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ClinicalTrials.gov identifier: NCT00699998.
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Current guidelines recommend use of a proton pump inhibitor (PPI) to decrease the risk of gastrointestinal bleeding in patients taking clopidogrel (Plavix) with aspirin. A recent issue of The Medical Letter considered whether omeprazole (Prilosec, and others) or other PPIs could interfere with the antiplatelet effect of clopidogrel. The conclusion was that patients taking both drugs should probably continue to do so until more data became available. Several new publications require reconsideration of that recommendation.
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This survey was performed in 102 level 2 hospitals from 15 provinces or autonomous region in China. Patients admitted to these hospitals with acute coronary syndrome during September 2011 to May 2012 were eligible for this study. Information on TCM use was obtained from their medical records. Chi-square test and logistic regression analysis were used to explore the related factors of TCM use in these patients.
Those of us who see patients with cardiovascular disorders frequently use antiplatelet and anticoagulant agents; the common agents are aspirin, clopidogrel, and warfarin. This editorial is a personal viewpoint about commonly used drugs, not so commonly used drugs, and drugs that are yet to be used clinically.
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Polypharmacy in patients undergoing coronary artery stenting or in those presenting with an acute coronary syndrome is common. Nevertheless, the risk of drug-drug interactions in patients treated simultaneously with P2Y12 receptor inhibitors is less well considered in routine clinical practice. Whereas the irreversible P2Y12 receptor inhibitors clopidogrel and prasugrel are prodrugs requiring cytochrome P450 (CYP) enzymes for metabolic activation, such activation is not necessary for the direct-acting reversible P2Y12 receptor inhibitor ticagrelor. Several drugs frequently used in cardiology have been shown to interact with the metabolism of P2Y12 receptor inhibitors in pharmacodynamic studies. Whereas several drug-drug interactions have been described for clopidogrel and ticagrelor, prasugrel seems to have a low potential for drug-drug interactions. The clinical implications of these interactions have raised concern. In general, concomitant administration of P2Y12 receptor antagonists and strong inhibitors or inducers of CYP3A/CYP2C19 should be performed with caution in patients treated with clopidogrel/ticagrelor. Under most circumstances, clinicians have the option of prescribing alternative drugs with less risk of drug-drug interactions when used concomitantly with P2Y12 receptor inhibitors.
EUCLID is a randomized, double-blind, parallel-group, multinational clinical trial designed to evaluate the efficacy and safety of ticagrelor compared with clopidogrel for the prevention of major adverse cardiovascular events in subjects with symptomatic PAD. Subjects with established PAD will be randomized in a 1:1 fashion to ticagrelor 90 mg twice daily or clopidogrel 75 mg daily. The primary end point is a composite of cardiovascular death, myocardial infarction, or ischemic stroke. Other end points address limb events including acute leg ischemia, need for revascularization, disease progression by ankle-brachial index, and quality of life. The primary safety objective is Thrombolysis in Myocardial Infarction-defined major bleeding. Recruitment began in December 2012 and was completed in March 2014; 13,887 patients were randomized. The trial will continue until at least 1,364 adjudicated primary end points occur.
Neovascularisation is mainly mediated by vascular endothelial growth factor (VEGF). Bevacizumab is a monoclonal antibody specific for VEGF. We assessed the safety of a bevacizumab-eluting stent, a dedicated stent for inhibition of plaque neovascularisation.
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Combined prescription has decreased since the first warning, above all in patients with a primary circulatory heart disease. Omeprazole is a potent CYP2C19 inhibitor, so it was used in lower rates than pantoprazole in association with clopidogrel. Medical departments related to cardiovascular disease followed the warning more than others.
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The efficacy and safety of ENOX and clopidogrel given together in STEMI remains to be defined.
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Retrospective cohort study of 8205 patients with ACS taking clopidogrel after discharge from 127 Veterans Affairs hospitals between October 1, 2003, and January 31, 2006. Vital status information was available for all patients through September 30, 2006.
Data were independently collected and verified by two reviewers. Data from different trials were pooled where appropriate.
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Proton pump inhibition (PPI) administrated together with adenosine diphosphate (ADP) receptor blockers (ADPRB) significantly reduces the risk of gastrointestinal bleeding. Nevertheless, there is a heated discussion about an interaction between PPI and ADPRB that leads to high on-treatment platelet reactivity (HTPR).
