Journal articles: 'Tirofiban'

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&NA;. "Tirofiban." Reactions Weekly &NA;, no. 1207 (June 2008): 33. http://dx.doi.org/10.2165/00128415-200812070-00101.

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&NA;. "Tirofiban." Reactions Weekly &NA;, no. 1320 (September 2010): 44. http://dx.doi.org/10.2165/00128415-201013200-00156.

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&NA;. "Tirofiban." Reactions Weekly &NA;, no. 1257 (June 2009): 40–41. http://dx.doi.org/10.2165/00128415-200912570-00130.

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&NA;. "Tirofiban." Reactions Weekly &NA;, no. 1276 (October 2009): 29. http://dx.doi.org/10.2165/00128415-200912760-00090.

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&NA;. "Tirofiban." Reactions Weekly &NA;, no. 1309 (July 2010): 38–39. http://dx.doi.org/10.2165/00128415-201013090-00124.

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&NA;. "Tirofiban." Reactions Weekly &NA;, no. 1310 (July 2010): 40. http://dx.doi.org/10.2165/00128415-201013100-00132.

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McClellan, Karen J., and Karen L. Goa. "Tirofiban." Drugs 56, no. 6 (1998): 1067–80. http://dx.doi.org/10.2165/00003495-199856060-00017.

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&NA;. "Tirofiban." Reactions Weekly &NA;, no. 1059 (July 2005): 22. http://dx.doi.org/10.2165/00128415-200510590-00067.

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&NA;. "Tirofiban." Reactions Weekly &NA;, no. 1062 (July 2005): 13. http://dx.doi.org/10.2165/00128415-200510620-00036.

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&NA;. "Tirofiban." Reactions Weekly &NA;, no. 1071 (October 2005): 13. http://dx.doi.org/10.2165/00128415-200510710-00037.

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&NA;. "Tirofiban." Reactions Weekly &NA;, no. 1301 (May 2010): 49. http://dx.doi.org/10.2165/00128415-201013010-00175.

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&NA;. "Tirofiban." Reactions Weekly &NA;, no. 1243 (March 2009): 43. http://dx.doi.org/10.2165/00128415-200912430-00137.

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&NA;. "Tirofiban." Inpharma Weekly &NA;, no. 1151 (August 1998): 16. http://dx.doi.org/10.2165/00128413-199811510-00032.

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&NA;. "Tirofiban." Reactions Weekly &NA;, no. 1365 (August 2011): 44. http://dx.doi.org/10.2165/00128415-201113650-00170.

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&NA;. "Tirofiban." Reactions Weekly &NA;, no. 1164 (August 2007): 23. http://dx.doi.org/10.2165/00128415-200711640-00065.

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&NA;. "Tirofiban." Reactions Weekly &NA;, no. 1133 (January 2007): 25. http://dx.doi.org/10.2165/00128415-200711330-00088.

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&NA;. "Tirofiban." Reactions Weekly &NA;, no. 1144 (March 2007): 22. http://dx.doi.org/10.2165/00128415-200711440-00064.

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&NA;. "Tirofiban." Reactions Weekly &NA;, no. 1429 (November 2012): 40. http://dx.doi.org/10.2165/00128415-201214290-00155.

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Theroux, P. "Tirofiban." Drugs of Today 35, no. 1 (1999): 59. http://dx.doi.org/10.1358/dot.1999.35.1.522949.

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&NA;. "Tirofiban." Reactions Weekly &NA;, no. 1385 (January 2012): 42. http://dx.doi.org/10.2165/00128415-201213850-00155.

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&NA;. "Tirofiban." Reactions Weekly &NA;, no. 1386 (January 2012): 34. http://dx.doi.org/10.2165/00128415-201213860-00122.

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Yang, Jianhong, Yuefei Wu, Xiang Gao, Andrew Bivard, Christopher R. Levi, Mark W. Parsons, Longting Lin, et al. "Intraarterial Versus Intravenous Tirofiban as an Adjunct to Endovascular Thrombectomy for Acute Ischemic Stroke." Stroke 51, no. 10 (October 2020): 2925–33. http://dx.doi.org/10.1161/strokeaha.120.029994.

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Background and Purpose: This study aimed to evaluate the treatment effect of intraarterial versus intravenous tirofiban during endovascular thrombectomy in acute ischemic stroke. Methods: This study retrospectively examined 503 patients with acute ischemic stroke with large vessel occlusion who received endovascular thrombectomy within 24 hours of stroke onset. Patients were divided into 3 groups: no tirofiban (n=354), intraarterial tirofiban (n=79), and intravenous tirofiban (n=70). The 3 groups were compared in terms of recanalization rate, symptomatic intracerebral hemorrhage, in-hospital death rate, 3-month death, and 3-month outcomes measured by modified Rankin Scale score (good clinical outcome of 0–2, poor outcome of 5–6). The comparison was statistically assessed by propensity score matching, followed by Freidman rank-sum test and pairwise Wilcoxon signed-rank test with Bonferroni correction. Results: The propensity score matching resulted in 92 matched triplets. Compared with the no-tirofiban group, the intravenous tirofiban group showed significantly increased recanalization (96.7% versus 64.1%, P <0.001), an increased rate of 3-month good outcome (69.5% versus 51.2%, P =0.034), and a lower rate of 3-month poor outcome (12.2% versus 41.4%, P <0.001). There was no significant difference between the tirofiban intravenous and no-tirofiban groups in terms of symptomatic intracerebral hemorrhage (2.2% versus 0%, P =1.000). However, symptomatic intracerebral hemorrhage was significantly increased in the intraarterial-tirofiban group compared with the no-tirofiban group (19.1% versus 0%, P <0.001), with an increased rate of in-hospital death (23.6% versus 0% P <0.001), and increased rate of 3-month death (26.8% versus 11.1%, P =0.021). The intraarterial-tirofiban and no-tirofiban group showed no significant difference in recanalization rate (66.3% versus 64.1%, P =1.000). Conclusions: As an adjunct to endovascular thrombectomy, intravenous tirofiban is associated with high recanalization rate and good outcome, whereas intraarterial tirofiban is associated with high hemorrhagic rate and death rate.

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&NA;. "Clopidogrel/tirofiban." Reactions Weekly &NA;, no. 1214 (August 2008): 13–14. http://dx.doi.org/10.2165/00128415-200812140-00033.

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&NA;. "Abciximab/tirofiban." Reactions Weekly &NA;, no. 797 (April 2000): 6. http://dx.doi.org/10.2165/00128415-200007970-00012.

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&NA;. "Heparin/tirofiban." Reactions Weekly &NA;, no. 852 (May 2001): 9. http://dx.doi.org/10.2165/00128415-200108520-00026.

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&NA;. "Streptokinase/tirofiban." Reactions Weekly &NA;, no. 946 (April 2003): 14–15. http://dx.doi.org/10.2165/00128415-200309460-00050.

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&NA;. "Heparin/tirofiban." Reactions Weekly &NA;, no. 1230 (November 2008): 20–21. http://dx.doi.org/10.2165/00128415-200812300-00058.

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&NA;. "TIROFIBAN (AGGRASTAT)." American Journal of Nursing 98, no. 8 (August 1998): 63. http://dx.doi.org/10.1097/00000446-199808000-00048.

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&NA;. "Antithrombotics/tirofiban." Reactions Weekly &NA;, no. 1429 (November 2012): 9. http://dx.doi.org/10.2165/00128415-201214290-00029.

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Hartman, G. D. "Tirofiban Hydrochloride." Drugs of the Future 20, no. 9 (1995): 897. http://dx.doi.org/10.1358/dof.1995.020.09.311591.

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Gruber, Philipp, Martin Hlavica, Jatta Berberat, Benjamin Victor Ineichen, Michael Diepers, Krassen Nedeltchev, Timo Kahles, and Luca Remonda. "Acute administration of tirofiban versus aspirin in emergent carotid artery stenting." Interventional Neuroradiology 25, no. 2 (November 4, 2018): 219–24. http://dx.doi.org/10.1177/1591019918808777.

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Background Carotid artery stenting requires antiplatelet therapy for prevention of in-stent thrombosis. Patients suffering from acute ischemic stroke undergoing intravenous thrombolysis and emergent carotid artery stenting (eCAS) are at high risk for intracranial bleeding. We assessed efficacy and safety of acute administration of intravenous tirofiban versus aspirin in these patients. Methods A retrospective, single center, cohort study was carried out of 32 patients who underwent eCAS (18 received tirofiban, 14 received aspirin) at our comprehensive stroke center (2008–2016). Results Of our 32 consecutive eCAS patients, favorable clinical outcomes (modified Rankin scale ≤ 2) were achieved in eight (47%) tirofiban patients and six (46%) aspirin patients ( p = 0.96). Overall rates were similar for symptomatic intracranial bleeding (tirofiban 22%, aspirin 29%, p = 0.68) and mortality (tirofiban 18%, aspirin 23%, p = 0.71). Conclusions Tirofiban and aspirin demonstrated similar efficacy and safety in thrombolyzed stroke patients who underwent eCAS in our cohort. Intravenous tirofiban with its short half-life might represent an alternative to aspirin in select patients.

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Fu, Zhiyong, Chuanli Xu, Xin Liu, Zhengze Wang, and Lianbo Gao. "Safety and Efficacy of Tirofiban in Acute Ischemic Stroke Patients Receiving Endovascular Treatment: A Meta-Analysis." Cerebrovascular Diseases 49, no. 4 (2020): 442–50. http://dx.doi.org/10.1159/000509054.

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Objectives: Tirofiban is widely used in clinical practice for acute ischemic stroke (AIS). However, whether tirofiban increases the bleeding risk or improves the outcome of AIS patients with endovascular treatment (ET) is unknown. The aim of this meta-analysis is to evaluate the safety and efficacy of tirofiban compared with those without tirofiban in AIS patients receiving ET. Methods: Systematic literature search was done in PubMed and EMBASE databases without language or time limitation. Safety outcomes were symptomatic intracranial hemorrhage (sICH) and mortality. Efficacy outcomes were recanalization rate and favorable functional outcome. Review Manager 5.3 and Stata Software Package 15.0 were used to perform the meta-analysis. Results: Eleven studies with a total of 2,028 patients were included. A total of 704 (34.7%) patients were administrated tirofiban combined with ET. Meta-analysis suggested that tirofiban did not increase the risk of sICH (odds ratio (OR) 1.08; 95% confidence interval (CI) 0.81–1.46; p = 0.59) but significantly decreased mortality (OR 0.68; 95% CI 0.52–0.89; p = 0.005). There was no association between tirofiban and recanalization rate (OR 1.26; 95% CI 0.86–1.82; p = 0.23) or favorable functional outcome (OR 1.21; 95% CI 0.88–1.68; p = 0.24). Subgroup analyses indicated that preoperative tirofiban significantly increase recanalization rate (OR 3.89; 95% CI 1.70–8.93; p = 0.001) and improve favorable functional outcome (OR 2.30; 95% CI 1.15–4.60; p = 0.02). Conclusions: Tirofiban is safe in AIS patients with ET and can significantly reduce mortality; preoperative tirofiban may be effective, but further studies are needed to confirm the efficacy.

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Zhao, Lili, Yating Jian, Tao Li, Heying Wang, Zhang Lei, Man Sun, Ye Li, et al. "The Safety and Efficiency of Tirofiban in Acute Ischemic Stroke Patients Treated with Mechanical Thrombectomy: A Multicenter Retrospective Cohort Study." Biochemistry Research International 2020 (May 1, 2020): 1–8. http://dx.doi.org/10.1155/2020/5656173.

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Introduction. Limited comparative studies have reported the safety and efficacy of tirofiban in acute ischemic stroke (AIS) patients after mechanical thrombectomy (MT). Additionally, the available studies are inconsistent with each other, which makes application of tirofiban unclear in neuro-intervention. Here, we performed a comparative retrospective study to investigate whether tirofiban combined with MT improves short- and long-term prognosis in AIS patients and whether its use is associated with complications. Method. Retrospective data were collected for AIS patients admitted between January 2013 and January 2019 at three stroke centers. According to whether tirofiban was used during the operation, patients were divided into tirofiban group and control group. Multivariate and COX regression analyses were performed to determine the association of tirofiban treatment with safety and efficiency in subjects treated with MT. Result. A total of 174 patients were analyzed, of whom 89 (51.1%) were treated with tirofiban. There were no differences in the incidence of symptomatic intracerebral hemorrhage (10.2% vs. 10.6%, p=0.918), parenchymal hemorrhage type 2 (18.0% vs. 16.5%, p=0.793), and reocclusion at 24 h (3.4% vs. 10.6%, p=0.060) between the tirofiban group and control group. Multivariate regression showed that tirofiban was not associated with intracerebral hemorrhage, early neurological deterioration, neurological improvement at 7 days, functional independence at 3-month and 9-month follow-up, or death at 9-month follow-up (adjusted p>0.05 for all). However, AIS patients treated with MT + tirofiban showed a trend towards acquiring faster functional independence, with a median time to acquire functional independence of 4.0 months compared with 6.5 months in the control group (risk ratio = 1.49, 95% confidence interval 0.98–2.27; long rank p=0.066). Conclusion. Tirofiban may help AIS patients given MT to gain functional independence faster, without increasing the risk of complications.

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Velibey, Yalcin, Tolga Sinan Guvenc, Koray Demir, Ahmet Oz, Evliya Akdeniz, Rengin Cetin Guvenc, Ozge Guzelburc, et al. "Effects of Bailout Tirofiban on In-Hospital Outcomes and Long-Term Mortality in Patients With ST-Segment Elevation Myocardial Infarction Undergoing Primary Percutaneous Intervention." Angiology 70, no. 5 (October 28, 2018): 431–39. http://dx.doi.org/10.1177/0003319718808911.

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We retrospectively analyzed short- and long-term outcomes of patients who received bailout tirofiban during primary percutaneous intervention (pPCI). A total of 2681patients who underwent pPCI between 2009 and 2014 were analyzed; 1331 (49.6%) out of 2681 patients received bailout tirofiban. Using propensity score matching, 2100 patients (1050 patient received bail-out tirofiban) with similar preprocedural characteristics were identified. Patients who received bailout tirofiban had a significantly higher incidence of acute stent thrombosis, myocardial infarction, and major cardiac or cerebrovascular events during the in-hospital period. There were numerically fewer deaths in the bailout tirofiban group in the unmatched cohort (1.7% vs 2.5%, P = .118). In the matched cohort, in-hospital mortality was significantly lower (1.1% vs 2.4%, P = .03), and survival at 12 and 60 months were higher (96.9% vs 95.2%, P = .056 for 12 months and 95.1% vs 92.0%, P = .01 for 60 months) in the bailout tirofiban group. After multivariate adjustment, bailout tirofiban was associated with a lower mortality at 12 months (odds ratio [OR]: 0.554, 95% confidence interval [CI], 0.349-0.880, P = .012) and 60 months (OR: 0.595, 95% CI, 0.413-0.859, P = .006). In conclusion, bailout tirofiban strategy during pPCI is associated with a lower short- and long-term mortality, although in-hospital complications were more frequent.

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Umemura, K., K. Kondo, Y. Ikeda, and M. Nakashima. "Enhancement by Ticlopidine of the Inhibitory Effect on In Vitro Platelet Aggregation of the Glycoprotein IIb/IIIa Inhibitor Tirofiban." Thrombosis and Haemostasis 78, no. 05 (1997): 1381–84. http://dx.doi.org/10.1055/s-0038-1665415.

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SummaryWe determined the effects of combining the glycoprotein IIb/IIIa inhibitor tirofiban (MK-383, Aggrastat) and ticlopidine on inhibition of ADP-induced platelet aggregation, inhibition of collagen-induced platelet aggregation, and prolongation of bleeding time in 5 healthy male volunteers. The study consisted of 2 periods. In period 1, tirofiban was administered intravenously as a bolus injection at a dose of 5.0 µg/kg for 5 min, then as a continuous infusion at a rate of 0.05 µg/kg/min for 5 h 55 min. In period 2, ticlopidine was given orally at a dose of 200 mg once daily for 4 days, after which tirofiban was administered in the same manner as in period 1, starting 2 h after the last dose of ticlopidine. The percent inhibition of platelet aggregation induced by ADP 5 µM at the end of tirofiban infusion in periods 1 and 2 was 73.6 ± 2.6 and 87.1 ± 5.7% (mean ± SD), respectively. The corresponding values for inhibition of platelet aggregation induced by collagen 2 µg/ml were 45.4 ± 36.1 and 82.8 ± 27.0%, respectively. In contrast, the percent inhibition of platelet aggregation induced by ADP and collagen after treatment with ticlopidine alone was 15.8 ± 20.2 and p ± 4.8%, respectively. Compared with tirofiban alone, the combination of tirofiban and ticlopidine significantly enhanced inhibition of platelet aggregation induced by both ADP and collagen (p <0.02 and p <0.012, respectively). The inhibitory effects of ticlopidine alone were not statistically significant. Tirofiban prolonged bleeding time both in period 1 and in period 2. However, tirofiban and ticlopidine combined did not affect bleeding time. Ticlopidine administration did not alter the pharmacokinetics of tirofiban. In conclusion, at the doses of tirofiban and ticlopidine used in this study, the combination of the two drugs enhanced inhibition of platelet aggregation but did not prolong bleeding time, suggesting that appropriate doses of tirofiban can be used concomitantly with ticlopidine with no further safety concerns but with potential additional clinical effects.

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Stahle, Mary, Gray Jerome, Chandrasekaran Nagaswami, John Weisel, and Roy Hantgan. "Tirofiban Blocks Platelet Adhesion to Fibrin with Minimal Perturbation of GpIIb/IIIa Structure." Thrombosis and Haemostasis 87, no. 05 (2002): 910–17. http://dx.doi.org/10.1055/s-0037-1613104.

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SummaryA biophysical approach tested the hypothesis that tirofiban, like eptifibatide, perturbs GpIIb/IIIa structure. Tirofiban bound tightly to platelet GpIIb/IIIa (EC50 ∼ 24 nmol/L) and effectively inhibited platelet aggregation (IC50 ∼ 37 nmol/L) but blocked platelet adhesion to clotted fibrin only at much higher doses (IC50 ∼ 580 nmol/L). Electrophoretic analyses demonstrated that tirofiban protected GpIIb/IIIa from SDSinduced subunit dissociation. However, saturating tirofiban concentrations had little or no effect on GpIIb/IIIa secondary or tertiary structure, as determined by circular dichroic spectroscopy, dynamic light scattering, and sedimentation velocity measurements performed with purified receptors in octyl glucoside. Moderate dose-dependent effects on GpIIb/IIIa quaternary structure were detected by sedimentation equilibrium. Transmission electron microscopy showed minimal tirofiban-induced receptor activation or oligomerization. Thus, even at the increased concentrations needed to block platelet:fibrin adhesive interactions, tirofiban exhibited only limited effects on GpIIb/IIIa conformation and clustering. Our results provide new insights into the mechanisms and potential prothrombotic complications of integrin antagonists.

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Zanaty, Mario, Carlos Osorno-Cruz, Stefano Byer, Jorge A. Roa, Kaustubh Limaye, Daizo Ishii, Daichi Nakagawa, et al. "Tirofiban Protocol Protects Against Delayed Cerebral Ischemia: A Case-Series Study." Neurosurgery 87, no. 5 (May 16, 2020): E552—E556. http://dx.doi.org/10.1093/neuros/nyaa170.

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Abstract BACKGROUND There has not been any effective prophylaxis for delayed cerebral ischemia delayed cerebral ischemia (DCI) since the introduction of nimodipine. Platelet inhibition may reduce the risk by preventing the formation of microthrombi. Tirofiban has been used as a single monotherapy bridge given its safety profile and controlled platelet inhibition. OBJECTIVE To assess the risk of DCI in aneurysmal subarachnoid hemorrhages (aSAH) patients treated with the tirofiban protocol. METHODS aSAH patients between December 2010 and March 2019 who were treated with stent assisted coiling or flow-diverting device were started on a continuous tirofiban infusion protocol and were compared with patients who underwent coil embolization without antiplatelet therapy. Safety analysis was performed to assess DCI, hemorrhagic, and ischemic events. RESULTS A total of 21 patients were included in the tirofiban series and 81 in the control group. There was no statistical difference in age, gender, Hunt-Hess grade, and Fisher scale between the 2 groups except for a higher Fisher grade II in the tirofiban group. Multivariate analysis revealed tirofiban to reduce the risk of vasospasm by 72 percent (OR .28, P = .03), without affecting the risk of hemorrhagic complications (OR = 0.50, P = .26). Tirofiban reduced the risk of symptomatic stroke endovascular procedure but it did not reach significance (P = .06). DCI, older age, and postprocedural symptomatic stroke were significant predictors of mortality. Tirofiban reduced the mortality risk, but this association was not statistically significant. CONCLUSION The tirofiban protocol in aSAH patients reduces the risk of DCI without conferring additional risks. This supports previous findings were antiplatelet therapy reduced DCI in human and animal models.

