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Plavix (Clopidogrel)

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Plavix is the medication of high quality which is taken in treatment of heart attacks and strokes by preventing blood clots. It is also taken to prevent other heart or blood vessels disorders. Plavix is acting by preventing blood clots.

Other names for this medication:

Similar Products:
Argatroban, Salagen, Arixtra, Persantine


Also known as:  Clopidogrel.


Plavix target is the treatment of heart attacks and strokes by preventing blood clots. It is also taken to prevent other heart or blood vessels disorders.

Plavix is acting by preventing blood clots. It is antiplatelet agents.

Plavix is also known as Clopidogrel, Clopitab, Caplor, Iscover, Clopilet, Ceruvin.

Generic name of Plavix is Clopidogrel.

Brand name of Plavix is Plavix.


Take Plavix at the same time every day, with or without food.

Take Plavix tablets orally with water.

If you want to achieve most effective results do not stop taking Plavix suddenly.


If you overdose Plavix and you don't feel good you should visit your doctor or health care provider immediately. Symptoms of Plavix overdosage: vomiting, abnormal bleeding or bruising, problems with breathing.


Store at room temperature between 15 and 30 degrees C (59 and 86 degrees F) away from moisture and heat. Throw away any unused medicine after the expiration date. Keep out of the reach of children in a container that small children cannot open.

Side effects

The most common side effects associated with Plavix are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.


Do not take Plavix if you are allergic to Plavix components.

Do not take Plavix if you're pregnant or you plan to have a baby, or you are a nursing mother.

Be careful with Plavix if you suffer from or have a history of stroke, stomach ulcer or ulcerative colitis; liver or kidney disease, hemophilia.

Be careful with Plavix if you are taking such medicines as aspirin or other NSAIDs (non-steroidal anti-inflammatory drugs such as naproxen (Aleve, Naprosyn), diclofenac (Voltaren), diflunisal (Dolobid), etodolac (Lodine), flurbiprofen (Ansaid), indomethacin (Indocin), ibuprofen (Motrin, Advil), (Toradol), ketoprofen (Orudis), nabumetone (Relafen), piroxicam (Feldene), ketorolac mefenamic acid (Ponstel), meloxicam (Mobic) and the others), phenytoin (such as Dilantin); torsemide (such as Demadex); medication used to prevent blood clots (alteplase (such as Activase), anistreplase (such as Eminase), dipyridamole (such as Persantine), streptokinase (such as Kabikinase, Streptase), ticlopidine (Ticlid) and urokinase (such as Abbokinase); fluvastatin (such as Lescol); a blood thinner (warfarin (such as Coumadin), heparin, ardeparin (such as Normiflo), dalteparin (such as Fragmin), danaparoid (such as Orgaran), enoxaparin (such as Lovenox), or tinzaparin (such as Innohep); tamoxifen (such as Nolvadex); tolbutamide (such as Orinase).

It is not recommended to do sport while taking Plavix because it can cause bleeding or bruising injury.

If you are going to have a surgery you should stop taking Plavix for 5 days before the surgery.

Do not use potassium supplements or salt substitutes.

If you want to achieve most effective results without any side effects it is better to avoid alcohol.

Do not stop taking Plavix suddenly.

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Observational design, selection bias of study cohort.

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Thienopyridines are metabolized to active metabolites that irreversibly inhibit the platelet P2Y(12) adenosine diphosphate receptor. The pharmacodynamic response to clopidogrel is more variable than the response to prasugrel, but the reasons for variation in response to clopidogrel are not well characterized.

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Clopidogrel is a prodrug that has to be converted in vivo to its active metabolite by cytochrome (CYP)P450 iso-enzymes. As calcium channel blockers (CCBs) are inhibitors of CYP3A4, concomitant use of these drugs might play a role in the wide inter-individual variability in the response to clopidogrel. However, some CCBs also have strong inhibitory effects on the drug transporter P-glycoprotein (Pgp), which mediates clopidogrel's intestinal absorption. It was the aim of this study to evaluate the effect of co-administration of Pgp-inhibiting and non-Pgp-inhibiting CCBs on on-clopidogrel platelet reactivity in patients on dual antiplatelet therapy undergoing elective percutaneous coronary intervention (PCI). In a total of 623 consecutive patients undergoing elective PCI treated with clopidogrel and aspirin, platelet reactivity to 5 and 20 muM adenosine diphospate (ADP) and clopidogrel poor-response (defined as > 70% platelet aggregation to 20 muM ADP) were evaluated by light transmittance aggregometry. A total of 222 patients (35.6%) were on CCB treatment, of which 98 used Pgp-inhibiting CCBs (verapamil, nifedipine, diltiazem, barnidipine) and 124 patients used the non-Pgp-inhibiting CCB amlodipine. Adjusted mean ADP-induced on-clopidogrel platelet reactivity was significantly higher in both users of Pgp-inhibiting CCBs and amlodipine as compared to CCB non-users (all p<0.05). However, only the use of amlodipine was significantly associated with a 2.3-fold increased risk of clopidogrel poor-response. This study demonstrates that concomitant use of Pgp-inhibiting CCBs and amlodipine increases on-clopidogrel platelet reactivity. Only amlodipine was associated with clopidogrel poor-response. The drug-drug interaction between clopidogrel and amlodipine might be more clinically relevant as compared to P-glycoprotein-inhibiting CCBs.

