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We enrolled 133 acute myocardial infarction and 67 stable angina patients undergoing intracoronary stenting into our study. Maximal aggregation was determined with light transmission aggregometry. Aggregation >50% induced by 5 μM ADP was indexed with high on-clopidogrel treatment platelet reactivity. In these cases 75 mg clopidogrel was doubled and control test was performed. Patients effectively inhibited with 150 mg clopidogrel were defined as clopidogrel pseudo non-responders. Patients with high platelet reactivity even on 150 mg clopidogrel were considered as clopidogrel real non-responders and were switched to ticlopidine.
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With the arrival of the potent P2Y12 antagonists, ticagrelor and prasugrel, the need for co-treatment with aspirin in acute coronary syndromes must be re-examined. This study assessed whether high-dose aspirin: a) provides additional anti-platelet efficacy, assessed in vivo and ex vivo, when combined with P2Y12 inhibition; and/or b) has a negative effect on vascular function.
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Thienopyridines have become the cornerstone of treatment of percutaneous coronary intervention although no survival benefit has ever been shown with clopidogrel despite increasing loading doses. Newly developed P2Y(12) inhibitors are more potent, more predictable and have a faster onset of action than clopidogrel, characteristics that make them particularly attractive for high-risk PCI. Four new P2Y(12) inhibitors have been tested each of them having particular individual properties. Prasugrel is an oral prodrug leading to irreversible blockade of the P2Y(12) receptor and is approved worldwide for ACS PCI. Ticagrelor is a direct-acting and reversible inhibitor of the P2Y(12) receptor with potentially more pleiotropic effects. Cangrelor is an intravenous direct and reversible inhibitor of the P2Y(12) receptor providing the highest level of inhibition and elinogrel is an intravenous and oral P2Y(12) antagonist with a direct and reversible action. Both prasugrel and ticagrelor, opposed to clopidogrel, have shown that stronger P2Y(12) inhibition led respectively to significant 19 % and 16 % relative risk reduction of a similar primary endpoint combining cardiovascular death, nonfatal myocardial infarction, or nonfatal stroke. Both drugs showed a significant 0.6 % absolute excess of TIMI major bleeding not related to CABG surgery. The effect of these new compounds is prompt, predictable and powerful as compared to clopidogrel. Their net benefit is particularly marked in PCI for STEMI patients, in which there is no significant increase in major bleeding when compared with clopidogrel. However, because in clinical trials patients perceived to be at higher risk for bleeding usually are excluded, the risk of major and even fatal bleeding might even be higher in a "real-world" setting i.e. in the elderly patient with comorbidities.
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Some studies have recently suggested a potential pharmacodynamic interaction between aspirin and some non-selective non-steroidal anti-inflammatory drugs (NSAIDs). We have evaluated the reality of this pharmacodynamic interaction and analyse its clinical pertinence.
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In our series, biliary-pancreatic surgical and endoscopic procedures were safely performed in 11 consecutive patients on dual antiplatelet therapy with no evidence of bleeding.
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Recent studies suggest a high interindividual variability of response to clopidogrel associated with adverse cardiovascular outcome. Different clinical factors are considered to influence a persistent residual platelet aggregation (RPA) despite conventional antiplatelet therapy.
In patients with acute coronary syndrome initially intended for non-invasive management, the benefits of ticagrelor over clopidogrel were consistent with those from the overall PLATO results, indicating the broad benefits of P2Y12 inhibition with ticagrelor regardless of intended management strategy.
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The results of our preliminary study suggest that the [(13)C]pantoprazole breath test can predict the anti-platelet efficacy of clopidogrel.
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To determine the effects of prasugrel loading on platelet function in patients on clopidogrel and high platelet reactivity undergoing percutaneous coronary intervention for acute coronary syndrome (ACS).
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We carried out a cross sectional retrospective analysis of 1468 ACS patients hospitalized between January 2008 and December 2010 and followed up for 1 year in the Institute of Cardiovascular Diseases, Madras Medical Mission, Chennai. Mortality at 1 year, its determinants and 1 year major adverse cardiac events (MACE) were determined.
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In the final quarter of 2008, pantoprazole represented 23.7% of all PPI prescriptions dispensed to patients receiving clopidogrel. Following the publications and FDA advisory in early 2009, pantoprazole use increased substantially. By the end of 2009, this medication accounted for 52.5% of all PPI prescriptions issued to patients receiving clopidogrel; by the end of the study period, it accounted for 71.0% of all PPI prescriptions dispensed to such patients (p < 0. 001). We also observed a modest drop in overall PPI use among clopidogrel recipients beginning in early 2009.
