Effects of drug-eluting stents on systemic inflammatory response in patients with unstable angina pectoris undergoing percutaneous coronary intervention

Abstract

Inflammatory markers are elevated in acute coronary syndromes, and are also known to play a crucial role in the pathogenesis of neointimal proliferation and stent restenosis. Drug-eluting stents (DESs) have been shown to decrease stent restenosis in different studies. In this study, we aimed to investigate the effect of treatment with DESs on systemic inflammatory response in patients with unstable angina pectoris who underwent percutaneous coronary intervention (PCI). We compared plasma high-sensitivity C-reactive protein (hsCRP), human tumor necrosis factor alpha (Hu TNF-alpha), and interleukin 6 (IL-6) levels after DES (dexamethasone-eluting stent [DEXES], and sirolimuseluting stent [SES]) implantation with levels after bare metal stent (BMS) implantation. We performed PCI with a single stent in 90 patients (62 men; 59 +/- 9 years of age; n = 30 in the BMS group, n = 30 in the DEXES group, n = 30 in the SES group) who had acute coronary syndrome. Plasma hsCRP, Hu TNF-alpha, and IL-6 levels were determined before intervention and at 24 h, 48 h, and 1 week after PCI. The results were as follows. Plasma hsCRP levels at 48 h (11.19 +/- 4.54, 6.43 +/- 1.63 vs 6.23 +/- 2.69 mg/l, P = 0.001) after stent implantation were significantly higher in the BMS group than in the DES group; this effect persisted for 7 days (P = 0.001). Plasma Hu TNF-alpha levels at each time point were higher in the SES group than in the BMS and DEXES groups (P < 0.05). The time course of Hu TNF-alpha values was similar in all groups. Although IL-6 levels at baseline and at 24 and 48 h showed no statistically significant difference between the study groups, postprocedural values at 7 days were slightly statistically significant in the SES group (P = 0.045). Drug-eluting stents showed significantly lower plasma hsCRP levels after PCI compared with BMSs. This may reflect the potent effects of DESs on acute inflammatory reactions induced by PCI.

Comparison of inflammatory markers and angiographic outcomes after implantation of sirolimus and paclitaxel-eluting stents

“…Kim et al 15 compared the inflammatory response after the implantation of a DES with that of a BMS and showed that a DES significantly reduced the plasma hs-CRP levels at 48 hours (13.4 mg/l vs 5.9 mg/l, p<0.01) and 72 hours (16.7 mg/l vs 5.4 mg/l, p<0.01) after the coronary stenting. Similar results are shown in another study 16. Kim et al 15 also compared the inflammatory response of two DES (SES and PES) without investigating the relation between the inflammatory response and angiographic outcomes and reported that there was no difference between the two groups.…”

C-Reactive Protein and Inflammatory Cytokines during Percutaneous Coronary Intervention

“…Although our study included both the patients with and without diabetes mellitus, many other studies have shown that serum IL-6, IL-1β, and CRP levels increased during PCI at similar ranges of concentrations compared to those detected in our procedures [23,24,25,26]. In contrast, most investigators have found that serum cytokines and CRP were related with the angiographic and PCI characteristics of the vessel, such as lesions in the vessels, the number of stents implanted, and other PCI procedures [27,28,29]. …”

“…Most of these studies focus on the relationship of these inflammation markers with restenosis, major clinical events, drug-eluting stent, or angiographic lesion progression, etc. [23,24,25,26,27,28,29]. Thus, many such studies have selected unstable angina, acute myocardial infarction, or multiple lesions in multiple coronary arteries for their study population [23,24,25,26,27,28,29].…”

“…In our current study, treatment with pathological concentrations of IL-6 and IL-1β, alone or in combination, failed to induce CRP expression in cultured human internal mammary arterial VSMCs. Cotreatment with both IL-1β and IL-6 led to a synergistic effect on CRP expression in human VSMCs, although the concentrations of these cytokines and the lengths of the interventions were much higher than the PCI-associated pathophysiological ranges [23,24,25,26,27,28]. In the current study, the concentrations of IL-6 and IL-1β capable of inducing CRP expression in VSMCs at 48 h were more than 1,000-fold higher than their serum expression levels detected following stent implantation.…”

Stent thrombosis: Nightmare of the interventional cardiology era

“…Mostly accused mechanisms for late and very late stent thrombosis are noncompliance to dual antiplatelet therapy and resistance to antiplatelet therapy, inflammatory responses to drug or polymer, delayed or incomplete reendothelialization of the DES, impaired endothelial function and late stent malapposition (LSM) [9][10][11][12]. LSM is defined as a separation of the stent struts from the intimal surface of the arterial wall that was not present immediately after implantation.…”