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The present work identifies decreased platelet miR-223 expression as a novel mechanism involved in blunted platelet response to clopidogrel in a Chinese population.

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Vorapaxar, a novel antiplatelet thrombin protease-activated receptor 1 (PAR-1) inhibitor, has been evaluated in the successful TRA2P trial and failed TRACER trial. The drug is currently approved for post myocardial infarction and peripheral artery disease indications on top of clopidogrel and/or aspirin. The stroke data after vorapaxar are mixed, dominated with heavy excess of intracranial bleeding risks and slightly worsened second stroke rates, but show less primary ischemic strokes. Fortunately, these conflicting data do not belong purely to vorapaxar per se but rather, reflect unreasonably aggressive strategies, including predominantly triple antiplatelet therapy, utilized in both Trial to Assess the Effects of SCH 530348 in Preventing Heart Attack and Stroke in Patients with Arteriosclerosis (TRA2P) and especially in Thrombin-Receptor Antagonist Vorapaxar in Acute Coronary Syndromes (TRACER). The FDA-confirmed evidence strongly suggests that unique pharmacokinetics and a very mild "comfort zone" antiplatelet profile makes vorapaxar a good candidate for improved secondary stroke prevention. The outcome-driven, randomized trial should test head-to-head monotherapy with vorapaxar (Zontivity®) versus clopidogrel (Plavix®) and versus dipyridamole with very low dose aspirin (Aggrenox®). The advantages and potential pitfalls of such a trial are discussed in this article.

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Transcatheter aortic valve implantation (TAVI) has been adopted worldwide as the standard treatment for severe aortic stenosis in symptomatic patients at prohibitive or high surgical risk, but there are still several areas where consensus and evidence are lacking. The purpose was to obtain a global view of current practice related to TAVI with the potential to identify the main areas of consensus and divergence between centers.

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A 35-year-old man with primary antiphospholipid syndrome and no risk factors for atherosclerosis presented with postinfarction angina.

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TAVR is a new technology that compresses a tissue valve onto an expandable stent. Technical and procedural issues have been solved, but strokes and major bleeding still affect patients' life despite double antiplatelet therapy given to reduce MACCE. To balance pros and cons, antithrombotic therapy with Warfarin or new anticoagulants can be used in patients with previous AF or NOAF to prevent stroke; while single antiplatelet with PPI is a better alternative in patients with liver disease, gastric ulcer or drug abuse to avoid bleeding events. While waiting for randomized trials, a tailored therapy based upon physician's experience and close patient follow-up is the safest, most effective treatment.

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Direct caroticocavernous fistula (CCF) has traditionally been treated by detachable balloon placement within the affected cavernous sinus. We describe a case of a direct CCF treated solely with flow-diverting stents. These novel devices may offer a simpler and potentially safer vessel-sparing option in this rare condition.

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There is some controversy as to whether tirofiban or eptifibatide, two small anti-aggregating drugs (AAD), may reduce the incidence of composite ischemic events within one year in patients undergoing percutaneous coronary intervention (PCI) in the real clinical world.

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One hundred fifty-three elective percutaneous coronary intervention patients were randomized to clopidogrel 150 mg/day (n = 58) or 75 mg/day (n = 95) for 4 weeks, with vasodilator-stimulated phosphoprotein assay-guided switching to clopidogrel 150 mg/day after 2 weeks in low responders (platelet reactivity index >or=69%). All patients received aspirin 75 mg/day.

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Discussion of a patient with non-ST elevation ACS illustrates some of the clinical issues surrounding PCI and stent implantation, including selection and use of antiplatelet therapy.

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CYP2C19*2 genotype was associated with diminished platelet response to clopidogrel treatment and poorer cardiovascular outcomes.

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We included eight RCTs involving 625 participants. Only one study was judged as 'low risk' of bias. There were insufficient published data from the eight studies for all planned primary and secondary outcomes. No patients died from ischemic stroke or from adverse drug effects, bleeding or infections among the 444 participants in the six studies where these outcomes were reported. Statin treatment did not reduce all-cause mortality compared with placebo or no treatment (OR 1.51, 95% CI 0.60 to 3.81) in the 431 patients enrolled in seven studies. No cases of rhabdomyolysis (the breakdown of muscle fibres resulting in the release of muscle fibre contents (myoglobin) into the bloodstream) occurred in 274 patients enrolled in three studies.

