Cv3: Influence of Diabetes and Baseline St-Segment Change Status on the Cost-Effectiveness of an Early Invasive vs. Conservative Strategy for the Treatment of Acute Coronary Syndromes:application of a Net-Benefit Regression Approach to Data From the Tactics-Timi 18 Trial

Mahoney, EM; Chu, Haitao; Jurkovitz, CT; Cp, Cannon; Alexander, Charles M.; Nag, Soma S.; Weintraub, WS

doi:10.1016/s1098-3015(10)63802-8

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“…[1][2][3] There are data suggesting that the delay in the antiplatelet treatment may have adverse consequences for patients who undergo coronary intervention. 4 Moreover, the degree of platelet inhibition during the procedure is critical for the protection from ischemic events. 5 Studies have also suggested that the benefit provided by the platelet GPIIb/IIIa antagonists is greater when patients are not adequately pretreated with thienopyridines.…”

Section: Introductionmentioning

confidence: 99%

Effects of Coronary Prestenting Platelet Inhibition on Coronary Poststenting Inflammation

Sacristán

López‐Farré²,

Zamorano-León³

et al. 2008

Journal of Cardiovascular Pharmacology

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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.

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