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The feasibility and safety of left atrial appendage closure with the Amplatzer cardiac plug (AGA Medical Corp., Minneapolis, MN) have been recently published; no thrombus formation on the device surface has been reported previously. We describe a case of a 66-year-old man with permanent atrial fibrillation, previous stroke, and contraindication for long-term oral anticoagulant therapy. A 22-mm ACP device was deployed successfully without complications. The patient was discharged on acetyl salicylic acid 100 mg and clopidogrel 75 mg daily. After 4 weeks, the patient was admitted for a lower gastrointestinal bleeding and clopidogrel was stopped. A 3-month follow-up echocardiogram confirmed the exclusion of the LAA but it demonstrated the presence of a thrombus on the atrial surface of the device. It was decided to keep the patient on acetyl salicylic acid 100 mg with the addition of enoxaparin 60 mg bid. Transesophageal echocardiogram demonstrated total resolution of the thrombus after 2 months.
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Currently available evidence does not substantiate the widespread use of long-term aspirin with clopidogrel for the secondary prevention of ischemic stroke or TIA.
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74 participants responded; 56.8% were from academic centers. Participants treated an average of 5.5 aneurysms per month. They placed an average of 1.6 intracranial stents and 1.4 cervical stents per month. Mean number of pipeline embolization devices (PEDs) placed per year was 15.2. Heterogeneity existed regarding AP regimens; the most frequent included acetylsalicylic acid (ASA) 325 mg+Plavix 75 mg daily (for 7 days prior) and ASA 325 mg+Plavix 75 mg daily (for 5 days prior) for routine placement of intracranial and cervical stents, respectively. For emergency placement, ASA 325 mg+Plavix 600 mg (at time of surgery) was the most frequently used. 46.8% routinely used POC testing, most frequently VerifyNow (Accumetrics, San Diego, California, USA); the most common threshold determining a non-responder was <30% inhibition. 85.7% used POC for PED placement. Management changes based on POC testing were diverse.
An update on and a brief review of the current knowledge on antiplatelet resistance were presented. Evidence available from studies evaluating aspirin resistance and high and low on-treatment platelet reactivity to ADP during P2Y12 receptor blocker therapy was collected from a selective literature search.
MEDLINE and Cochrane Controlled Trials Register databases were searched from January 1980 through January 2010. Randomized, placebo-controlled trials that compared new P2Y(12) antagonists with clopidogrel in PCI were selected. Data from 8 studies were evaluated and analyses performed for all randomized patients, PCI patients (any PCI), and PCI for ST-segment elevation myocardial infarction (STEMI) patients. All-cause mortality was the primary efficacy end point. Thrombolysis In Myocardial Infarction major bleeding was the primary safety end point.
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The MIG registry prospectively collects demographical, clinical, and procedural characteristics of consecutive patients undergoing PCI. We assessed medication use (aspirin, clopidogrel, ACE inhibitors, angiotensin receptor blockers, beta-blockers, and lipid-lowering agents) at 30 days and 12 months in patients alive and able to provide the information.
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Interindividual variability in the pharmacological response to antiplatelet drugs has been reported in some studies. Suboptimal response to aspirin, as determined by specific tests (serum thromboxane B(2)), appears to be rare and in most cases is caused by poor compliance. In contrast, studies using specific tests to measure the pharmacological effect of clopidogrel showed a wide variability of responses, with a significant number of subjects (approximately one-third) who were very poor responders. Interindividual differences in the extent of metabolism of clopidogrel to its active metabolite is the most plausible mechanism for the observed interindividual variability in platelet inhibition. Tailored treatment based on laboratory monitoring of platelet function has been proposed as a solution to poor responsiveness to clopidogrel. However, we still need to identify the ideal laboratory test and to answer basic questions on its clinical utility and cost-effectiveness before monitoring clopidogrel therapy can be recommended in clinical practice.
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Cardiac events in patients with acute stroke are frequent. Urgent PCI in myocardial infarction is crucial to improve outcome. However, the situation is complex as intracranial hemorrhage is a frequent complication of stroke but antithrombotic medication is indispensable during and after PCI. Therefore in this study, we aimed to investigate the safety of percutaneous coronary intervention (PCI) in patients hospitalized with acute ischemic stroke and concomitant acute coronary syndrome (ACS).
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There is considerable interindividual variation in response to the antiplatelet agent clopidogrel. Hyporesponse predicts negative outcomes in patients presenting with a variety of ischemic cardiac conditions and following intracoronary stent placement. Many tests of clopidogrel activity are time consuming and complex. Short thromboelastography (s-TEG) allows rapid measurement of platelet clopidogrel response.