Uncertainty exists concerning the relative merits of pharmacological versus mechanical coronary reperfusion in patients presenting early with ST-elevation myocardial infarction (STEMI) with extensive myocardium at risk. Accordingly, we investigated whether the extent of baseline ST-segment shift was related to the response of either reperfusion modality in patients with STEMI presenting within 3 h of symptoms.
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We believe that stent-assisted coiling with the Neuroform2 stent is very effective and safe without pretreatment with antiplatelets in ruptured as well as in unruptured aneurysms.
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In addition to reducing the risk of gastrointestinal bleeding, statistically significant benefits with prophylactic omeprazole use on both pain and nonpain symptoms were evident at 4 weeks and sustained through 24 weeks. The clinical significance of these overall results is unclear, but greater in patients with pain at baseline.
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In ISAR-REACT 3, 30-day 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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This study is intended to provide information about the safety characteristics of warfarin and ticagrelor in persistent or permanent AF patients after PCI-eS. No prospective randomized study has been conducted on the issue of antithrombotic therapy using warfarin and ticagrelor in these patients. Therefore, the MANJUSRI trial will help to explore and determine a new potential therapeutic regimen for AF patients after PCI-eS.
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Antiplatelet drug resistance is a well-known problem, causing recurrent cardiovascular events. Multiple genetic polymorphisms have been related to antiplatelet resistance by several large trials, however data from common clinical practice is limited. We examined the influence of previously described polymorphisms, related to aspirin and clopidogrel resistance, on treatment outcome in a real life unselected population of patients presenting with ST-segment elevation myocardial infarction (STEMI) treated with percutaneous coronary intervention.
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Antiplatelet therapy is recommended after coronary artery bypass grafting, because it improves saphenous vein graft (SVG) patency and clinical outcomes. We investigated the association between prehospital antiplatelet regimens and outcomes after SVG intervention. Patients who underwent SVG intervention from 2003 to 2008 were divided into 3 groups: (1) no antiplatelet therapy, (2) the use of aspirin or clopidogrel, and (3) the use of dual antiplatelet therapy (DAPT) at admission. Clinical follow-up examinations were performed at 30 days and 1 year. The primary outcome was the composite of all-cause mortality, myocardial infarction, the need for revascularization, and stroke at 30 days. The relation between antiplatelet therapy and outcomes was adjusted for factors associated with the outcomes. A total of 225 patients underwent SVG intervention, 87% were men, and the mean age was 70 years. Of the 225 patients, 21 (9.4%) were not receiving antiplatelet therapy, 102 (45.3%) were receiving aspirin/clopidogrel, and 102 (45.3%) were receiving DAPT. The patients without antiplatelet therapy were more frequently women, had presented earlier after coronary artery bypass grafting, and were less frequently taking other cardiac-related medications. The patients taking aspirin or DAPT were more often smokers and had a greater peripheral vascular burden. The incidence of the 30-day and 1-year primary outcomes was greater in patients without preadmission antiplatelet use (38.1% vs 14.9% and 13.9%, overall p = 0.01; 52.4% vs 29.5% and 28.3%, overall p = 0.03). After adjustment, antiplatelet use remained associated with the primary outcome. In conclusion, prehospital use of antiplatelet therapy was associated with a lower occurrence of major adverse cardiac events after SVG intervention. We did not find that DAPT improved outcomes compared to single antiplatelet therapy.
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Antiplatelet therapy (AT) is indicated in hypertensive patients with increased cardiovascular risk. The literature about the adequate or inadequate prescription of AT is scarce. We conducted a prospective descriptive study to quantify therapeutic inertia and non-guideline-recommended prescription (NGRP) of AT (aspirinor clopidogrel or both), and to assess associated factors, calculating the adjusted odds ratios (ORs) from multivariate models. In 2007-2009, 712 primary health-care hypertensive patients in a Spanish region were enrolled. Inertia was defined as the lack of an AT prescription, despite being indicated by guidelines, whereas NGRP was defined as AT prescription when there was no guideline recommendation. We also recorded cardiovascular variables. Inertia and NGRP were quantified for primary and secondary prevention. Of 108 patients in secondary prevention, 53 had inertia (49.1%, 95% confidence interval (CI): 39.6-58.5%). Associated profile: female (OR=0.460, P=0.091), no dyslipidemia (OR=0.393, P=0.048), no coronary heart disease (OR=0.215, P=0.001) and high diastolic blood pressure (OR=1.076, P=0.016). In primary prevention, NGRP was present in 69 of 595 patients (11.6%, 95% CI: 9.0-14.2%). Associated profile: male (OR=1.610, P=0.089), smoking (OR=2.055, P=0.045), dyslipidemia (OR=3.227, P<0.001) and diabetes (OR=2.795, P<0.001). Although certain factors were clearly associated with these phenomena much still remains to be learnt.
