Why the study?
Does simultaneous administration of clopidogrel and tirofiban reduce poststenting inflammation compared to sequential administration in patients with acute myocardial infarction?
Does simultaneous administration of clopidogrel and tirofiban reduce poststenting inflammation compared to sequential administration in patients with acute myocardial infarction?
Greater inhibition of platelet activation before stenting with simultaneous clopidogrel and tirofiban does not correlate with a different early inflammatory response after stenting compared to sequential administration.
No difference in post-stent inflammation despite greater initial platelet inhibition; leaves open optimal clopidogrel-tirofiban timing in AMI.
The aim of this study was to analyze the effect of 2 antiplatelet regimens on the inhibition of GP IIb/IIIa-dependent platelet activation and their association with the poststenting inflammatory response. Seventeen patients with acute myocardial infarction were divided into 2 groups: (A) clopidogrel plus tirofiban infusion administered together during inclusion (n = 10); (B) clopidogrel administered at inclusion and followed 2 hours after by tirofiban (n = 7). Blood samples were obtained at inclusion and at 24 and 48 hours after stenting. Before stenting, a greater reduction of GP IIb/IIIa-dependent platelet activation was found in both groups, although it was greater in group A than in group B. This statistical difference was not observed at 24 and 48 hours after the procedure. At 48 hours after stenting, interleukin-6, interleukin-10, soluble intracellular adhesion molecule-1, and soluble CD40 ligand plasma values were not different between experimental groups. By proteomics, different isoforms of the following proteins were identified: alpha 1-antitrypsin (ATT-1), fibrinogen gamma chain, apolipoprotein A-IV, apolipoprotein A-I, vitamin D binding protein, haptoglobin, and serotransferrin. At 48 hours after stenting, only the plasma expression of the ATT-1 isoform 5 was significantly increased in group A compared with group B. In conclusion, a greater inhibition of GP IIb/IIIa-dependent platelet activation before stenting was not correlated with a different inflammatory activity early after stenting.
No takes yet. Share an insight, caveat, or question.
Sacristán et al. (2008) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: