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      Bivalirudin plus loading dose of cilostazol-based triple-antiplatelet in treatment of non-ST-elevation myocardial infarction following percutaneous coronary intervention

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          Abstract

          Objective

          To study the effect of bivalirudin plus loading dose of cilostazol-based triple-antiplatelet therapy strategy in patients undergoing percutaneous coronary intervention (PCI).

          Methods

          One hundred and fifty-three patients with non-ST-segment elevation myocardial infarction who underwent PCI were divided into control group and cilostazol group. Patients in control group were given aspirin and clopidogrel and those in cilostazol group were given aspirin, clopidogrel, and cilostazol once 2 hours before PCI and for 30 days after PCI. Bivalirudin was given to all patients before and during the PCI.

          Results

          After PCI, the Thrombolysis In Myocardial Infarction myocardial perfusion grade (TMPG) III in cilostazol group was higher than that in control group (89.19% versus 72.15%, P<0.05). At 30 days, the incidence of major adverse cardiac events was significantly lower in cilostazol group compared with that in control group (6.76% versus 17.72%, P<0.05). However, the rates of cardiac death, nonfatal reinfarction, target vessel revascularization, new congestive heart failure, and subacute stent thrombosis did not significantly differ between the two groups. In addition, the rates of minor or major bleeding or thrombocytopenia did not significantly differ between the two groups.

          Conclusion

          Bivalirudin plus loading dose of cilostazol-based triple-antiplatelet therapy strategy in PCI increased TMPG III, decreased major adverse cardiac events, and did not increase the incidence of bleeding and thrombocytopenia.

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          Most cited references 20

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          Bivalirudin during primary PCI in acute myocardial infarction.

          Treatment with the direct thrombin inhibitor bivalirudin, as compared with heparin plus glycoprotein IIb/IIIa inhibitors, results in similar suppression of ischemia while reducing hemorrhagic complications in patients with stable angina and non-ST-segment elevation acute coronary syndromes who are undergoing percutaneous coronary intervention (PCI). The safety and efficacy of bivalirudin in high-risk patients are unknown. We randomly assigned 3602 patients with ST-segment elevation myocardial infarction who presented within 12 hours after the onset of symptoms and who were undergoing primary PCI to treatment with heparin plus a glycoprotein IIb/IIIa inhibitor or to treatment with bivalirudin alone. The two primary end points of the study were major bleeding and combined adverse clinical events, defined as the combination of major bleeding or major adverse cardiovascular events, including death, reinfarction, target-vessel revascularization for ischemia, and stroke (hereinafter referred to as net adverse clinical events) within 30 days. Anticoagulation with bivalirudin alone, as compared with heparin plus glycoprotein IIb/IIIa inhibitors, resulted in a reduced 30-day rate of net adverse clinical events (9.2% vs. 12.1%; relative risk, 0.76; 95% confidence interval [CI] 0.63 to 0.92; P=0.005), owing to a lower rate of major bleeding (4.9% vs. 8.3%; relative risk, 0.60; 95% CI, 0.46 to 0.77; P<0.001). There was an increased risk of acute stent thrombosis within 24 hours in the bivalirudin group, but no significant increase was present by 30 days. Treatment with bivalirudin alone, as compared with heparin plus glycoprotein IIb/IIIa inhibitors, resulted in significantly lower 30-day rates of death from cardiac causes (1.8% vs. 2.9%; relative risk, 0.62; 95% CI, 0.40 to 0.95; P=0.03) and death from all causes (2.1% vs. 3.1%; relative risk, 0.66; 95% CI, 0.44 to 1.00; P=0.047). In patients with ST-segment elevation myocardial infarction who are undergoing primary PCI, anticoagulation with bivalirudin alone, as compared with heparin plus glycoprotein IIb/IIIa inhibitors, results in significantly reduced 30-day rates of major bleeding and net adverse clinical events. (ClinicalTrials.gov number, NCT00433966 [ClinicalTrials.gov].). Copyright 2008 Massachusetts Medical Society.
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            The Thrombolysis in Myocardial Infarction (TIMI) trial. Phase I findings. TIMI Study Group.

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              CYP2C19 genotype, clopidogrel metabolism, platelet function, and cardiovascular events: a systematic review and meta-analysis.

              The US Food and Drug Administration recently recommended that CYP2C19 genotyping be considered prior to prescribing clopidogrel, but the American Heart Association and American College of Cardiologists have argued evidence is insufficient to support CYP2C19 genotype testing. To appraise evidence on the association of CYP2C19 genotype and clopidogrel response through systematic review and meta-analysis. PubMed and EMBASE from their inception to October 2011. Studies that reported clopidogrel metabolism, platelet reactivity or clinically relevant outcomes (cardiovascular disease [CVD] events and bleeding), and information on CYP2C19 genotype were included. We extracted information on study design, genotyping, and disease outcomes and investigated sources of bias. We retrieved 32 studies of 42,016 patients reporting 3545 CVD events, 579 stent thromboses, and 1413 bleeding events. Six studies were randomized trials ("effect-modification" design) and the remaining 26 reported individuals exposed to clopidogrel ("treatment-only" design). In treatment-only analysis, individuals with 1 or more CYP2C19 alleles associated with lower enzyme activity had lower levels of active clopidogrel metabolites, less platelet inhibition, lower risk of bleeding (relative risk [RR], 0.84; 95% CI, 0.75-0.94; absolute risk reduction of 5-8 events per 1000 individuals), and higher risk of CVD events (RR, 1.18; 95% CI, 1.09-1.28; absolute risk increase of 8-12 events per 1000 individuals). However, there was evidence of small-study bias (Harbord test P = .001). When analyses were restricted to studies with 200 or more events, the point estimate was attenuated (RR, 0.97; 95% CI, 0.86-1.09). In effect-modification studies, CYP2C19 genotype was not associated with modification of the effect of clopidogrel on CVD end points or bleeding (P > .05 for interaction for both). Other limitations included selective outcome reporting and potential for genotype misclassification due to problems with the * allele nomenclature for cytochrome enzymes. Although there was an association between the CYP2C19 genotype and clopidogrel responsiveness, overall there was no significant association of genotype with cardiovascular events.
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                Author and article information

                Journal
                Ther Clin Risk Manag
                Ther Clin Risk Manag
                Therapeutics and Clinical Risk Management
                Therapeutics and Clinical Risk Management
                Dove Medical Press
                1176-6336
                1178-203X
                2015
                28 September 2015
                : 11
                : 1469-1473
                Affiliations
                Department of Cardiology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, People’s Republic of China
                Author notes
                Correspondence: Yongjun Li, Department of Cardiology, The Second Hospital of Hebei Medical University, Shijiazhuang, 215 Hepingxi Road, Shijiazhuang, Hebei 050000, People’s Republic of China, Tel +86 311 6600 2126, Fax +86 311 6600 2126, Email liyongjun@ 123456fexmail.cn
                Article
                tcrm-11-1469
                10.2147/TCRM.S86799
                4592053
                © 2015 Wang et al. This work is published by Dove Medical Press Limited, and licensed under Creative Commons Attribution – Non Commercial (unported, v3.0) License

                The full terms of the License are available at http://creativecommons.org/licenses/by-nc/3.0/. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

                Categories
                Original Research

                Medicine

                triple-antiplatelet therapy, bivalirudin, percutaneous coronary intervention

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