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Data from 67 patients with intermittent claudication taking part in a randomised controlled trial and who received clopidogrel in addition to aspirin was analysed.
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Novel adenosine diphosphate (ADP) P2Y(12) antagonists such as prasugrel, ticagrelor, cangrelor, and elinogrel are in various phases of clinical development. These ADP P2Y(12) antagonists have advantages over clopidogrel ranging from faster onset to greater and less variable inhibition of platelet function. Novel ADP P2Y(12) antagonists are under investigation to determine whether their use can result in improved antiplatelet activity, faster onset of action, and/or greater antithrombotic effects than clopidogrel without an unacceptable increase in hemorrhagic or other side effects. Prasugrel (CS-747; LY-640315), a novel third-generation oral thienopyridine, is a specific, irreversible antagonist of the platelet ADP P2Y(12) receptor. Pre-clinical and early phase clinical studies have shown prasugrel to be characterized by more potent antiplatelet effects, lower inter-individual variability in platelet response, and faster onset of activity compared to clopidogrel. Recent findings from large-scale phase-III testing show prasugrel to be more efficacious in preventing ischemic events in acute coronary syndrome patients undergoing percutaneous coronary intervention (PCI); however, this is achieved at the expense of an increased risk of bleeding. Prasugrel provides more rapid and consistent platelet inhibition than clopidogrel.
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Oral antiplatelet therapy is routinely administered to ACS patients as well as to patients undergoing percutaneous coronary intervention (PCI) with the primary aim of inhibiting platelet-mediated thrombus formation and subsequent abrupt vessel occlusion. Individual platelet response to aspirin and especially to clopidogrel is highly variable and evidence has grown in recent years linking an attenuated response to therapy with the occurrence of ischemic events. At present, the antiplatelet therapy landscape is changing with the emergence of prasugrel and ticagrelor as alternative and more potent treatment options. In addition, tests for near-patient monitoring of platelet function in clinical practice are available and are being increasingly employed for the optimization of antiplatelet treatment. It is hypothesized that platelet function testing may prove useful for achieving an optimized balance of proven platelet inhibition at a cost of moderate bleeding risk. This is also why first centers have already included testing in day-to-day routine. Extensive clinical evaluations with a range of currently-available assays for platelet function testing are ongoing and the current and future role of platelet function testing in clinical practice is a topic of much debate. Widespread adoption of this practice and its incorporation into clinical guidelines awaits the results of ongoing trials where treatment is changed based on platelet function testing data. This review paper summarizes the key characteristics of platelet function tests available, presents an overview of relevant studies and examines the present role of platelet function testing in clinical practice with a focus on antiplatelet therapy in patients undergoing coronary stent placement.
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Clinical studies have reported a clustering of thrombotic events after stopping clopidogrel treatment. The hypothesis of a rebound phenomenon of platelets has been declared causative, but its existence has never been confirmed. Tapering of clopidogrel over a certain period of time before stopping the drug completely might provide a way to attenuate this supposed phenomenon.
A retrospective chart review was performed on patients taking AC/AP agents who were undergoing transconjunctival sutureless vitrectomies with subconjunctival anesthesia between January 2007 and June 2009. Intra- and postoperative complications (such as massive hemorrhage), anatomical results, satisfactory analgesia (informed by patients and recorded by surgeon), anatomical results, and visual acuity were documented.
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The prevalence of patent foramen ovale among patients with cryptogenic stroke is higher than that in the general population. Closure with a percutaneous device is often recommended in such patients, but it is not known whether this intervention reduces the risk of recurrent stroke.
Randomized trials of clopidogrel, prasugrel, or ticagrelor that examined clinical outcomes among subgroups of smokers and nonsmokers.
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We included patients admitted in a 24-month period. During the first 12-month period, the patients received tirofiban and clopidogrel (group A). In the second one, clopidogrel was not administered (group B). Urgent cardiac catheterism was requested if recurrent ischemic chest pain with ST segment changes, left ventricular failure or hemodynamic instability were present. PRIMARY VARIABLES: A composite of recurrent ischemic chest pain with ST segment changes or death during ICCU admission was evaluated as an efficacy variable. A variable of safety was defined as the occurrence of intracranial or gastrointestinal bleeding, or any hemorrhagic event accompanied by a drop of at least 3 g/dl of hemoglobin. The rate of urgent cardiac catheterisms was recorded.