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Chalouhi, Nohra, Pascal Jabbour, David Kung, and David Hasan. "Safety and Efficacy of Tirofiban in Stent-Assisted Coil Embolization of Intracranial Aneurysms." Neurosurgery 71, no. 3 (June 4, 2012): 710–14. http://dx.doi.org/10.1227/neu.0b013e31826213f9.

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Abstract BACKGROUND: Thromboembolic complications are a major concern in stent-assisted coiling of intracranial aneurysms that may be prevented with adequate antiplatelet therapy. OBJECTIVE: To assess the safety and efficacy of tirofiban in stent-assisted coiling. METHODS: Two protocols were used. In the initial protocol, tirofiban was administered intravenously as a 0.4 μg/kg per min bolus for 30 minutes followed by 0.10 μg.kg−1 min−1 maintenance infusion. The revised protocol consisted of a 0.10 μg.kg−1 min−1 maintenance infusion alone. RESULTS: Sixty-seven patients received tirofiban, 16 under the initial protocol and 51 under the revised protocol. Thirty (44.8%) patients had sustained a subarachnoid hemorrhage (SAH). Tirofiban infusion was initiated after thromboembolic events in 9 (13.4%) patients and prophylactically in 58 (86.6%). Four (6.0%) intracranial hemorrhages were noted. Three (18.8%) intracranial hemorrhages occurred with the initial protocol in patients treated electively and were fatal in 2 (66.7%) cases. The only complication (1.9%) under the revised protocol was a subclinical worsening of the computed tomographic appearance of an SAH. There was no tirofiban-related morbidity or deaths with the revised protocol. Of 9 patients that received tirofiban as a rescue treatment, 7 (77.8%) had complete and 2 (22.2%) had partial arterial recanalization. No thromboembolic events occurred in patients receiving prophylactic tirofiban. CONCLUSION: A bolus followed by a maintenance dose of tirofiban appears to have a high risk of cerebral hemorrhage. A maintenance infusion without an initial bolus, however, has an exceedingly low risk of hemorrhage and appears to be very safe and effective, even in the setting of SAH.

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Mansur, Antonio de Padua, Alessandra Roggerio, Júlio Yoshio Takada, Pérola Michelle Vasconcelos Caribé, Solange Desirée Avakian, and Célia Maria Cassaro Strunz. "Gene mutations of platelet glycoproteins and response to tirofiban in acute coronary syndrome." Sao Paulo Medical Journal 134, no. 3 (January 19, 2016): 199–204. http://dx.doi.org/10.1590/1516-3180.2015.00650808.

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CONTEXT AND OBJECTIVES: Glycoprotein inhibitors (abciximab, eptifibatide and tirofiban) are used in patients with unstable angina and non-ST-segment elevation myocardial infarction before percutaneous coronary intervention. Of these, tirofiban is the least effective. We hypothesized that the response to tirofiban might be associated with glycoprotein gene mutations. DESIGN AND SETTING: Prospective study at Emergency Unit, Heart Institute (InCor), University of São Paulo. METHOD: Intrahospital evolution and platelet aggregation in response to tirofiban were analyzed in relation to four glycoprotein mutations in 50 patients indicated for percutaneous coronary intervention: 17 (34%) with unstable angina and 33 (66%) with non-ST-segment elevation myocardial infarction. Platelet aggregation was analyzed using the Born method. Blood samples were obtained before and one hour after tirofiban infusion. Glycoproteins Ia (807C/T ), Ib (Thr/Met) , IIb (Ile/Ser ) and IIIa (PIA ) were the mutations selected. RESULTS: Hypertension, dyslipidemia, diabetes, smoking, previous coronary artery disease and stroke were similar between the groups. Mutant glycoprotein IIIa genotypes had lower platelet aggregation before tirofiban administration than that of the wild genotype (41.0% ± 22.1% versus 55.9% ± 20.8%; P = 0.035). Mutant glycoprotein IIIa genotypes correlated moderately with lower platelet inhibition (r = -0.31; P = 0.030). After tirofiban administration, platelet glycoprotein Ia, Ib, IIb and IIIa mutations did not influence the degree of inhibition of platelet aggregation or intrahospital mortality. CONCLUSIONS: Mutations of glycoproteins Ia, Ib, IIb and IIIa did not influence platelet aggregation in response to tirofiban in patients with unstable angina and non-ST-segment elevation myocardial infarction.

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Jagroop, I. Anita, and Dimitri P. Mikhailidis. "The Effect of Tirofiban on Fibrinogen/Agonist-Induced Platelet Shape Change and Aggregation." Clinical and Applied Thrombosis/Hemostasis 14, no. 3 (June 19, 2008): 295–302. http://dx.doi.org/10.1177/1076029608316014.