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The above in vivo data suggest that the inactive metabolite displaces the active metabolite from binding sites. Thus, the inactive metabolite might increase the free concentration of the active metabolite leading to enhanced inhibition of platelet aggregation. The plasma protein binding mechanism would offer an additional therapeutic strategy to optimize clopidogrel pharmacotherapy.

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The incidence of MACE in patients undergoing NCS after previous PCI is high in spite of adequate perioperative antiplatelet therapy.

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Three thousand and eighty confirmed ACS patients enrolled in this registry were followed up for 1 year at 3-month intervals. Patient data on medical interventions as well as clinical events were recorded and analyzed by descriptive statistics.

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We found no association between discharge clopidogrel use and long-term risk of major adverse cardiac events among older, unrevascularized non-ST-segment elevation myocardial infarction patients. Clopidogrel use in this population requires further prospective evaluation.

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Dual antiplatelet therapy is associated with increased rates of intracerebral hemorrhage, especially in the context of subarachnoid hemorrhage. We present a case of a spontaneous hemorrhage in a patient treated with a Pipeline stent for a ruptured dissecting vertebrobasilar aneurysm and the novel use of direct application of platelets during surgery to control bleeding.

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This article provides an overview of the available antiplatelet pharmacogenetics literature. Evidence supporting the significance of candidate genes and their potential influence on antiplatelet response and clinical outcomes are summarized and evaluated. Additional focus is directed at CYP2C19 and clopidogrel response, including the availability of clinical testing and genotype-directed antiplatelet therapy.

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We included 2099 patients, with a mean age of 64 (SD=13) years, 69% males. In our sample, 55.1% presented with ST-segment elevation ACS and 13.1% in Killip class ≥ 2. Only 25% were known diabetic at admission. In-hospital mortality was 5.8% and 9.7% at one-year follow-up. The best cut-point for blood glucose was 160 mg/dl (sensitivity 62% and specificity 68%), and 35.2% of the patients had increased levels. This group was elderly, had more prevalence of cardiovascular risk factors, worse renal function and GRACE score as well as more frequently Killip class ≥2. Treatment was similar in both groups besides less frequent use of clopidogrel in high glycaemic patients. The hyperglycaemia group had higher one-year mortality (17.2% vs. 5.6%, p<0.001). Moreover, binary blood glucose remained a predictor of death independently of the GRACE risk score and the presence of diabetes (odds ratio (OR) 1.99, 95% CI 1.40-2.84, p<0.001). The inclusion of blood glucose, as a continuous variable, in a logistic regression model with GRACE score, increased the area under the ROC curve from 0.80 to 0.82 (p=0.018) as well as the goodness-of-fit and was associated with an improvement in both the NRI (37%) and the IDI (0.021), suggesting effective reclassification.

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Data were collected from 100 dentists. Of these, 17 had no knowledge of coronary stents, but only one did not interrupt dual therapy: 12 consulted a cardiologist and the remaining four discontinued therapy themselves. Of the 83 who knew about stents, only 28 (34%) understood the difference between bare metal and drug-eluting stents. The drug clopidogrel's name was known by 21%, while 60% recognized one of the drug's commercial names and 45% recognized the other. Of the 83 aware of stents, 48 (58%) knew of the possibility of stent thrombosis, but only three knew about possible mortality. Cardiologists were consulted before dental procedures in 83% of cases. Only 36% knew about the existence of the guidelines.

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Surgery increased TG in vascular-patients despite intra-operative unfractioned heparin administration when compared to orthopedic patients (MRI:P=0.039, ETP:P=0.001, PGT:P=0.003), but this perioperative prothrombotic status was reversed by postoperative thromboprophylaxis. No thromboembolic events were observed. Similar TG parameter values between the 8th and 32nd postoperative day indicate that vascular patients were adequately protected after prophylaxis withdrawal, probably due to the synergic action of clopidogrel, while orthopedic patients increased TG on day-32 compared to the 8th postoperative day (P=0.03, for both lag-time and ttPeak). Furthermore, on day-32, a prothrombotic status (increased TG) was observed in the orthopedic patients (P=0.034, and 0.004 for ttPeak and lag-time, respectively). Inter-individual variability to enoxaparin response was observed in both groups:7/15 vascular and 10/15 orthopedic patients increased TG despite anticoagulant administration, which reveals heparin-resistance. Among the heparin-resistant patients, 4 vascular and 6 orthopedic increased TG after anticoagulant withdrawal, depicting a rebound effect to activation of coagulation.

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After undergoing routine EMG, if any of seven predetermined high-risk muscles were tested, study subjects then underwent ultrasound to evaluate for hematoma formation.