The mean perioperative blood loss was 899±496 ml for patients not on clopidogrel, 1091±654 ml for patients on clopidogrel (p=0.005) and 1312±686 ml for those on combined clopidogrel and aspirin (p=0.0003 vs. all others). Increased blood loss was also associated with a shorter time to operation (p=0.0012) and prolonged surgical time (p=0.0002). There were no cases of mortality in the early postoperative period.
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Stopping aspirin intake within the first 72 hours of the acute stroke drastically increases TXA2 synthesis. During the same time window, the freshly prescribed clopidogrel manages to reduce the ADP-induced aggregation only slightly (13%). This study offers analytic proof that the common practice of replacing aspirin with clopidogrel does not leave stroke patients fully protected during the first days after an ischemic stroke. Possible solutions could be to preserve aspirin during a few days or to use loading doses of clopidogrel at hospital admission.
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Anticoagulation therapy during percutaneous coronary intervention (PCI) has been the focus of numerous clinical trials. Low-anticoagulant doses have been successfully used in patients undergoing elective PCI, a situation with low-thrombogenic milieu.
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An 82-year-old female with an extensive history of coronary disease who had undergone placement of a drug-eluting stent was admitted following continued problems with her surgically repaired right hip. Radiographic imaging of the area revealed mechanical failure of the surgically repaired hip, requiring intervention. Clopidogrel and aspirin therapy was discontinued and intravenous eptifibatide 1 μg/kg/min was initiated prior to surgery; the drugs were then discontinued 4 hours before the procedure. During this admission, the patient received a total of 155 hours of eptifibatide to prevent acute coronary stent thrombosis while awaiting surgical intervention. Postoperatively, the patient experienced anemia and severe thrombocytopenia and required 11 units of packed red blood cells, but displayed no signs of stent thrombosis.
Patients with coronary artery disease who undergo stent implantation and have concomitant indication for long-term oral anticoagulation represent a considerable proportion of the overall population. To date there is still no consensus about the optimal antithrombotic strategy to choose in this kind of patients, due to the difficult balance between an increased risk of bleeding and thromboembolic complications. Therefore, the aim of this study was to perform a meta-analysis to evaluate the risk and benefits of triple antithrombotic therapy versus dual antithrombotic therapy in patients undergoing coronary stent implantation, requiring long-term oral anticoagulation.
Patients with CKD exhibit increased platelet activation, and an attenuated response to dual antiplatelet therapy compared with patients without renal insufficiency.
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A case of rhabdomyolysis occurring shortly after the addition of ranolazine to a stable simvastatin regimen is reported.
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We performed a systematic review to define the relative and absolute risk of clinically relevant adverse events with the antiplatelet agents, aspirin and clopidogrel.
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Increasing evidence suggests that angiotensin converting enzyme (ACE) inhibitors exert antithrombotic effects. Based on the assumption of differential effects of various ACE inhibitors on coagulation, the aim of the present study was to evaluate the coagulative activities of cardiovascular (CV) patients treated with either ramipril, captopril, and enalapril, and to compare these with patients treated with established antithrombotics such as aspirin (ASA) and clopidogrel or none of these medication.
All consecutive patients (pts) included in the Portuguese Registry on Acute Coronary Syndromes (ProACS) between January 1, 2002 and August 31, 2011 were analysed. Compliance with Guidelines for the management of NSTE-ACS was evaluated with a 6-point therapeutic score (ThSc), comprising the treatment with: aspirin, clopidogrel, heparin, beta-blocker, angiotensin-converting enzyme inhibitor and statin. One point was assigned for each drug prescribed and zero if not given. The total therapeutic compliance was defined as ThSc =6 points.