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There is evidence linking raised plasma fibrinogen (fib) and platelet hyperactivity with vascular events. One way to inhibit platelets is to block the platelet membrane glycoprotein (GP) IIb/IIIa receptor, which binds circulating fib or von Willebrand factor and cross-links platelets at the final common pathway to platelet aggregation. Tirofiban is a potent and specific fib receptor antagonist, used in the treatment of unstable angina. The authors assessed the effect of tirofiban on spontaneous platelet aggregation (SPA), fib-induced, serotonin (5HT)-induced, and adenosine diphosphate (ADP)-induced aggregation in whole blood by calculating the percentage free platelet count. These various agonists were used alone and in combination. The authors also measured the effect of tirofiban on agonists-induced (ADP, 5HT) platelet shape change (PSC). The effect of fib on PSC was also evaluated in platelet-rich plasma using a high-resolution (0.07 fL) channelyzer. Tirofiban significantly inhibited SPA, fib (2, 4, 8 g/L), ADP, ADP + fib combination, and 5HT-induced aggregation. Tirofiban had no effect on agonist-induced PSC. There was no apparent change in platelet volume with fib. In conclusion, tirofiban does not appear to have an effect on PSC, an early phase of platelet activation. Tirofiban seems to be a nonspecific and an effective inhibitor of platelet aggregation (a later phase of platelet activation) in whole blood. The clinical significance of these findings remains to be established.

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K, Thamayanthi, Arun Ranganathan, and Vasanthira K. "EFFECT OF TIROFIBAN ON THE OUTCOME DURING HOSPITALIZATION IN PATIENTS WITH ACUTE CORONARY SYNDROME AN OBSERVATIONAL STUDY." Asian Journal of Pharmaceutical and Clinical Research 11, no. 8 (August 7, 2018): 388. http://dx.doi.org/10.22159/ajpcr.2018.v11i8.26065.

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Objective: The present study was intended to know the effect of tirofiban on the prognostic outcome of patients with acute coronary syndrome (ACS) during their stay in the hospital.Methods: Registers and case sheets of patients admitted for ACS during May 2014–April 2015 were analyzed retrospectively. The duration of stay in hospital/Intensive Care Unit (ICU) and the outcomes were recorded in patients who received tirofiban. ACS patients who did not receive tirofiban served as control. During the study period, there were 720 patients with ACS, and among them, 216 did not receive tirofiban and 504 patients received tirofiban.Results: ICU stay (days, mean±standard deviation [SD]) for tirofiban group was longer (2.5±0.5) when compared to the controls (1.5±0.5). However, this was not statistically significant. The duration of hospitalization (days, mean±SD) was not significantly different in both groups (6±0.81 vs. 6±0.82). None of the patients developed reinfarction or persistent pain during their stay in the hospital. There were no major adverse events with tirofiban.Conclusion: Therefore, it was concluded that tirofiban does not affect the outcome during hospitalization in patients with ACS.

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Fang, Ching-Chang, Fresner Yeun Tarl, Yi Chen, Ching-Lung Yu, and Shih-Pu Wang. "Glycoprotein IIb/IIIa Inhibitor (Tirofiban) in Acute ST-Segment Elevation Myocardial Infarction." Angiology 60, no. 2 (April 29, 2008): 192–200. http://dx.doi.org/10.1177/0003319708316168.

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Studies have shown conflicting results for glycoprotein IIb/IIIa inhibitor (tirofiban) use in ST-segment elevation myocardial infarction (STEMI). The authors aimed to determine if an upstream conventional dose of tirofiban in addition to a standard treatment regimen improved coronary patency and clinical outcomes in patients with STEMI. A retrospective analysis of consecutive patients with STEMI, who underwent emergent percutaneous coronary intervention (PCI) in the authors' hospital from July 2000 to April 2006 was performed. All patients received loading doses of aspirin, clopidogrel or ticlopidine, and unfractionated heparin with or without tirofiban in the emergency department prior to PCI. It was found that adding a conventional dose of tirofiban to the standard treatment regimen prior to PCI did not improve coronary patency in STEMI patients. Tirofiban also failed to show favorable outcomes for 90 days of follow-up, but there was a favorable trend for short-term 30-day survival.

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Zhang, Jing, and Guomin Ding. "Improved Cardiac Function and Attenuated Inflammatory Response by Additional Administration of Tirofiban during PCI for ST-Segment Elevation Myocardial Infarction Patients." Evidence-Based Complementary and Alternative Medicine 2021 (June 16, 2021): 1–9. http://dx.doi.org/10.1155/2021/8371996.

