Enhanced Inflammatory Response to Coronary Angioplasty in Patients With Severe Unstable Angina

Abstract

Our data suggest that plaque rupture per se is not the main cause of the acute-phase protein increase in unstable angina and that increased baseline levels of acute-phase proteins are a marker of the hyperresponsiveness of the inflammatory system even to small stimuli. Thus, an enhanced inflammatory response to nonspecific stimuli may be involved in the pathogenesis of unstable angina.

Marcadores inflamatórios intracoronarianos após intervenções coronarianas percutâneas

“…TNF-a values, observed in patients in our study, showed similar Inflammatory marker Pre-ICP Post-ICP p TNF alfa (mean ± DP) 9.5±1.5 9.9±1.8 0.017 pg/ml IL-1(mean ± DP) 2.1±0.1 2.1±0.1 1.0 pg/ml IL-6 (mean ± DP) 5.9±2.4 6.9±2.9 <0.001 pg/ml ICAM-1 221.9±53.7 ng/ml 208.2±69.8 ng/ml 0.6 (mean ± DP) E-selectina 52±17.5 ng/ml 49.3±18.7 ng/ml 0.009 (mean ± DP) P-selectina 74.2±30.7 ng/ml 74.3±31.5 ng/ml 1.0 (mean ± DP) concentrations to those found in CAD carriers in CARE study 9 , approximately 95% with values over 4.18 pg/ml. Similarly, IL-6 concentrations, found in our research patients, were higher than 5.0 pg/ml, corresponding to findings by Liuzo et al 10 , who studied CAD carriers submitted to percutaneous coronary interventions. In both studies, the dosages of those markers were performed through an analogous methodology to the one used in our work (Quantikine human TNF-a, IL-6 R&D system).…”

“…In acute event, variable concentrations of cytokines and adhesion molecules 9 are released in the coronary flow. To a certain extent, that situation can be reproduced in percutaneous coronary interventions (PCI) 10 . Simultaneously to the release of inflammatory mediators, originated from plaque rupture, additional quantities of inflammatory markers (IM) originated from brief myocardial ischemia occurred during PCIs, can be added.…”

Abciximab Suppresses the Rise in Levels of Circulating Inflammatory Markers After Percutaneous Coronary Revascularization

“…[5][6][7][8] Inflammatory markers have also been shown to increase in the period immediately after percutaneous revascularization procedures in patients with or without unstable myocardial ischemia, and the magnitude of rise in these markers has been correlated with subsequent myocardial infarction and restenosis. [1][2][3][4]19 The efficacy of percutaneous revascularization is considerably improved by the administration of GP IIb/IIIa receptor antagonists. In randomized placebo-controlled trials, the risk of death, myocardial infarction, or emergency repeat revascularization within 30 days after coronary intervention was reduced by Ϸ40% to 60% with abciximab and by 15% to 35% with eptifibatide (Integrilin, COR Therapeutics) or tirofiban (Aggrastat, Merck).…”

“…IL-6 is expressed in a number of cell types, including those within atherosclerotic plaque, and its production seems to be controlled in part by IL-1␤ and TNF-␣. 6,19 CRP is an acute-phase reactant produced by the liver under the influence of inflammatory cytokines, principally IL-6. 19 In addition to acting as a marker of a systemic inflammatory state, CRP may also have a direct pro-inflammatory effect, 27 and it may influence thrombosis and inflammation through complement activation.…”

Preinterventional peak monocyte count and in-stent intimal hyperplasia after coronary stent implantation in human coronary arteries

“…22 Systemic inflammatory reaction may play a pivotal role in neointima formation within stent struts in addition to the local vessel wall injury, with the subsequent release of chemotactic and growth factors. 8,23 Fukuda et al 24 reported that the circulating monocyte count increased and reached its peak 2 days after stent implantation and that the maximum monocyte count after stent implantation showed a positive correlation with in-stent neointimal volume at 6-month follow-up. They concluded that circulating monocytes after stent implantation play a role in the process of in-stent neointimal hyperplasia.…”