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A 48-year-old man was admitted to our cardiac catheterization unit with severe chest pain 75 minutes after onset of symptoms. Two years before he had undergone percutaneous coronary intervention (PCI) for stable angina pectoris with implantation of a drug-eluting stent (TAXUS) into the proximal left anterior descending artery. Antiplatelet therapy with 75 mg clopidogrel was given for one year, together with 100 mg aspirin. Subsequently he was put on low-dose aspirin monotherapy. Eight days before admission aspirin was discontinued because a tooth extraction was planned.

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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.

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A total of 68 (65%) of the 104 enrolled patients were carriers of the CYP2C19 reducedfunction allele. On-clopidogrel platelet aggregation (PA), measured using light transmittance aggregometry and the VerifyNow(®) P2Y12 system, and the platelet reactivity index (PRI) were significantly higher at all time points in the carriers than in the noncarriers (p<0.05), whereas there were no differences in the levels of the coagulation and inflammatory biomarkers or serum hs-TnT. Simple and multiple logistic regression analyses identified on-clopidogrel PA and PRI as being significant predictors of carriers of the CYP2C19 reduced-function allele.

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Several methods provide new insights into understanding clinical trial composite endpoints, using both conventional and novel methods. The TRILOGY ACS trial is used as a contemporary example to prospectively compare these methods side by side.

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Patients with atrial fibrillation usually are elderly and may have cognitive dysfunction. These patients may receive less effective oral anticoagulation, resulting in more vascular events and bleeding.

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Combined antiplatelet agents (cAPA), aspirin plus clopidogrel, increase the risk of bleeding. We hypothesised that recombinant activated FVIIa (rFVIIa), which normalises thrombin generation in platelet-rich plasma from patients treated with cAPA, could limit this bleeding risk. It was the objective of this study to investigate the efficacy and safety of rFVIIa compared to placebo, in a bleeding and thrombosis model in rabbits treated with aspirin and clopidogrel. New-Zealand rabbits, randomised into two groups (Placebo1, n=36 ; cAPA, n=34), were anaesthetised, ventilated and monitored for blood pressure, temperature and carotid blood flow. The Folts model was applied to a carotid artery. Cyclic flow reductions (CFR) were recorded over a first 20-min period (Obs1). Each rabbit was then randomly assigned into one of three subgroups (Placebo2, 40μg/kg rFVIIa, 160 μg/kg rFVIIa) and CFR were monitored for a second 20-min period (Obs2). Ear bleeding time (BT) was measured at the end of each period. Hepatosplenic (HS) section was performed at the end of the experiment and HS blood loss defines the primary endpoint. Secondary endpoints were thrombosis (CFR), prothrombin time, platelet aggregation, and thrombin generation. Non- parametric statistical tests were used (p<0.05). cAPA significantly increased HS blood loss, BT and suppressed CFR compared to Placebo1 (p<0.05). rFVIIa injection did not modify HS blood loss, BT or CFR rate in Placebo1 rabbits nor in cAPA animals. These effects were unaffected by either rFVIIa dose. rFVIIa accelerated thrombin generation but had no effect on platelet aggregation in citrated platelet-rich plasma. rFVIIa did not modify HS blood loss associated with cAPA in rabbits.

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Therapy with clopidogrel and aspirin after ACS does not seem to increase the risk of real-life bleeding following OS, regardless of the platelet activity response to DAPT. © 2015 S. Karger AG, Basel.

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The anticoagulants and antiplatelet agents that patients are receiving preoperatively apart from unfractionated heparin include low-molecular-weight heparins (LMWHs); a pentasaccharide (fondaparinux); oral anticoagulants: vitamin K antagonists (warfarin), new oral Xa inhibitors (rivaroxaban, apixiban), or the oral direct thrombin inhibitor (DTI) dabigatran; platelet inhibitors: thienopyridines (clopidogrel, ticlopidine, prasugrel) or IIb/IIIa receptor antagonists (tirofiban, abciximab, eptifibatide); or DTIs (r-hirudin, bivalirudin, argatroban).

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Controlled localised bipolar conjunctival cautery before STA injection may significantly reduce the frequency of SCH, especially in patients on warfarin or aspirin.

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Observational study.

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Our registry showed that underlying medical conditions may affect antiplatelet prescriptions at discharge. During the first year following an ACS episode, the prescription rate of dual antiplatelet therapy declined over time, mainly due to physician's judgment leading to the discontinuation of clopidogrel. Adherence to dual antiplatelet treatment was associated with lower total mortality at 1 year.

