Effect of high bolus dose tirofiban on the inflammatory response following percutaneous coronary intervention
| Autor: | Elie Salamé, Righab Hamdan, Roland Kassab, Vanda Barakett, Mirna Germanos, Antoine Sarkis, Rabih R. Azar, Simon Aboujaoudé, Georges Badaoui |
|---|---|
| Rok vydání: | 2009 |
| Předmět: |
Male
medicine.medical_specialty Ticlopidine Time Factors Platelet Aggregation medicine.medical_treatment Clinical Investigations Bolus (medicine) Interquartile range Internal medicine Medicine Creatine Kinase MB Form Humans Prospective Studies Thrombus Angioplasty Balloon Coronary CD40 Antigens Saline Inflammation biology business.industry Interleukin-6 Percutaneous coronary intervention General Medicine Tirofiban Middle Aged medicine.disease Troponin Clopidogrel C-Reactive Protein Anesthesia Conventional PCI biology.protein Cardiology Tyrosine Female Cardiology and Cardiovascular Medicine business Biomarkers Platelet Aggregation Inhibitors medicine.drug |
| Zdroj: | Clinical cardiology. 33(1) |
| ISSN: | 1932-8737 |
| Popis: | Background Tirofiban at the bolus dose of 10 µg/kg does not suppress the inflammatory response following percutaneous coronary intervention (PCI). This may be due to less than optimal inhibition of platelet aggregation. High bolus dose tirofiban (25 µg/kg) allows better inhibition of platelet aggregation but its anti-inflammatory effect remains unknown. Hypothesis High bolus dose tirofiban exhibits anti-inflammatory activity. Methods A total of 100 patients referred for PCI were randomized to receive high bolus dose tirofiban followed by a 24-h infusion or a bolus and an infusion of saline. Patients with elevated troponin or with thrombus in the culprit lesion were excluded. Inflammatory markers were measured at baseline and at 24 h. Results Levels of soluble CD40 ligand (sCD40L) were not affected by PCI while those of interleukin-6 (IL-6) and of high sensitivity C-reactive protein (hs-CRP) significantly increased. Despite inhibiting platelet's aggregation by > 90%, tirofiban did not suppress the rise of IL-6 and hs-CRP. Median (interquartile range) elevation of IL-6 was 0.6 pg/mL (−1.5–3.6) versus 0.4 pg/mL (−0.7–1.8) and that of hs-CRP was 2.1 mg/L (0.7–5.2) versus 2.4 mg/L (1–4.7) in the tirofiban and the control groups, respectively (p = ns). However, in patients with diabetes mellitus, tirofiban significantly suppressed the rise of hs-CRP by 65% (p = 0.01), but did not significantly affect the rise of IL-6. Conclusion In low-risk patients undergoing PCI, tirofiban did not attenuate the rise of inflammatory markers. However, the significant effect in diabetics suggests that tirofiban may have anti-inflammatory activity in higher risk patients. Copyright © 2009 Wiley Periodicals, Inc. |
| Databáze: | OpenAIRE |
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