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The management of unstable angina/non ST elevation myocardial infarction (UA/NSTEMI) has evolved substantially in recent years. Multiple new antithrombotic options are available; in addition, the use of interventional strategies in patients with UA/NSTEMI has become the dominant strategy, particularly in tertiary centers. On the one hand, we are doing more percutaneous interventions more rapidly in ACS patients. On the other hand, we have an ever-expanding therapeutic armamentarium to apply in these complex clinical circumstances. Much of the controversy surrounding modern-day management is not so much about the specific the choice of agent or strategy, but rather how to use these agents most effectively in a clinical environment where patients may come forward to the catheterization laboratory, sometimes rapidly, and may require percutaneous or surgical revascularization. All available antithrombotic agents act on one (or more) of the four steps of coagulation: platelet activation, platelet aggregation, thrombin generation, and thrombin activity. The antiplatelet agents, aspirin, thieno-pyridines, and glycoprotein (GP) IIb/IIIa antagonists, target the early steps of platelet activation and aggregation. The antithrombin agents, unfractionated heparin, low molecular weight (LMW) heparin, Xa inhibitors, and direct thrombin antagonists, act specifically to target thrombin generation, thrombin activity, or both. We will review the major recent trials that comprise the current state of knowledge regarding these new antithrombotic agents in ACS, and discuss some of the near-future additions to our armamentarium, including prasugrel, Cangrelor, and AZD6140. The most recent ACC/AHA and ESC unstable angina guidelines have emphasized that multiple options are available, and no one agent can be recommended over the others in all cases. There is NOT one perfect antithrombotic regimen for all patients. Antithrombotic therapy needs to be individualized, and that so-called ''standard'' therapy may need to be supplemented (or even replaced) in specific circumstances. Ultimately, determining optimal therapy means understanding the physiology, understanding the therapeutic options - not just how they work, but how they may work together, and being able to interpret a never-ending supply of new clinical trial data that have to be applied in the ''real world''.
MGuard based PCI of NC and VG appears encouraging especially in view of unfavorable patient and lesion characteristics. Efficacy needs to be further established in larger randomized trials.
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We analysed 2995 consecutive PPCI patients enrolled in the Clinical Center of Serbia STEMI Register, between February 2007 and March 2012. All patients were pretreated with 600 mg clopidogrel and 300 mg aspirin. Major adverse cardiovascular events, comprising all-cause death, nonfatal infarction, nonfatal stroke, and ischaemia-driven target vessel revascularization, was the primary efficacy end point. TIMI major bleeding was the key safety end point.
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Eighty-four patients were randomized into four treatment groups: prasugrel 10/2.5mg (loading dose [LD]/maintenance dose [MD]), 15/3.75 mg or 20/5mg, and clopidogrel 300/75 mg. The LD of each regimen was administered the day before PCI, followed by 28-day MD on aspirin background therapy (81-100mg). Antiplatelet effects were evaluated by light transmission aggregometry and VASP assay. The mean inhibition of platelet aggregation (IPA) induced by 20 μM of adenosine diphosphate at 4 hours after LD was higher among the prasugrel 10/2.5mg, 15/3.75 mg and 20/5mg groups compared with the clopidogrel group (12.3%, 20.9%, 29.8% vs. 8.4%, respectively). The proportion of subjects with an IPA of <10% on Day 28 was lower among the prasugrel 15/3.75 mg, and 20/5mg groups than in the clopidogrel group (0%, 6.3% vs. 15.8%, respectively). No "major" or "clinically relevant non-major" bleeding was observed.
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To determine the effect of various SNPs on post-clopidogrel platelet reactivity and clinical outcome.
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This is the largest population-scale genetic epidemiology study that provides a high-resolution map of variants associated with clopidogrel response that could be potentially valuable to clinicians to rationally plan appropriate dosage for therapy in resource poor conditions based on population level allele frequencies.
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Aspirin utilisation increased by 19.55% (95% CI: 19.39-19.70), clopidogrel by 2.93% (95% CI: 2.88-2.97) and dipyridamole decreased by 0.65% (95% CI: -0.70 to -0.59). Utilisation of aspirin with clopidogrel increased by 1.78% (95% CI: 1.74-1.81) and aspirin with dipyridamole increased by 0.54% (95% CI: 0.50-0.58%).Warfarin decreased by 0.87% (95% CI: -0.96 to -0.78) and dabigatran increased by 0.65% (95% CI: 0.60-0.70). Statins increased by 7.0% (95% CI: 6.82-7.18) and bisphosphonates decreased by 2.37% (95% CI: -2.44 to -2.30). Aspirin, clopidogrel, dabigatran and statins utilisation showed a greater increase in males. Interestingly, clopidogrel, warfarin and statins use increased in older adults aged 85+ compared to the younger age groups (65-84 years).
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Major adverse cardiovascular events occurred in 19 patients (8.6%), including 14 patients with periprocedural MI and 5 patients with stroke. Correlations were weak between the 2 tests in the arachidonic acid-induced (Spearman r = 0.189, P = .006) and ADP-induced platelet reactivity (Spearman r = 0.390, P < .001). Although the VerifyNow P2Y12 Assay (Accumetrics) was able to predict periprocedural MI (area under the aggregation curve 0.680, P = .024) and 30-day MACE (area under the aggregation curve 0.649, P = .032), VerifyNow Aspirin Assay (Accumetrics), MEA ASPI test, and MEA ADP test failed to predict such clinical events. Hyporesponsiveness to clopidogrel based on the VerifyNow Assay was associated with about a 6-fold increased risk of MACE at 30 days.