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We retrospectively identified patients who had aspirin and P2Y12 assays at the time of stenting. Aspirin (325 mg) and clopidogrel (75 mg) were started 7-10 days pre-intervention. If not possible, aspirin (650 mg) and clopidogrel (600 mg) loading doses were given pre-intervention. Assays were checked on postoperative day 0/1. Outcomes included neurological ischemic sequela at 30 days, 1 and 2 years, as well as 30 day death/hemorrhage/myocardial infarction.
While the data on the risk of late stent thrombosis are not definitive, several general conclusions may be drawn from the available data. Late thrombosis, while associated with high mortality and morbidity, is an uncommon complication of both drug-eluting stents and bare metal stents. Randomized trials of approved drug-eluting stents versus bare metal stents have shown additional cases of late stent thrombosis in drug-eluting stents, but no significant difference in the cumulative incidence of stent thrombosis, myocardial infarction, or cardiac death at 4 years of follow-up. Observational studies suggest higher very late stent thrombosis incidence, but the relative risks of drug-eluting stents versus bare metal stents in specific high-risk groups require further study. Although the etiology of late stent thrombosis is multifactorial, premature discontinuation of clopidogrel appears to be the most important risk factor.
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Platelet activation is a major component in the pathogenesis of coronary thrombosis and myocardial infarction. Therefore, antiplatelet therapy has become the cornerstone in the therapy of ischemic heart disease. Thienopyridines, especially clopidogrel, have a highly significant effect on treated patients with regard to reduction of stent thrombosis and functional inhibition of adenosine diphosphate-(ADP-)induced platelet activation. Clopidogrel, a specific inhibitor of the P2Y(12) ADP receptor, is a prodrug which releases the active compound after metabolization. Actual ACC/AHA/SCAI guidelines recommend the use of 75 mg clopidogrel once daily after stent implantation. Nevertheless, there is a high incidence of impaired clopidogrel responsiveness in patients potentially leading to subacute stent thrombosis and other adverse cardiovascular events following coronary interventions (incidence of about 1% within the first 4 weeks). Therefore, individual risk testing and adjusted antiplatelet therapy might be recommendable under certain circumstances, e.g., high-risk interventions such as last patent vessel, dominant vessel, or planned drug-eluting stent implantation. Furthermore, identification of a nonresponder requires increased clinical attention. Newly developed antiplatelet substances might overcome the nonresponse problem and allow sufficient platelet inhibition in all patients. Further prospective studies are needed to determine the risk reduction by an individually adjusted antiplatelet therapy.
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We compared the effects of a 600- versus a 300-mg LD of clopidogrel on inhibition of platelet aggregation, myonecrosis, and clinical outcomes in patients with NSTEACS undergoing an early invasive management strategy. Patients with NSTEACS (n = 256, mean age 63 years, 81.6% elevated troponin) without thienopyridine for at least 7 days were randomized to receive 600- or 300-mg LD of clopidogrel. Percutaneous coronary intervention was performed in 140 patients, with glycoprotein IIb/IIIa inhibitor use in 68.6%. Adenosine diphosphate (ADP)-induced platelet aggregation was measured by optical platelet aggregometry immediately before coronary angiography.
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Diabetes mellitus is an independent predictor of adverse clinical events after drug-eluting stent implantation.
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Coronary revascularization with conventional CABG has the best evidence for improving outcome in patients with ischemic heart disease. Three main complications after CABG are myocardial infarction, heart failure and atrial fibrillation. Although preoperative statin and aspirin therapy are established treatment for post CABG myocardial infarction when to stop and restart aspirin is still debatable. Evidence on the use of clopidogrel and prasugrel may be unfavourable but ticagrelor may be beneficial. In post CABG heart failure mixture of GIK, changing the cardioplegic solution and careful intra-operative management to reduce myocardial stunning may prove beneficial. Intra aortic balloon pump and ischemic preconditioning have shown benefit in the postoperative heart failure. Instead of post hoc treatment for atrial fibrillation new upstream therapies are available.