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Of 13,819 patients enrolled, 1,539 (11.1%) underwent CABG before discharge. Clopidogrel-exposed patients had a longer median duration of hospitalization (12.0 days vs. 8.9 days, p < 0.0001), but fewer adverse composite ischemic events (death, myocardial infarction, or unplanned revascularization) at 30 days; 12.7% vs. 17.3%, p = 0.01), with nonsignificantly different rates of non-CABG-related major bleeding (3.4% vs. 3.2%, p = 0.87) and post-CABG major bleeding (50.3% vs. 50.9%, p = 0.83) compared with those patients not administered clopidogrel. By multivariable analysis, clopidogrel use before CABG was an independent predictor of reduced 30-day composite ischemia (odds ratio: 0.67, 95% confidence interval: 0.48 to 0.92, p = 0.001) but not of increased post-CABG major bleeding (odds ratio: 0.98, 95% confidence interval: 0.80 to 1.19, p = 0.80).
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Stroke, myocardial infarction (MI), and death are complications of carotid artery stenting (CAS). The effect of baseline patient demographic factors, processes of care, and technical factors during CAS on the risk of stroke, MI, or death within 30 days of CAS in the International Carotid Stenting Study (ICSS) were investigated.
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Clopidogrel and ticagrelor, antagonists to P2Y(12) receptor molecules on platelet membranes, significantly ameliorate acute myocardial infarction due to coronary artery thrombosis, the most common cause of death in the developed world. A personal account is given here of the foundational research that lead to the identification of P2Y receptors, carried out 50 years ago in the Melbourne University Zoology Department headed by Geoffrey Burnstock. In Christmas 1962, I made the serendipitous observation of large hyperpolarizing changes across the membranes of smooth muscle cells in the taenia coli of the intestine on stimulating its nerve supply. I then showed that these potentials relaxed the muscle and were not due to noradrenaline or acetylcholine, which were then the only substances known to be released from nerves. I called these non-adrenergic, non-cholinergic (NANC) terminals in the laboratory and showed that this NANC transmitter acted at receptor molecules on the muscle cells, promoting efflux of potassium ions, and so the observed potential changes. In 1968, Graeme Campbell showed that ATP relaxed the taenia coli muscle, and in 1969, David Satchell, using purine chromatography, showed that ATP was likely to be released from NANC terminals. The receptor molecules involved were shown to be exceptionally sensitive to 2-methylthio-ATP (Satchell and Macguire, 1975, J Pharmacol Exp Ther, 195, 540), and so belonged to the class P2Y receptors as designated by Abbracchio and Burnstock, with subclasses P2Y(1)-P2Y(12). The discovery of the role of P2Y(12) receptors in increasing thrombosis lead to the focused research that resulted in clopidogrel and ticagrelor.
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There is no difference for definite stent thrombosis in patients taking low dose versus standard aspirin.
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Residual platelet reactivity after dual antiplatelet treatment measured before stenting did not predict poststenting SECI. However, the longer stent and the serial increase of PRU values after stenting were related to SECI. Continuous increase of platelet activation after endovascular procedure may be important in poststent cerebral infarction.
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Transient ischemic attack is one of the most common causes of transient neurologic deficit. Anemic hypoxia results from reduced hemoglobin content with normal arterial oxygen tension and saturation. Anemic hypoxia caused by blood loss or hemolysis has not been considered as an independent factor leading to significant neurologic problems because cerebral homeostasis adjusted by the physiologic regulation in cerebral hemodynamics and oxygenation would meet the brain oxygen requirement in most circumstances even with profound anemia. We report a case of severe anemia associated with transient ischemic attack involving vertebrobasilar circulation.
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Ticagrelor vs. clopidogrel post-ACS was associated with a lower risk of death, MI, or stroke, as well as death alone. Risk of bleeding was higher with ticagrelor. These real-world outcomes are consistent with randomized trial results.