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Increased expression of CD40 ligand and C-reactive protein in patients with restenosis after percutaneous coronary intervention

Jin-Chuan Yan, Yi Liang, Gen-Shan Ma, Jian Zhu, Yi Feng, Dan Luo, Zong-Gui Wu, Xian-Tao Kong, Ren-Qian Zong and Lin-Zen Zhan

Background: Inflammation plays a pathogenic role in restenosis after percutaneous transluminal coronary angioplasty. Elevated levels of C-reactive protein are one of the strongest prognostic factors in atherosclerosis. Increasing evidence demonstrates that the CD40–CD40 ligand (L) interaction plays a crucial role in the pathogenesis of atherosclerosis and coronary artery disease. However, its role in the pathophysiology of restenosis is still unclear.

Methods: A total of 150 patients with percutaneous coronary intervention were investigated. The expression of CD40 and CD40L on platelets was analyzed by indirect immonofluorescence flow cytometry and serum-soluble CD40L level and C-reactive protein was determined by commercially available enzyme-linked immunosorbent assay. Patients with restenosis within a 6-month follow-up were observed in 150 consecutive patients who underwent percutaneous coronary intervention.

Results: Restenosis occurred in 38 patients (25.3%). Patients who developed restenosis showed higher levels of CD40–CD40L system compared with nonrestenotic patients before percutaneous coronary intervention. All restenotic patients demonstrated a significant increase of CD40 (66.8 ± 4.4 mean fluorescence intensity [MFI]) and CD40L (14.2 ± 1.7 MFI) coexpression on platelets as well as soluble CD40L (14.0 ± 1.6 ng/ml) compared with nonrestenotic patients and controls at 6-month follow-up (p < 0.001). Elevated sCD40L and CD40L were significantly correlated with serum C-reactive protein levels after percutaneous transluminal coronary angioplasty and with lumen loss at 6-month follow-up.

 Conclusion: Our results suggest that the CD40L system levels are associated with late restenosis after percutaneous coronary intervention. This would suggest that restenosis is, in part, an inflammatory disorder.