Clopidogrel improves outcomes in patients with ST-segment elevation myocardial infarction (STEMI) and is recommended in the guidelines. We sought to determine the incremental cost-effectiveness of clopidogrel therapy in this patient population. We used primary patient-level resource use and clinical outcomes data from 3491 STEMI patients treated with fibrinolysis and either clopidogrel or placebo prior to a diagnostic coronary angiogram in the Clopidogrel as Adjunctive Reperfusion Therapy-Thrombolysis in Myocardial Infarction 28 (CLARITY-TIMI 28) trial. Costs for each patient were calculated based on diagnosis-related groups-specific Medicare reimbursement rates for all hospitalizations and the average wholesale price of clopidogrel. Cost per event prevented and cost per life year gained (LYG) were calculated using standard methods. The estimate of LYG due to clopidogrel therapy was based on recurrent myocardial infarction and death outcomes. The bootstrap method was used to produce bias-corrected confidence intervals for cost and efficacy estimates as well as the cost per LYG ratio. Total costs and resource use were not significantly different for the clopidogrel and placebo groups ($8128 vs. $8134), indicating that short-term clopidogrel therapy is an economically dominant treatment strategy. Even in a sensitivity analysis accounting for higher long-term medical costs due to greater life expectancy, clopidogrel remained under $6000 per LYG. Clopidogrel therapy was dominant in 35% of the bootstrap simulations and cost less than $50,000 per LYG in 67% of simulations. In conclusion, this analysis finds short-term clopidogrel therapy to be a highly economically attractive therapy, improving patient outcomes at no increase in costs.
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AZD6140 exhibited greater mean inhibition of platelet aggregation than a standard regimen of clopidogrel in ACS patients. In addition, AZD6140 further suppressed platelet aggregation in clopidogrel pretreated patients.
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A double maintenance dose of clopidogrel at 150 mg daily was associated with a reduction in adenosine diphosphate-induced platelet aggregation in South Korean patients who previously exhibited clopidogrel resistance.
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Clopidogrel coprescription with low-dose ASA increased from 1.6% to 25.2% between the two study periods; PPI coprescription increased from 11.6% to 28.3%. Low-dose ASA indications of myocardial infarction [odds ratio (OR) 11.7, 95% confidence interval (CI) 10.2 to 13.4] and unstable angina (OR 1.73, 95%CI 1.09 to 2.75) were positive predictors of clopidogrel coprescription in 2006-2007, relative to chronic ischaemic heart disease. Patients at high risk of upper gastrointestinal bleeding were more likely to receive a PPI than those at lower risk in 2006-2007 (OR 4.36, 95%CI 3.93 to 4.84). In this period, 65.5% of patients who required a clopidogrel coprescription according to guideline recommendations received one, and 44.3% of patients at high risk of upper gastrointestinal bleeding received a PPI.
About 40% of clopidogrel-treated patients display high platelet reactivity (HPR). Alternative treatments of HPR patients, identified by platelet function tests, failed to improve their clinical outcomes in large randomized clinical trials. A more appealing alternative would be to identify HPR patients a priori, based on the presence/absence of demographic, clinical and genetic factors that affect PR. Due to the complexity and multiplicity of these factors, traditional statistical methods (TSMs) fail to identify a priori HPR patients accurately. The objective was to test whether Artificial Neural Networks (ANNs) or other Machine Learning Systems (MLSs), which use algorithms to extract model-like 'structure' information from a given set of data, accurately predict platelet reactivity (PR) in clopidogrel-treated patients.
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Three hundred and twenty-two patients with (n = 74) or without (n = 248) bleeding (anterior segment, choroidal, intravitreal and/or subretinal) during or after RD surgery were included in this case-control study. Exclusion criteria were: history of trauma, vitreoretinal surgery, diabetic retinopathy, and taking clopidogrel and/or a vitamin K antagonist. Univariate and multivariate analyses were performed to identify risk factors of perioperative bleeding.
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A total of 20 patients with AD and CVD were randomly assigned to a cilostazol group (n=11, 100 mg daily) or control group (n=9, aspirin 100 mg or clopidogrel 50 mg-75 mg daily) for 6 months.