Platelets are critical for haemostasis and blood clotting. However, since under normal circumstances blood should flow without clotting, its function is regulated via a complex interplay of activating and inhibiting signal transduction pathways. Understanding this network is crucial for treatment of cardiovascular and bleeding diseases. Detailed protein interaction and phosphorylation data are explored to establish a simplified Boolean model of the central platelet cascades. We implemented the model by means of CellNetAnalyzer and showed how different signalling events coalesce into a fully activated system state. Furthermore, we examined the networks' inherent threshold behaviour using the semi-quantitative modelling software SQUAD. Finally, predictions are verified monitoring phosphorylations which mark different activation phases as modelled. The model can also be applied to simulate different pharmacological conditions as they modify node activity (aspirin, clopidogrel, milrinon, iloprost, combination) and is available for further studies. It agrees well with observations. Activatory pathways are diversified to cope with complex environmental conditions. Platelet activation needs several activation steps to integrate over different network subsets, as they are formed by the interplay of activating kinases, calcium mobilization, and the inhibiting cAMP-PKA system. System stability analysis shows two phases: a sub-threshold behaviour, characterized by integration over different activatory and inhibitory conditions, and a beyond threshold phase, represented by competition and shutting down of counter-regulatory pathways. The integrin network and Akt-protein are critical for stable effector response. Dynamic threshold-analysis reveals a dependency of the relative activating input strength necessary to irreversibly engage the system from the absolute inhibitory signal strength.
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The majority of ISR treated occurred in bare metal stents [BMS (n=52, 87%)] and had a focal (<10 mm) pattern of ISR (53%). In-stent restenosis of DES occurred in eight (13%) patients. The majority of ISR were treated with additional stenting with a preference for DES over BMS in almost all cases. At 12 months, one patient died of non-cardiac cause and four patients (7%) presented with recurrent ISR. The incidence of recurrent ISR in DES was 5% (n=3). No late thrombosis was reported despite only 50% of patients having >or=12 months of clopidogrel therapy.
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In our experience, CAS followed immediately by cardiac surgery is safe and represents a reasonable option for selected patients presenting with severe carotid and coronary disease.
Sixty-five rabbits were randomly divided into 7 groups: normal, model (collagen encapsulated thread-drawing),model+aspirin (ASA), model+clopidogrel (CP),model+ASA+CP, model+ low dosage DZ (DZL), and model+high dosage DZ (DZH). All rabbits except the normal group were fed with the drugs repectively for 8 days,and sacrificed at 2 hours after the last feeding, obtained aortae. The pathological changes in the aortae were observed under microscope,and the level of FDP, D-dimer and tissue factor (TF) were measured by enzyme-linked immunosorbent assay (ELISA).
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The Elderly-ACS 2 study is a multicenter, randomized trial comparing a strategy of dual antiplatelet therapy with a reduced dose of prasugrel with a standard dose of clopidogrel in elderly patients with ACS undergoing percutaneous revascularization (the Elderly ACS 2 trial: NCT01777503).
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Clopidogrel reduces long-term ischemic events in patients with acute coronary syndrome or stable angina (SA) undergoing percutaneous coronary intervention (PCI). Endothelial function improvement has been proposed, among other factors, for this beneficial effect of clopidogrel, but whether this might be associated to its anti-platelet action remains unclear. We tested the hypothesis that clopidogrel improvement of peripheral vascular endothelial function might be associated with inhibition of platelet aggregation. Endothelial function was evaluated before and at least 12 h after 600 mg clopidogrel in 43 SA pts undergoing elective PCI by: (a) reactive hyperemia peripheral arterial tonometry (measuring the Endoscore); (b) circulating endothelial microparticles (EMPs). Response to clopidogrel was measured with point-of-care VerifyNow P2Y12 assay and expressed as platelet reaction unit (PRU) and percent platelet inhibition (%PI). High platelet reactivity after clopidogrel was defined as PRU ≥ 240. Endothelial function improved after clopidogrel in 20 pts. Changes in Endoscore (Δ Endoscore) were significantly correlated with both PRU (r = -0.61, P < 0.001) and %PI (r = 0.57, P < 0.001). Endoscore significantly increased after clopidogrel in pts with PRU < 240 (0.38 ± 0.26 to 0.57 ± 0.33, P < 0.001), but did not in pts with PRU ≥ 240 (0.53 ± 0.31 to 0.40 ± 0.37, P = 0.12). EMPs were also significantly reduced in pts with PRU < 240 (222 [140-593] to 142 [83-371]/μl, P = 0.001), while no changes were observed in pts with PRU ≥ 240 (256 [178-531] to 388 [238-499]/μl, P = 0.55). In patients with stable coronary artery disease, a single 600 mg clopidogrel loading dose improves vascular endothelial function. This improvement is associated with optimal platelet inhibition and it is not observed in patients with post-clopidogrel high platelet reactivity.
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In our population, concomitant CCB therapy did not alter clopidogrel-mediated platelet aggregation and did not have a measurable impact on ST and mortality after coronary stenting.