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ST-segment elevation myocardial infarction (STEMI) is one of the acute coronary syndromes, and it is the main cause of cardiac death worldwide. The purpose of this study was to investigate whether tirofiban improves cardiac function and attenuates inflammatory response in STEMI patients undergoing percutaneous coronary intervention (PCI). From May 2016 to May 2019, a total of 124 patients who admitted into our hospital due to STEMI fulfilled inclusion and exclusion criteria and were randomly assigned to PCI + tirofiban and PCI groups, 62 cases per groups. Intravenous administration of 10 μg kg−1 min−1 tirofiban was performed 30 min prior to PCI. During PCI, tirofiban infusion through a micropump with 0.15 μg kg−1 min−1 lasted for 48 h. It was found that the PCI + tirofiban group was significantly different from the PCI group in total corrected TIMI frame count (CTFC) after PCI (15.88 ± 5.11 vs. 22.47 ± 6.26, P < 0.001 ). At day 7 and day 30 post-PCI, a significant time-dependent decrease in the levels of brain natriuretic peptide (BNP), cardiac troponin I (cTnI), and creatine kinase isoenzyme (CK-MB) in both groups was observed after PCI ( P < 0.001 ). More importantly, the patients in the PCI + tirofiban group had much lower levels of BNP, cTnI, and CK-MB compared with those in the PCI group at days 7 and 30 post-PCI ( P < 0.001 ). At day 7 following PCI, the left ventricular ejection fraction (LVEF) was statistically higher in the PCI + tirofiban group than in the PCI group ( P < 0.05 ). At day 30 post-PCI, increased LVEF concomitant with reduced left ventricular end diastolic diameter (LVEDD) and left ventricular end systolic diameter (LVESD) was observed in the PCI + tirofiban group compared with the PCI group. At day 7 and day 30 post-PCI, both groups displayed a time-dependent decline in the levels of C reactive protein (CRP), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and procalcitonin (PCT) after PCI ( P < 0.05 ). Additionally, the patients in the PCI + tirofiban group had lower levels of CRP, TNF-α, IL-6, and PCT compared with those in the PCI group at days 7 and 30 post-PCI ( P < 0.05 ). All patients in the PCI + tirofiban and PCI groups were followed up for 12 months by outpatient or telephone after discharge. There were fewer patients with LVEF < 50% in the PCI + tirofiban group than the PCI group ( P = 0.044 ). Furthermore, it was found that the incidence rate of major adverse cardiovascular events (MACEs) in the PCI + tirofiban group was evidently lower than that in the PCI group (12.90% vs. 29.03%, P = 0.028 ). Taken together, our data suggest that additional administration of tirofiban could improve cardiac function and attenuate inflammatory response in STEMI patients undergoing PCI, which is worthy of promotion in clinic.

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&NA;. "Enoxaparin sodium/tirofiban." Reactions Weekly &NA;, no. 772 (October 1999): 8. http://dx.doi.org/10.2165/00128415-199907720-00026.

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Cook, Jacquelynn J., Bohumil Bednar, Joseph J. Lynch, Robert J. Gould, Melissa S. Egbertson, Wasyl Halczenko, Mark E. Duggan, et al. "Tirofiban (Aggrastat®)." Cardiovascular Drug Reviews 17, no. 3 (June 7, 2006): 199–224. http://dx.doi.org/10.1111/j.1527-3466.1999.tb00015.x.

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&NA;. "Alteplase/heparin/tirofiban." Reactions Weekly &NA;, no. 1414 (August 2012): 8–9. http://dx.doi.org/10.2165/00128415-201214140-00018.

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Cheng, Liang, Tingxiang Chen, Hang Li, Zhenghua Feng, Zhijie Li, and Dingsheng Lin. "Effects of Tirofiban on Random Skin Flap Survival in Rats." Journal of Reconstructive Microsurgery 34, no. 02 (October 9, 2017): 138–44. http://dx.doi.org/10.1055/s-0037-1607304.

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Background Tirofiban is a glycoprotein IIb/IIIa receptor antagonist that is widely used clinically. In the present study, we investigated whether tirofiban promotes flap survival in rat random skin flap model. Methods “McFarlane flaps” models were developed in 60 male rats. The rats were divided into a tirofiban-treated group (n = 30) and a saline-treated group (n = 30). The flap surviving rate was calculated 7 days after surgery. Tissue samples were collected and subjected to histopathological evaluation. Lead oxide–gelatin angiography and immunohistochemical staining analysis were taken to evaluate angiogenesis. Analysis of oxidative stress was performed by measuring the activity of superoxide dismutase (SOD) and malondialdehyde (MDA). Results Compared with controls, the tirofiban-treated groups exhibited significantly larger mean areas of flap survival, significantly increased SOD activity, and vascular endothelial growth factor (VEGF) expression, and significantly reduced MDA level. Hematoxylin and eosin staining revealed that naringin promoted angiogenesis and inhibited inflammation. Conclusion These findings demonstrate that tirofiban increases flap survival of random skin flaps in rats.

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Moriguchi, Akira, Masashi Maeda, Kayoko Mihara, Toshiaki Aoki, Nobuya Matsuoka, and Seitaro Mutoh. "FK419, a Novel Nonpeptide GPIIb/IIIa Antagonist, Restores Microvascular Patency and Improves Outcome in the Guinea-Pig Middle Cerebral Artery Thrombotic Occlusion Model: Comparison with Tirofiban." Journal of Cerebral Blood Flow & Metabolism 25, no. 1 (January 2005): 75–86. http://dx.doi.org/10.1038/sj.jcbfm.9600009.