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Out of 535 IS patients, 208 (38.88%) were CR and 327 (61.12%) were clopidogrel sensitive (CS). Diabetes was independently associated with risk of CR (odds ratio: 2.42, 95% confidence interval [CI], 1.22-4.97, P <.01). During the follow-up period, the incidence of ischemic vascular events was higher in the CR group than in the CS group; the proportion of patients with mRS score of 0-2 points at 6 months was significantly lower in CR group than in CS group. CR (hazard ratio [HR]: 2.82, 95% CI, 1.23-6.94, P <.01), diabetes (HR: 1.61, 95% CI, 1.01-3.49, P = .02), and hypertension (HR: 1.84, 95% CI, 1.12-4.72, P = .03) were independent risk factors for ischemic vascular events.

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In contrast to the negative drug interaction of PPI reported elsewhere, in the present study the intake of PPI buy plavix was not associated with an increased risk for adverse clinical outcomes in patients treated with stents.

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The routine off-label use of drug-eluting stents (DESs) has been associated with a higher prevalence of stent thrombosis in clinical practice than was suggested in US Food and Drug Administration (FDA) preapproval studies. Consequently, the early identification of patients at risk for stent thrombosis has become a major goal in cardiology. Although a number of factors may be involved in DES thrombosis, the biologic cascade begins with local platelet activation and culminates in platelet aggregation, the generation of coagulation factors, the formation of a fibrin network, and the creation of a stable occlusive thrombus. Current data show that the premature discontinuation of dual-antiplatelet therapy is an important risk factor for DES thrombosis, but the occurrence of stent thrombosis in patients adhering to this drug regimen suggests that some patients are nonresponsive to clopidogrel therapy, primarily because of functional and genetic variability in the cytochrome P450 enzymes. Patients with high platelet reactivity to adenosine diphosphate (ADP) during dual-antiplatelet therapy may be at increased risk for adverse ischemic events, including stent thrombosis. Using a point-of-service assay, Price et al measured platelet function in patients treated with DESs and demonstrated that 75% of patients who developed stent thrombosis were in the lowest quartile of platelet inhibition and the highest quartile of platelet reactivity. Data from the authors' center suggest that there may be a threshold of platelet reactivity, as measured by light-transmittance aggregometry after ADP stimulation, that predicts an increased risk for stent thrombosis. Large prospective studies designed to identify which patients are at risk for stent thrombosis on the buy plavix basis of platelet function testing are under way and may eventually lead to personalized antithrombotic therapy.

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Recent European Society of Cardiology (ESC) Guidelines declare superiority of prasugrel and ticagrelor over clopidogrel in non-ST segment elevation myocardial infarction (NSTEMI) and STEMI patients with acute coronary syndromes (ACS). The recommendations for NSTEMI and especially STEMI are based on a subgroup analyses yielded from a single trial with either prasugrel (TRITON), or ticagrelor (PLATO). In contrast, the United States (US) Guidelines present a more balanced, conservative, and evidence-based outlook suggesting no proven extra benefit of one P2Y12 antagonist over the other(s). It was the purpose of this study to scrutinise the evidence leading to the current ESC ACS Guidelines on oral antiplatelet agents and compare them with US recommendations. Matching the evidence from TRITON and PLATO primary publications with the data reported in the Food and Drug Administration (FDA) official reviews in light of their impact on current regional ACS Guidelines on antiplatelet P2Y12 inhibitors. The available body of evidence on the efficacy and safety of the new oral P2Y12 inhibitors challenge the ESC Guidelines, and supports the US recommendations. Some of the pivotal data with regard to the newer P2Y12 inhibitors (prasugrel and ticagrelor) on event definition, adjudication, questionable efficacy, and serious safety concerns were ignored by the European Task Force Members, while the other "beneficial" findings were exaggerated to a disproportional extent. We conclude that current ESC Guidelines, with regard to their recommendation of superiority of prasugrel or ticagrelor over clopidogrel, in contrast to the Voltaren Gel Side Effects Pregnancy US, are overoptimistic, and not evidence based. Low clinical utilisation of prasugrel and especially ticagrelor worldwide in general, and Europe in particular suggests mismatch of prescription habits with issued ESC recommendations.

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The hemostatic effect of rFVIIa and NN1731 was demonstrated in thrombocytopenic and clopidogrel-treated rats, showing efficacy in situations with decreased platelet number or Cleocin T Solution Reviews functionality. Our findings are consistent with the hypothesis that rFVIIa/NN1731 contribute to hemostasis by thrombin generation even in situations with platelet disorders. Furthermore, NN1731 demonstrated a higher hemostatic potential than rFVIIa.

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Various drug therapies may be used to manage stable angina Indocin Medication Indomethacin Side Effects , with coronary revascularization as an option in patients who are refractory to drug therapy. However, antianginal drug therapies may prove inadequate for managing anginal episodes for a variety of reasons, and revascularization is not always effective.

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In ISAR-REACT 3, 30-day Famvir Cold Sore Tablets outcomes in 4570 biomarker negative patients undergoing percutaneous coronary intervention (PCI) > or =2 h after pre-treatment with 600 mg of clopidogrel revealed less bleeding with bivalirudin compared with unfractionated heparin, but no difference in 30-day net clinical benefit. The objective of the present analysis was to assess the impact of bivalirudin vs. heparin on 1-year outcomes in ISAR-REACT 3.