Methyl (R)-o-chloromandelate (R-CMM) is an intermediate for the platelet aggregation inhibitor clopidogrel. Its preparation through enzymatic resolution of the corresponding ester has been hindered by the lack of an enzyme with satisfying enantioselectivity and activity. In the present work, we aimed to improve the enzymatic enantioselectivity towards methyl (S)-o-chloromandelate (S-CMM) by rational design, using esterase BioH as a model enzyme. Based on the differences in the binding mode of S- and R-enantiomers at the active cavity of the enzyme, the steric and electronic interactions between the key amino acids of BioH and the enantiomers were finely tuned. The enantioselectivity of esterase BioH towards S-CMM was improved from 3.3 (the wild type) to 73.4 (L123V/L181A/L207F). Synergistic interaction was observed between point mutations, and insight into the source of enzymatic enantioselectivity was gained by molecular dynamics simulations. The results can provide a reference for the enzyme design of other enzymes towards S-CMM for the enhancement of enantioselectivity.
Traditionally, unfractionated heparin has been the most commonly used parenteral anticoagulant, but owing to its variable dose response and narrow therapeutic indices, it is being replaced by low molecular weight heparin, fondaparinux, and bivalrudin. New oral factor Xa inhibitors like apixaban and rivaroxaban are still on the horizon, awaiting definite evaluation in ACS, DVT and atrial fibrillation. On the contrary, a dramatic advance in the arena of oral anticoagulants has occurred with the introduction of dabigatran, an oral direct thrombin inhibitor. This agent showed better outcomes than oral vitamin K antagonists in patients with atrial fibrillation. The antiplatelet field has also expanded by the addition of two new agents, prasugrel and ticagrelor. These agents have been tested against clopidogrel, in patients with ACS, with superior efficacy outcomes for both agents and higher bleeding events with prasugrel.
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Thrombin-activatable fibrinolysis inhibitor (TAFI) is a plasma carboxypeptidase that renders a fibrin-containing thrombus less sensitive to lysis. In the present study, we describe the development of a murine model of vena cava thrombosis and its use to characterize the antithrombotic activity of potato carboxypeptidase inhibitor (PCI) of TAFIa (activated TAFI) in mice.
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The composite endpoint of cardiovascular adverse events occurred more often in patients with high platelet reactivity (HPR) to both agonists ADP and AA (37.5%) than in those with isolated HPR to ADP (33.3%), AA (25.6%) or without any HPR (18.6%; p=0.003). Classification tree analysis indicated that any HPR emerged as an independent predictor influencing outcome, which was associated with a 1.75 higher risk of cardiac adverse events (OR=1.75: 95%CI=1.1-2.9). Interestingly, the predictive value of HPR tended to be greater among patients with diabetes mellitus (OR=2.18; 95%CI=1.20-3.95). C-reactive protein and diabetes mellitus were independent predictors of high platelet reactivity to both agonists.
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We conducted a retrospective study using the GP computer database (Hatfield, UK) on all 9400 patients to assess the quality of anticoagulation in patients with a recorded diagnosis of AF.
There were 44 patients in the esomeprazole group and 44 in the famotidine group. The baseline PRUs of the 2 groups were comparable (esomeprazole vs famotidine, 229.1 ± 85.6 vs 220.4 ± 83.0, P = .63). The PRUs on day 28 were 242.6 ± 89.7 and 237.5 ± 79.2 in the groups receiving esomeprazole and famotidine, respectively (mean difference 5.1, 95% CI -30.8 to 41.0, P = .78).
The following features of inhospital management of pts diagnosed as ACS at CCU (or its equivalent) admission could be object of improvement: low rate of reperfusion therapy and use of PCI, long interval between admission and initiation of PCI, insufficient use of some standard medications, frequent use of subcutaneous UFH, rare transferal of PCI eligible pts from noninvasive to invasive hospitals. However existing management was associated with reported low hospital mortality in patients labeled as NSTEACS.
