) was used to assess ISR. All ISR analyses were restricted to participants who completed 12-month imaging (the imaging-complete cohort). Multivariable logistic regression adjusted for prespecified clinical/lesion/stent covariates and imaging modality. Model performance was compared for a Clinical model vs. an immune-enhanced model (clinical + aPL + IL-6) with internal bootstrap validation. ICA-only analyses were prespecified. Clinically driven target-lesion revascularization (TLR) was evaluated with Cox models in all enrolled patients. Results: Of the 2,503 enrolled participants, 2,388 completed 12-month imaging, with ISR occurring in 193 participants (8.1%; 95% CI 6.9-9.1). In adjusted analyses, any aPL positivity (OR 1.92, 95% CI 1.34-2.74) and IL-6 (per doubling) (OR 1.25, 95% CI 1.10-1.42) were independently associated with ISR. Adding aPL and IL-6 improved discrimination (AUC 0.79 vs. 0.72, Δ = 0.07, Conclusion: Baseline aPL seropositivity and higher IL-6 were associated with 12-month ISR and clinically driven TLR. Incorporating these immune markers improves risk discrimination beyond clinical and angiographic factors. External validation and interventional studies are warranted.
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