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The results of this study substantiate the occurrence of severe drug interactions among Indian elderly inpatients. In order to provide safer pharmaceutical care, the Generic Viagra Price Australia active involvement of clinical pharmacists is a potential option.

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Oral anticoagulants and platelet receptor blockers are widely used in clinical practice with the aim of reducing Crestor Gone Generic the risk of thrombotic complications in patients with cardiovascular diseases. Their regular intake and adequate antithrombotic action is vital and this is way numerous assays have been developed for laboratory testing and monitoring of these agents. Available assays can be stratified into pharmacokinetic and pharmacodynamic assays. Such assays are increasingly used in clinical routine and their daily use is triggered by the advent of the novel direct oral anticoagulants (DOACs) as an alternative for vitamin K antagonist (VKA) treatment, which are dabigatran, rivaroxaban and apixaban, and by the advent of prasugrel or ticagrelor as an alternative for clopidogrel with regard to platelet P2Y12 receptor inhibition. In this review the most important and most commonly used laboratory assays are summarized as well as their clinical implications with the focus on DOACs as an alternative for VKAs and the different P2Y12 receptor blockers for antiplatelet treatment.

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A reversed phase liquid chromatographic method with UV detection for the simultaneous determination of clopidogrel and acetylsalicylic acid and their related substances in combined oral formulations was developed and validated. Good separation was achieved on a Luna C18 column (150 mm × 4.6 mm, 3 μm) using gradient elution at a flow rate of 1 mL/min and a column temperature of 35 °C. UV detection was performed at 220 nm. The validation was performed according to the ICH guidelines. The method proved to be specific, sensitive (LOQ=0.975 μg/mL and 0.0384 μg/mL for clopidogrel and acetylsalicylic acid, respectively), linear in the concentration range from LOQ to 325 μg/mL for clopidogrel and from LOQ to 650 μg/mL for acetylsalicylic acid, precise (RSD values for intermediate precision <1%) and accurate with mean recovery values of 100.7% and 100.2% for clopidogrel and acetylsalicylic acid, respectively. Moreover, the solution stability and method robustness were examined. The method gives satisfactory separation of impurities of clopidogrel and acetylsalicylic acid and so it is suitable for quantification of the related substances as well Glucophage 10 Mg as for the assay of the actives.

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Proton pump inhibitor (PPI) therapy Zanaflex Maximum Daily Dose has been shown to attenuate the antiplatelet effects of clopidogrel. The aim of this study was to compare the antiplatelet effects of cilostazol versus clopidogrel in patients co-administered a PPI.

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It Zovirax Generic Cream has not been clearly established whether percutaneous coronary intervention (PCI) can provide an incremental benefit in quality of life over that provided by optimal medical therapy among patients with chronic coronary artery disease.

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Using a mouse model of intra-abdominal sepsis and acute lung injury, we investigated the role of the P2Y12 receptor in neutrophil migration and lung inflammation in P2Y12 null mice and in mice pretreated with the P2Y12 antagonist clopidogrel. Our data show a decrease in circulating white blood cells and a decrease in platelet activation and platelet-leukocyte interactions in treated mice compared with untreated mice. Additionally, lung injury and platelet sequestration were diminished in clopidogrel-treated mice compared with their untreated septic littermates. Similar results were observed in P2Y12 null mice: platelet activation and platelet-leukocyte aggregates were decreased in septic P2Y12 null mice compared with wild-type mice. P2Y12 null mice were refractory to lung injury compared with wild-type mice. Finally, to evaluate P2Y12-independent effects of clopidogrel, we pretreated P2Y12 null mice. Interestingly, the number of circulating neutrophils was reduced in treated septic P2Y12 null mice, Voltaren Gel Dosage Card Online suggesting neutrophils as a target for clopidogrel pleiotropic effects. No difference was observed in P2Y1 null mice during sepsis, indicating that the P2Y12 receptor is responsible for the effects.

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This population-based, retrospective cohort study employed data from the Taiwanese National Health Insurance database (January 2001 through December 2006) for patients who had a history of hospitalization for GI complications before the initiation of antiplatelet therapy with aspirin or clopidogrel. Recurrent hospitalizations for major GI complications were analyzed using a Cox proportional hazards model, with adjustment for age, sex, ulcer-related medical history, ulcer-related risk factors, and use of ulcer-related medications during follow-up. The propensity score Elavil 50 Mg Uses method was applied to adjust for selection bias.

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In this analysis in patients at high GI risk who were receiving antiplatelet therapy for the secondary prevention of cardiovascular events, aspirin plus a PPI was associated with a Zofran 4 Mg Dosage reduced risk of recurrent hospitalization for major GI complications. This was not the case for clopidogrel plus a PPI.