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Ticagrelor has a greater antiplatelet efficacy than clopidogrel but may be accompanied by an increased risk of bleeding. This study evaluated the antiplatelet effect and pharmacokinetic profile of low-dose ticagrelor in healthy Chinese volunteers. Thirty healthy subjects were randomized to receive standard-dose ticagrelor (180-mg loading dose, 90-mg twice daily [bid] [n = 10]), low-dose ticagrelor (90-mg loading dose, 45-mg bid [n = 10]), or clopidogrel (600-mg loading dose, 75-mg once daily [n = 10]). Platelet reactivity was assessed by using the VerifyNow P2Y12 assay at baseline and 0.5, 1, 2, 4, 8, 24, 48, and 72 hours post-dosing. The ticagrelor and AR-C124910XX concentrations were measured for pharmacokinetic analysis. The percentage inhibition of P2Y12 reaction units was higher in the low-dose and standard-dose ticagrelor group than in the clopidogrel group at 0.5, 1, 2, 4, 8, and 48 hours post-dosing (P < 0.05 for all), but did not differ significantly between the two ticagrelor doses at any time-point (P > 0.05). The plasma ticagrelor and ARC124910XX concentrations were approximately 2-fold higher with standard-dose versus low-dose ticagrelor. No serious adverse events were reported. In conclusion, low-dose ticagrelor achieved faster and higher inhibition of platelet functions in healthy Chinese subjects than did clopidogrel, with an antiplatelet efficacy similar to that of standard-dose ticagrelor.
Predictive scores are important tools for stratifying patients based on the risk of future (cerebro)vascular events and for selecting potential prevention therapy. Recently, the Essen Stroke Risk Score (ESRS) was derived from cerebrovascular patients in the Clopidogrel versus Aspirin in Patients at Risk of Ischemic Events (CAPRIE) trial. We aimed to validate the ESRS in a large cohort of outpatients with previous transient ischemic attack or stroke from the REduction of Atherothrombosis for Continued Health (REACH) Registry.
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Heightened platelet activity plays a critical role in thrombus formation, which is central to acute coronary syndromes (ACS), including non-ST-segment elevation (NSTE)-ACS (comprising unstable angina pectoris and non-ST-segment elevation myocardial infarction [NSTEMI]) and ST-segment elevation myocardial infarction (STEMI), and has been implicated in poor clinical outcome. Platelets not only impact coronary thrombus but are major contributors to microcirculatory dysfunction and vascular inflammation. Efforts to inhibit platelet function, including antiplatelet therapy, are paramount to the management of ACS; thus, a growing recognition of the various pathways driving platelet activity has given rise to the need for multiple agents that impart complimentary mechanisms of action. While only inhibiting platelet activation will still allow for aggregation, i.e. the binding of glycoprotein (GP) IIb/IIIa receptors to fibrinogen, solely blocking aggregation may leave platelet-activating pathways free to sustain the production and release of various pro-inflammatory and pro-thrombotic compounds. The benefit of 'triple antiplatelet therapy', referring to the combination of aspirin, a thienopyridine or non-thienopyridine adenosine diphosphate (ADP)/P2Y12 receptor blocker and a GPIIb/IIIa inhibitor (GPI), has been demonstrated in patients with NSTE-ACS who ultimately undergo percutaneous coronary intervention (PCI) and are determined to be at an elevated risk for ischaemic events, and in patients undergoing primary PCI. It is therefore recommended by the European Society of Cardiology (ESC) and American College of Cardiology/American Heart Association. Furthermore, the rationale for adding a GPI, particularly in patients with STEMI, is backed by studies that have shown negligible effects of a 600 mg clopidogrel loading dose, despite being administered 4 hours prior to PCI. Moreover, it has been observed that the physiological state of STEMI may deem dual antiplatelet therapy ineffective, because during an acute event the absorption of clopidogrel may be impaired. Nonetheless, there is still considerable variability with respect to the use of triple antiplatelet therapy such as that documented in the Euro Heart Survey. The perception that the mortality benefit afforded by adding a GPI to dual oral antiplatelet therapy does not outweigh the risk is a likely factor. This may be fuelled by results of trials such as BRAVE-3, which, inconsistent with those for On-TIME 2, failed to prove the value of adding a GPI to dual oral antiplatelet therapy in patients with STEMI. Subsequent analyses have indeed demonstrated the positive benefit-risk ratio associated with adding a GPI and determined that the timing of GPI administration could have an impact on clinical outcome related to its impact on infarct size in patients with STEMI. Additionally, it has been presumed that a synergistic effect exists between P2Y12 inhibitors and GPIs. Triple antiplatelet therapy has a significant role to play in the management of patients with ACS managed with PCI. An understanding of patient risk status and timing of symptoms and bleeding risk is crucial to patient selection and ensuring that this therapy is optimized. Though no interaction has been noted in trials of newer, more potent antiplatelet agents, future studies are key to determining the role of this strategy in the era of these more potent agents.