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The antithrombotic efficacy of FK419, a novel nonpeptide platelet glycoprotein IIb/IIIa antagonist, was compared with tirofiban in guinea-pigs. FK419 and tirofiban similarly inhibited platelet aggregation in vitro (IC50 values: 0.43 ± 0.076 and 0.41 ± 0.053 μmol/L) and dispersed aggregated platelets (EC50 values: 2.3 ± 0.88 and 2.0 ± 0.81 μmol/L). FK419 inhibited retention of platelets and neutrophils in a collagen-coated bead column with greater potency than tirofiban (IC50 values of 0.90 ± 0.133 and 2.4 ± 0.21 μmol/L for platelet retention and 0.32 ± 0.078 and 0.57 ± 0.180 μmol/L for neutrophil retention). When FK419 or tirofiban were administered after photochemically induced middle cerebral artery (MCA) occlusion in guinea-pigs, they dose-dependently improved MCA patency. FK419 reduced neurological deficits and ischemic brain damage in a dose-dependent fashion, whereas tirofiban did not. Reduced regional cerebral blood flow in the striatum gradually returned to the preoccluded level with FK419 treatment; however, no restoration was observed with tirofiban even though the MCA was recanalized. These results indicate that FK419 ameliorates ischemic brain damage by not only lysing the obstructive thrombus in MCA but also preventing or restoring microcirculation deficits after occlusion/reperfusion, suggesting that FK419 would be an attractive intervention for the treatment of ischemic stroke patients.

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Zi-Liang, Wang, Liang Xiao-Dong, Li Tian-Xiao, Zhu Liang-Fu, Xue Jiang-Yu, Bai Wei-Xing, He Ying-Kun, et al. "Intravenous administration of tirofiban versus loading dose of oral clopidogrel for preventing thromboembolism in stent-assisted coiling of intracranial aneurysms." International Journal of Stroke 12, no. 5 (November 4, 2016): 553–59. http://dx.doi.org/10.1177/1747493016677989.

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Background Thromboembolic complications after stenting of intracranial aneurysms may be affected by antiplatelet administration. Aims This retrospective study aimed to assess the safety of intravenous tirofiban versus loading dose of oral clopidogrel for preventing thromboembolism in stent-assisted coiling of intracranial aneurysms. Methods From January 2006 to December 2013, 281 patients with cerebral aneurysms were treated with stent-coiling using two antiplatelet strategies in comparison: the initial strategy (a loading dose of ≥300 mg clopidogrel followed by dual antiplatelet, clopidogrel group) and the modified strategy (intravenous administration of tirofiban 8 µg/kg over 3 min followed by a maintenance dose of 0.1 µg/kg/min for 24 h, tirofiban group). The end points were rates of perioperative thromboembolic events and intracranial hemorrhages. Results Thromboembolic events were observed more often in the clopidogrel group (13/120 aneurysms, 10.83%) than the tirofiban group (6/178 aneurysms, 3.37%; P = 0.010), with no increase in the rate of intracranial hemorrhages ( P = 0.164). In the ruptured subgroups, thromboembolic events were significantly fewer in the tirofiban subgroup (5/128, 3.91%) compared with the clopidogrel subgroup (7/53, 13.21%; P = 0.043) with no increase in the rate of hemorrhage ( P = 0.360). Conclusions Intravenous administration of tirofiban is safe in intracranial aneurysms treated with stent-assisted coiling.

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Canedo, Leonardo F., Marcel Autran C. Machado, Ana M. M. Coelho, Sandra N. Sampietre, Telesforo Bachella, and Marcel C. C. Machado. "Efeito protetor de antagonista das gliproteínas IIb/IIa nas alterações hepáticas e pulmonares secundárias à isquemia e reperfusão do fígado em ratos." Arquivos de Gastroenterologia 44, no. 3 (September 2007): 276–81. http://dx.doi.org/10.1590/s0004-28032007000300018.

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RACIONAL: A lesão de isquemia e reperfusão hepática é um evento comum e responsável por considerável morbidade e mortalidade. OBJETIVO: Avaliar efeitos de inibidor da glicoproteína IIb/IIIa, cloridrato de tirofiban, nas alterações hepáticas e pulmonares da lesão de isquemia e reperfusão de fígado de ratos. MÉTODO: Vinte e três ratos Wistar divididos em três grupos: laparotomia (n = 6), isquemia e reperfusão que receberam solução fisiológica (n = 8), e submetidos a isquemia e reperfusão e tratados com o cloridrato de tirofiban (n = 9). Foram realizadas dosagens das aminotransferases e análise histológica hepática. Avaliação pulmonar foi realizada pelo teste do azul de Evans e pela dosagem tecidual da mieloperoxidase no parênquima pulmonar. A oxidação e fosforilação mitocondrial das células hepáticas também foram avaliadas. RESULTADOS: O grupo tratado com cloridrato de tirofiban apresentou menores níveis de aminotransferases, assim como alterações histológicas menos intensas. Avaliação pulmonar demonstrou diminuição no teste de azul de Evans no grupo tratado com cloridrato de tirofiban. Grupo tratado com cloridrato de tirofiban apresentou aumento significativo do estado 3 da respiração mitocondrial e das relações adenosina difosfato utilizado para fosforilação sobre o oxigênio consumido na reação e de coeficiente respiratório. CONCLUSÕES: O uso do cloridrato de tirofiban exerceu papel protetor da lesão hepática de isquemia e reperfusão e impediu o aumento da permeabilidade vascular secundária à lesão de reperfusão hepática.

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Journal articles on the topic 'Tirofiban'

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