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Using the evaluation of the CAPRIE (Clopidogrel versus Aspirin in Patients at risk of Ischemic Events) trial by the British National Institute for Health and Clinical Excellence (NICE) and the German Institute for Quality and Efficiency in Health Care (IQWiG), we illustrate that there was no consensus for Avelox Reviews the interpretation of possible heterogeneity in treatment comparisons across subgroups.

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The direct-acting platelet P2Y12 receptor antagonist ticagrelor can reduce the incidence of major adverse cardiovascular events when administered at hospital admission to patients with ST-segment elevation myocardial infarction (STEMI). Whether prehospital administration of ticagrelor can improve coronary reperfusion and the clinical outcome is unknown.

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Extracellular nucleotides have been implicated as signaling molecules used by microglia to sense adverse physiological conditions, such as neuronal damage. They act through purinoceptors, especially the G-protein-coupled P2Y receptor P2Y(12)R. Emerging evidence has indicated that activated spinal microglia responding to nerve injury are key cellular intermediaries in the resulting highly debilitating chronic pain state, namely neuropathic pain. However, the role of microglial P2Y(12)Rs in neuropathic pain remains unknown. Here, we show that the level of P2Y(12)R mRNA expression was markedly increased in the spinal cord ipsilateral to the nerve injury and that this expression was highly restricted to ionized binding calcium adapter molecule 1-positive microglia. An increase in the immunofluorescence of P2Y(12)R protein in the ipsilateral spinal cord was also observed after nerve injury, and P2Y(12)R-positive cells were double labeled with the microglial marker OX-42. Blocking spinal P2Y(12)R by the intrathecal administration of its antagonist AR-C69931MX prevented the development of tactile allodynia (pain hypersensitivity to innocuous stimuli), a hallmark of neuropathic pain syndrome. Furthermore, mice lacking P2ry(12) (P2ry(12)(-/-)) displayed impaired tactile allodynia after nerve injury without any change in basal mechanical sensitivity. Moreover, a single intrathecal administration of AR-C69931MX or oral administration of clopidogrel (a P2Y(12)R blocker clinically in use) to nerve-injured rats produced a striking alleviation of existing tactile allodynia. Together, our findings indicate that activation of P2Y(12)Rs in spinal microglia may be a critical event in the pathogenesis of neuropathic pain and suggest that blocking microglial P2Y(12)R might be a viable therapeutic strategy for treating neuropathic pain.

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The mechanical injury was exerted by pinching the abdominal aorta with hemostatic forceps for either 15 (moderate injury) or 60 (severe injury) seconds. Thrombus formation was monitored for 20min in real time using a fluorescent microscope coupled to a CCD camera. In the moderate injury, thrombus formation peaked at approximately 1min after injury and resolved within 3min, with the mean AUC (area under the curve) of 165.2±17.29mm(2), whereas a larger thrombus was observed upon the severe injury, with the mean AUC of 600.5±37.77mm(2). Using scanning electron microscopy and HE staining, a complete deformation of the endothelium in the moderate injury model and the exposure of the media in the severe injury model were observed. The model was also evaluate for its application on the effects of antithrombotic drugs targeting GP IIb-IIIa (eptifibatide), ADP receptor P2Y1 (MRS2500) and P2Y12 (clopidogrel), and thrombin (hirudin) on thrombus formation.

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Decision-makers in the US may be interested in the applicability to their populations of cost-effectiveness results generated from clinical trial populations.

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We consecutively enrolled 198 patients with stable CAD one month after successful PCI. All patients were receiving dual antiplatelet therapy (clopidogrel 75 mg and aspirin 100 mg/day). Platelet reactivity was measured by VerifyNow P2Y12 assay (Accumetrics, San Diego, CA). VerifyNow reports its results in P2Y12 reaction units (PRU) and the diagnostic cut-off value is 230. Endothelial function was evaluated by flow mediated dilation (FMD).

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DPFC embosurgery is effective and safe in managing uncontrollable epistaxis.

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Preoperative dual antiplatelet therapy does not result in significantly increased bleeding or perioperative transfusion requirements. If clinically indicated, it is reasonable to continue preoperative combination antiplatelet therapy in patients undergoing robotic-assisted coronary surgery.

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Patients with coronary artery aneurysms caused by Kawasaki disease are at increased risk of coronary thrombosis and ischemia. To prevent coronary thrombosis, long-term anti-thrombosis using anti-platelet drugs, such as aspirin, dipyridamole, ticlopidine, clopidogrel, and abciximab, with or without warfarin is recommended by official guidelines. In fact, aspirin or aspirin with warfarin are the most frequently administered regimen in these patients with coronary aneurysms. However, there has been paucity of data and no randomized controlled study to determine the efficacy of these drugs. This short article attempts to summarize the efficacy and safety of these drugs based on currently available literatures and our multi-institutional experience.

