Cytokine response after percutaneous coronary intervention in stable angina: effect of selective glycoprotein IIb/IIIa receptor antagonism.
BACKGROUND
It is unclear whether modulation of inflammatory markers by glycoprotein IIb/IIIa receptor inhibition after percutaneous coronary intervention (PCI) is caused by an interaction with the alpha(v)beta3 and alpha(M)beta2 receptor or it correlates with ischemic events during PCI. This study investigates the inflammatory profile after elective, nonacute PCI and whether and how administration of the glycoprotein IIb/IIIa receptor antagonist tirofiban modulates the postinterventional inflammatory myocardial response.


METHODS
The time course of inflammatory parameters (C-reactive protein [CRP], interleukin-1 [IL-1], interleukin-6 [IL-6], and tumor necrosis factor alpha [TNF-alpha]) of patients receiving peri- and postinterventional placebo (n = 46) or tirofiban infusion (n = 50) was analyzed by use of enzyme-linked immuno assays. Samples were collected before and 30 minutes, 2.5 hours, 6.5 hours, 12 hours, 24 hours, and 48 hours after elective PCI.


RESULTS
Among the inflammatory markers analyzed, TNF-alpha, IL-6, and CRP levels increased significantly. However, the latter markers followed individual time courses in patients given placebo and patients treated with tirofiban after PCI, compared with pre-PCI levels (P <.01), with no significant differences between the placebo and tirofiban-treated groups. However, by subgroup analysis, significant differences were revealed in TNF-alpha, IL-6, and CRP levels of patients who were troponin T-positive versus patients who were troponin T-negative after PCI.


CONCLUSIONS
The administration of the selective glycoprotein IIb/IIIa receptor antagonist tirofiban has no direct impact on the inflammatory profile after elective PCI. Change of the inflammatory profile was only related to the presence or absence of postinterventional troponin.
Bonz
Andreas W
AW
Department of Medicine/Cardiology, University of Würzburg, Würzburg, Germany. bonz_a@klinik.uni-wuerzburg.de
Lengenfelder
Björn
B
Jacobs
Martina
M
Strotmann
Jörg
J
Held
Stefanie
S
Ertl
Georg
G
Voelker
Wolfram
W
D000787:Angina Pectoris / Q000188:drug therapy; D015906:Angioplasty, Balloon, Coronary / Q000009:adverse effects*; D002097:C-Reactive Protein / Q000378:metabolism; D003327:Coronary Disease / Q000188:drug therapy* / Q000276:immunology / Q000378:metabolism; D016207:Cytokines / Q000187:drug effects*; D004311:Double-Blind Method; D006801:Humans; D007249:Inflammation / Q000188:drug therapy*; D007375:Interleukin-1 / Q000097:blood; D015850:Interleukin-6 / Q000097:blood; D019039:Platelet Glycoprotein GPIIb-IIIa Complex / Q000037:antagonists & inhibitors*; D011446:Prospective Studies; D000077466:Tirofiban; D014336:Troponin / Q000097:blood; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D014443:Tyrosine / Q000031:analogs & derivatives / Q000627:therapeutic use*
D016207:Cytokines; D007375:Interleukin-1; D015850:Interleukin-6; D019039:Platelet Glycoprotein GPIIb-IIIa Complex; D014336:Troponin; D014409:Tumor Necrosis Factor-alpha; D014443:Tyrosine; D002097:C-Reactive Protein; D000077466:Tirofiban