Short-term changes in interleukin 10 following drug-eluting stent placement in stable angina patients: Influence of hypertension

Background: Drug-eluting stents (DES) are widely used in percutaneous coronary interventions (PCI) to reduce restenosis. However, their effect on acute inflammatory and anti-inflammatory responses is not completely understood. Interleukin-10 (IL-10) is a key anti-inflammatory cytokine implicated in vascular healing and modulation of immune responses following endothelial injury.Objective: To evaluate the acute-phase response of IL-10 following DES implantation in patients with stable angina, with a particular focus on differences between hypertensive and normotensive individuals.Methods: Thirteen patients with stable angina undergoing elective DES implantation were included. Arterial blood samples were collected at baseline and immediately post-procedure, and venous samples were collected at 24 hours post-PCI. Serum IL-10 levels were measured using ELISA. Patients were stratified based on hypertensive status.Results: IL-10 levels significantly increased immediately after stenting (16.65 ± 1.49 pg/ml) compared to baseline (11.88 ± 0.42 pg/ml; P < 0.05). However, levels declined significantly at 24 hours post-procedure (10.15 ± 1.04 pg/ml). Hypertensive patients showed a greater post-procedure increase in IL-10 (18.16 ± 2.4 pg/ml) than normotensive patients (15.16 ± 1.08 pg/ml), though this difference was not statistically significant. At 24 hours, IL-10 levels fell below baseline in both groups. The IL-6/IL-10 ratio, used as an index of net inflammatory activity, significantly increased at 24 hours (1.05 ± 0.13), suggesting a delayed shift toward a pro-inflammatory state.Conclusion: DES implantation in patients with stable angina induces a transient increase in IL-10 levels, particularly among hypertensive individuals. The subsequent decline in IL-10 and rise in the IL-6/IL-10 ratio at 24 hours may indicate a pro-inflammatory rebound phase. These findings underscore the dynamic nature of cytokine regulation following PCI and support further investigation into IL-10’s role in modulating vascular inflammation and restenosis risk.