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Updated: Jul 17, 2026
A Murine Model of Stent Implantation in the Carotid Artery for the Study of Restenosis
Published on: May 14, 2013
Enhanced inflammatory response to coronary stenting marks the development of clinically relevant restenosis
Adriano M Caixeta1, Fábio S Brito, Marco A Costa
1Division of Interventional Cardiology, Brasília Heart Institute (InCor-DF), Zerbini Foundation, Estrada Parque Contorno do Bosque, s/n Parte, CEP:70658-900 Brasília, DF, Brazil. adriano.caixeta@incordf.zerbini.org.br
Insights
Coronary stenting triggers the release of inflammatory cytokines and cell-mediated immunity factors. Elevated levels of these markers post-procedure are linked to restenosis, a significant clinical outcome.
Area of Science:
- Cardiology
- Immunology
- Biochemistry
Background:
- Elevated inflammatory markers and cytokines are observed in acute coronary syndromes, correlating with poor prognosis.
- Coronary stenting is a common intervention for coronary artery disease.
Purpose of the Study:
- To investigate the impact of coronary stenting on cytokine and cell-mediated immunity factor release.
- To assess the relationship between inflammation and clinical outcomes at 6 months post-stenting.
Main Methods:
- Forty patients with native coronary artery disease undergoing stenting were studied.
- Blood samples were collected pre-stenting and at 6 hours, 48 hours, and 12 weeks post-stenting.
- Serum levels of high-sensitivity C-reactive protein, IL-6, IL-8, TNF-alpha, and soluble IL-2 receptor (sIL2-R) were measured. Clinical outcomes, including major adverse cardiac events, were tracked for 6 months.
Main Results:
- Proinflammatory cytokines (IL-6, IL-8, TNF-alpha) peaked at 6 hours post-stenting.
- High-sensitivity C-reactive protein peaked at 48 hours, and sIL2-R peaked at 12 weeks.
- Patients with restenosis showed significantly higher C-reactive protein and IL-8 levels compared to those without restenosis.
Conclusions:
- Coronary stenting induces the release of proinflammatory cytokines and inflammatory markers into circulation.
- Increased levels of specific inflammatory markers post-stenting are associated with clinically significant restenosis.
Objectives:
The aims of this study were to investigate the effect of coronary stenting on the release of cytokines and cell-mediated immunity factors and to evaluate the association between inflammation and clinical outcomes at 6 months.
Background:
Circulating levels of inflammatory markers and cytokines are elevated in patients with acute coronary syndromes and are related to an unfavorable outcome. The aims of this study were to investigate the effect of coronary stenting on the release of cytokines and cell-mediated immunity factors and to evaluate the association between inflammation and clinical outcomes at 6 months.
Methods:
Forty patients with single native coronary artery disease treated with stenting were enrolled. Peripheral venous blood samples were collected before and 6 h, 48 h, and 12 weeks after stenting. Serum concentrations of high-sensitivity C-reactive protein, interleukin-6, interleukin-8, tumor necrosis factor-alpha (markers of inflammation) and serum-soluble interleukin-2 receptor for T-lymphocyte activation (sIL2-R, marker of cell-mediated immunity) were measured. Patients also were evaluated clinically one, 3, and 6 months post-stenting or when they presented with cardiovascular symptoms to identify major adverse cardiac events (cardiac death, MI, revascularization).
Results:
Concentrations of interleukins 6 and 8 and tumor necrosis factor-alpha peaked at 6 h (11.0, 12.6, and 5.3 pg/ml, respectively). The peak level of high-sensitivity C-reactive protein (2.77 mg/dL) occurred 48 h post stenting, while sIL2-R peaked (495 U/ml) at 12 weeks. Patients who experienced restenosis had higher levels of C-reactive protein at 48 h (4.94 vs. 1.84 mg/dl; P = 0.043) and of IL-8 at 6 h (26.75 vs. 13.55 pg/mL; P = 0.048) than those without restenosis.
Conclusions:
Proinflammatory cytokines and inflammatory markers are released into the peripheral circulation early after coronary stenting, and increased levels of some are associated with clinically relevant restenosis.
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