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Interindividual heterogeneity in drug response is a central feature of all drug therapies. Studies in individual patients, families, and populations over the past several decades have identified variants in genes encoding drug elimination or drug target pathways that in some cases contribute substantially to variable efficacy and toxicity. Important associations of pharmacogenomics in cardiovascular medicine include clopidogrel and risk for in-stent thrombosis, steady-state warfarin dose, myotoxicity with simvastatin, and certain drug-induced arrhythmias. This review describes methods used to accumulate and validate these findings and points to approaches--now being put in place at some centers--to implementing them in clinical care.

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Eighty patients were enrolled and clinical and laboratory data were recorded. Albumin-creatinine ratio (ACR) was calculated in first-morning urine samples. Serum and urinary tumor necrosis factor-α (TNF-α) levels were determined by ELISA.

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Patients with BCVIs from January 1, 1997, to January 1, 2007.

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we included 206 patients (231 lesions) with a mean age of 67.46 ± 8.37 years, 40 patients (19.4 %) > 75 years, 66 % were symptomatic, 169 patients (82 %) with history of ischemic heart disease; in 213 lesions (92.2 %) cerebral protection filters were used; clopidogrel 300 mg; aspirin 325, heparin IV 70 UI/kg, temporary pacemaker prophylaxis in ostial lesions of the internal carotid artery were applied.

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Important correlates of ST were identified. Discontinuation of clopidogrel, undersizing of the coronary stent, present malignancy, and intermediate (>or=50% to <70% stenosis) coronary artery disease proximal to the culprit lesion were the strongest predictors of ST.

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Vertebral artery dissection has been increasingly identified as a cause of ischemic stroke in young adults. This condition is typically secondary to trauma, with spontaneous VA dissection accounting for only a minority of cases. We report the case of a patient with bilateral symptomatic spontaneous VA dissections, presenting in rapid succession. Each ictal event was successfully managed with stent reconstruction and antiplatelet therapy.

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No funding was received for the conduct of this study. DiDomenico received an honorarium from Amgen for the preparation of a heart failure drug monograph for Pharmacy Practice News and was a co-investigator on funded research for the Patient-Centered Outcomes Research Institute. DiDomenico also serves as an advisory board member for a heart failure program at Otsuka America Pharmaceuticals and as an advisory board member at Novartis Pharmaceuticals. Touchette has received unrestricted grant funding from Cardinal Health and Sunovion Pharmaceuticals and has also served as a consultant to and director of the American College of Clinical Pharmacy Practice-Based Research Network on a study funded by Pfizer. None of the authors of this study are involved in financial or personal relationships with agencies, institutions, or organizations that inappropriately influenced the statistical analysis plan or interpretation of the results. Study concept and design were contributed by Kim, Lee, Touchette, and Walton, with assistance from DiDomenico and Ardati. Kim and Lee collected the data, and data interpretation was performed by Lee, DiDomenico, and Ardati, along with Kim and Walton and assisted by Touchette. The manuscript was written by Kim and Walton, with assistance from the other authors, and revised by Kim, Walton, and Lee, with assistance from the other authors.

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Previous clinical studies have shown heterogeneity in individual patient responses to antiplatelet therapy and high residual platelet reactivity is associated with increased risk of adverse clinical events. Monitoring response to antiplatelet therapy and tailoring treatment accordingly is currently not recommended in routine clinical practice largely due to the lack of a standardized definition of antiplatelet therapy hyporesponse and the need for a widely accepted point-of-care platelet function test that can be reliably utilized in frontline clinical practice. Recent data have shown that titrating the dose of clopidogrel in patients undergoing percutaneous coronary intervention significantly reduces the incidence of major adverse cardiovascular events and large-scale clinical trials are currently underway to investigate whether individually tailored treatment based on results of platelet function testing leads to improved clinical outcome. Furthermore, genetic testing has demonstrated a link between CYP2C19 genetic polymorphisms, altered clopidogrel metabolite concentrations and adverse clinical events. Clinical studies are currently underway to investigate the potential clinical benefit associated with genotype-guided tailoring of antiplatelet therapy. With the advent of newer, more potent antiplatelet agents and their associated increased bleeding risks, it will become imperative in the future to select the most appropriate, safe and effective drug.

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Spontaneous MI following a medically managed UA/NSTEMI event is common. Baseline characteristics can be used to predict subsequent risk of spontaneous MI in this population. These findings provide insight into the long-term natural history of medically managed UA/NSTEMI patients and could be used to optimize risk stratification and treatment of these patients. (A Comparison of Prasugrel and Clopidogrel in Acute Coronary Syndrome Subjects [TRILOGY ACS]; NCT00699998).