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The risk of adverse events in patients with acute coronary syndrome remains substantial despite the use of regular aspirin. The addition of clopidogrel to regular aspirin therapy has been shown to be associated with significantly better outcomes in a variety of clinical settings within the spectrum of acute coronary syndromes. In this article, the evidence and therapeutic implications for the use of clopidogrel in patients with non-ST-elevation and ST elevation acute coronary syndromes is discussed, and also in those undergoing percutaneous coronary intervention. The use of clopidogrel in combination with other antithrombotics in the acute setting is considered, including glycoprotein IIb/IIIa receptor antagonists and direct thrombin inhibitors. Clopidogrel has changed the way in which patients with non-ST-elevation and, more recently, ST elevation acute coronary syndromes are treated.
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To determine the incidence of postoperative bleeding for oral osteotomy carried out under continued monoantiplatelet therapy with clopidogrel and dual therapy with clopidogrel/aspirin. Design. Retrospective single center observatory study of two study groups and a control group.
A 67 years old male presented with acute myocardial infarction. Emergency coronary angiography demonstrated subocclusive stenosis in the proximal Left Anterior Descending artery (LAD). Primary Percutaneous Coronary Intervention (PCI) was complicated with intraprocedural thrombosis in the distal Left Main Tract (LMT) following implantation of a stent in the mid LAD. The thrombus was successfully managed with heparin and quadruple antiplatelet therapy (abciximab, aspirin, clopidogrel, and cilostazol) after several attempts of thrombectomy adequate distal flow was achieved. The lesion in the proximal LAD was successfully treated using a kissing stent technique in the second stage.
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After 12 months, 24 patients were excluded because of major adverse cardiovascular events (MACEs). Three hundred and thirty six patients surviving without MACEs were further followed up for 6 months. Between 12 and 18 months, in 160 patients with standard clopidogrel therapy, 5.6% had very late stent thrombosis. In contrast, in 176 patients with prolonged clopidogrel therapy, 1.1% had very late stent thrombosis (p<0.01, versus standard clopidogrel therapy group).
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Antiplatelet drugs are widely used in the treatment of patients with coronary artery disease. Dual anti-platelet therapy with acetylsalicylic acid (ASA) and a P2Y12 inhibitor (clopidogrel, prasugrel or ticagrelor) is the recommended strategy for patients undergoing a percutaneous coronary intervention (PCI), while patients that undergo coronary artery bypass grafting (CABG) are treated with ASA monotherapy. However, the response to these drugs as assessed with platelet function tests varies between patients. Despite these drugs, many patients still exhibit high on-treatment platelet reactivity (HPR), while platelet reactivity seems to be excessively inhibited in other patients. This review will discuss the use of platelet function testing in the prediction of atherothrombotic and bleeding events in patients undergoing PCI or CABG. Furthermore, options for tailoring based on platelet function testing in these patients are described.
Clopidogrel is an important component of medical therapy for patients with acute coronary syndromes and those receiving coronary artery stents. Despite use of clopidogrel, a significant number of patients experience recurrent adverse ischemic events. Interindividual variability of platelet aggregation in response to clopidogrel may be an explanation for some of these recurrent events, and small trials have linked "clopidogrel resistance" as measured by platelet function tests to adverse events. Additionally, the degree of clopidogrel-induced platelet inhibition appears to be a factor determining bleeding risk at coronary artery bypass grafting. A point-of-care device that could accurately and rapidly measure the degree of platelet inhibition among patients taking clopidogrel could be clinically valuable. Such a device would have the potential to allow therapeutic decision-making based on the degree of platelet inhibition, especially for patients undergoing percutaneous coronary intervention or coronary artery bypass grafting.
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To determine whether the incidence of procedure-related myocardial injury, assessed by cardiac troponin T (cTnT) release, is altered when clopidogrel is coadministered with a statin that is predominantly CYP3A4-metabolized.
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Intraventricular hemorrhage (IVH) is a serious complication of intracerebral hemorrhage (ICH). We hypothesized that antiplatelet medication use and platelet activity would be associated with more IVH.
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The cumulative incidence of recurrent peptic ulcer during the 6-month period was 7.0% in famotidine group (n=114) and 11.4% in the placebo group (n=114). The two patient groups had comparable cumulative incidence of peptic ulcer (difference, 4.4%; 95% confidence interval (CI), -11.7 to 2.9%; P=0.239). Additionally, there was no difference in the cumulative incidence of ulcer bleeding (2.6% vs. 1.8%; difference, 0.8%; 95% CI, -0.6 to 2.4%, P=1.000) between famotidine and placebo groups. However, the former had a lower incidence of gastroduodenal erosion than the latter (21.1% vs. 36.8%; difference, 15.7%; 95% CI, -27.3 to -4.1%; P=0.013).