Enhanced inflammatory response to coronary stenting marks the development of clinically relevant restenosis.
OBJECTIVE
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.
Caixeta
Adriano M
AM
Division 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
Brito
Fábio S
FS
Costa
Marco A
MA
Serrano
Carlos V
CV
Petriz
João L
JL
Da Luz
Protásio L
PL
D000368:Aged; D000787:Angina Pectoris / Q000097:blood / Q000000981:diagnostic imaging / Q000628:therapy; D015906:Angioplasty, Balloon, Coronary; D015415:Biomarkers / Q000097:blood; D019917:Blood Vessel Prosthesis Implantation; D002097:C-Reactive Protein / Q000378:metabolism; D018849:Controlled Clinical Trials as Topic; D017023:Coronary Angiography; D023903:Coronary Restenosis / Q000097:blood* / Q000000981:diagnostic imaging / Q000209:etiology*; D023921:Coronary Stenosis / Q000097:blood / Q000000981:diagnostic imaging / Q000628:therapy*; D016207:Cytokines / Q000097:blood*; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood*; D015850:Interleukin-6 / Q000097:blood; D016209:Interleukin-8 / Q000097:blood; D008297:Male; D008875:Middle Aged; D015375:Receptors, Interleukin-2 / Q000097:blood; D012107:Research Design; D015607:Stents; D013997:Time Factors; D016896:Treatment Outcome; D019210:Troponin I / Q000097:blood; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
D015415:Biomarkers; D016207:Cytokines; D018836:Inflammation Mediators; D015850:Interleukin-6; D016209:Interleukin-8; D015375:Receptors, Interleukin-2; D019210:Troponin I; D014409:Tumor Necrosis Factor-alpha; D002097:C-Reactive Protein