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There was no difference in major bleeding complications overall or when ticagrelor or clopidogrel was used in accordance with guidelines. In patients on dual antiplatelet medication up to 1 day before surgery, there tended to be more bleeding complications in ticagrelor-treated patients.
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We report a case of epidural hematoma formation in the cervical spine following interlaminar epidural steroid injection in an elderly woman with chronic neck and arm pain, who was on clopidogrel therapy.
In addition to P2Y12 receptor antagonism, ticagrelor inhibits adenosine cell uptake. Prior data show that 7-day pretreatment with ticagrelor limits infarct size. We explored the acute effects of ticagrelor and clopidogrel on infarct size and potential long-term effects on heart function.
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Low response to antiplatelet agents has been associated to an increased risk of thrombotic complications and recurrent ischemic events. Platelet size has been proposed as a potential marker of platelet reactivity. Therefore, the aim of the present study was to evaluate the impact of platelet Larger Cell Ratio (p-LCR) on platelet aggregation and the prevalence of residual high-on treatment platelet reactivity (HRPR) in patients receiving dual antiplatelet therapy (DAPT) after a recent acute coronary syndrome or coronary revascularization.
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Our aim was to evaluate the effects of single and dual antiplatelet treatment on postoperative bleeding in patients having dental extractions. The prospective clinical study included 160 patients who were taking antiplatelet drugs. The first group (n=43) were taking 2 drugs, mostly aspirin and clopidogrel, and the second group (n=117) were taking a single antiplatelet drug in the form of aspirin (n=84), clopidogrel (n=20), and ticlopidine (n=13). All patients had simple dental extractions, and local haemostasis was with resorbable collagen sponges, without suturing of the wound. The control group comprised 105 healthy subjects with a similar number of dental extractions. Bleeding was an "event" if it continued for more than 12h, made the patient call or return to the dental practice or emergency department, induced a large haematoma or ecchymosis within the oral soft tissues, or required blood transfusion. A total of 110 teeth were extracted on 59 occasions in the dual drug group, and 232 teeth on 128 occasions in the single drug group. Bleeding was recorded after extraction in only one patient on dual aspirin-clopidogrel treatment, which was mild and easily controlled by local haemostasis. The incidence of postoperative bleeding did not differ significantly among the three groups (χ(2)=4.3, p=0.11). However, the wound was sutured to achieve effective initial local haemostasis in 4/59 (6.8%) and 2/128 (1.6%) occasions of tooth extractions in the dual and single drug groups, respectively, and none in the control group (χ(2)=10.02, p=0.007). Patients taking single or dual antiplatelet drugs may have teeth extracted safely without interruption of treatment using only local haemostatic measures.
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Because of the known CYP3A4 inhibition by calcium-channel blockers (CCBs), we hypothesized that there might be a drug-drug interaction between clopidogrel and dihydropyridines in patients with coronary artery disease.
This study indicates that a loading dose of ticagrelor does not significantly reduce post- PCI myonecrosis. Diabetes is associated with more post-PCI myonecrosis. A loading dose of ticagrelor effectively reduces platelet aggregation in diabetic patients.
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A 62-year-old man with a history of coronary artery disease, multiple acute coronary syndromes requiring percutaneous coronary interventions with multiple stent placements, and acute stent thrombosis resulting in ST segment elevation myocardial infarction presented to the hospital with chest pain. The chest pain was not relieved by 4 sublingual nitroglycerin tablets. Five days prior to his presentation, the patient had been instructed to discontinue both aspirin and clopidogrel in preparation for a left ankle fusion procedure. He was taken to the cardiac catheterization laboratory where he was found to have thrombosis in a sirolimus-eluting stent placed more than 3 years ago. Thrombectomy and balloon angioplasty were performed, and the patient completed his hospital course without complications.
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The strategy of leaving a mechanical heart valve in place at the time of LVAD implantation in five patients led to valvular thrombosis in three but did not provoke embolic events. It increased the complexity of postoperative anticoagulation.