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Twelve cases of EBUS-TBNA procedures performed on patients taking clopidogrel were identified. Mean age was 74 years (range 61-85). Seven patients (66.7%) were taking aspirin in addition to clopidogrel. There was no significant bleeding seen in any cases at the time of bronchoscopy and no additional complications were identified during follow-up (at least 4 weeks; median follow-up 3 months).
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1. Clopidogrel is one of the most important antithrombotic drugs but has different efficacies in different populations. The aim of the present study was to evaluate the contribution of CYP2C19 genetic polymorphisms to the inhibition of ADP-induced platelet aggregation by clopidogrel in healthy Chinese volunteers. 2. Eighteen healthy male volunteers (six CYP2C19*1/CYP2C19*1, six CYP2C19*1/CYP2C19*2and*3 and six CYP2C19*2/CYP2C19*2and*3) were enrolled in the study. Each subject took 300 mg clopidogrel on the first day and then 75 mg once daily for 2 consecutive days. Blood samples were taken to measure ADP-induced platelet aggregation at baseline and 4, 24 and 72 h after administration of the first dose of clopidogrel. 3. There were significant decrease in 2 and 5 micromol/L ADP-induced platelet aggregation at 4, 24 and 72 h after clopidogrel among the three CYP2C19 genotypes compared with baseline (P < 0.001). The change in 5 micromol/L ADP-induced platelet aggregation in subjects with the CYP2C19*1/CYP2C19*1 genotype was greater than that in subjects with the CYP2C19*2/CYP2C19*2and*3 genotype at 4 h (49.0 +/- 15.5 vs 29.7 +/- 17.4%, respectively; P = 0.029), 24 h (48.7 +/- 20.5 vs 25.0 +/- 17.6%, respectively; P = 0.035) and 72 h (45.5 +/- 15.2 vs 26.5 +/- 15.8%, respectively; P = 0.030) after clopidogrel administration. 4. In conclusion, CYP2C19*2 and CYP2C19*3 genetic polymorphisms reduced clopidogrel inhibition of ADP-induced platelet aggregation, with the degree of inhition dependent on the genetic polymorphism present.
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Whether patients with renal insufficiency (RI) undergoing percutaneous coronary interventions (PCI) benefit from abciximab added to clopidogrel plus aspirin is unknown.
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To review the best evidence for medical treatment of PAD.
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We used confocal videomicroscopy to measure in real time the volume of platelet thrombi forming upon blood perfusion over fibrillar collagen type I at a wall shear rate of 1500 s(-1). The average volume was significantly smaller in 31 patients receiving aspirin and clopidogrel (19) or ticlopidine (12) than in 21 controls, but individual values were above the lower limit of the normal distribution, albeit mostly within the lower quartile, in 61.3% of cases. Disaggregation of platelet thrombi at later perfusion times occurred frequently in the patients. Vasodilator-stimulated phosphoprotein phosphorylation, reflecting P2Y12 inhibition, was also decreased in the patient group, and only 22.6% of individual values were above the lower normal limit. We found no correlation between volume of thrombus formed on collagen fibrils and level of P2Y12 inhibition, suggesting that additional and individually variable factors can influence the inhibitory effect of treatment on platelet function.
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Out of 3410 patients undergoing PCI-S in the study period, indication for OAC was present in 4.8%. Femoral approach and bare metal stents were the most frequently used. During PCI-S, OAC was continued in about 30% of patients, whereas in about 20% heparin bridging was carried out. Glycoprotein IIb/IIIa inhibitors were rarely used (11%), whereas a standard bolus of unfractionated heparin was given in 93% of cases. Major adverse cardiovascular events (MACE) occurred in 4.8% of patients and major bleeding in 4.3%. No predictors of MACE or bleeding were identified, although the femoral approach was of borderline significance for major bleeding (OR 4.6, 95% CI 1.0-20.8; P = 0.05). A history of previous hemorrhage (OR 5.3, 95% CI 1.6-18.1; P = 0.007) predicted Carbofilm-coated stent implantation.
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We performed a cohort study using nationwide registries to identify all Danish patients surviving first-time hospitalization for AF between January 1, 1997, and December 31, 2006, and their posthospital therapy of warfarin, aspirin, clopidogrel, and combinations of these drugs. Cox proportional hazards models were used to estimate risks of nonfatal and fatal bleeding.
More and more patients are treated with antiplatelet drugs today. In this context a sufficient inhibition of platelet aggregation, on the one hand, is of essential importance to the efficiency of prophylaxis of myocardial and cerebral infarction and to avoiding thrombosis of drug-eluting stents. On the other hand, this medication can result in an increased risk of perioperative bleeding. In both situations control of the efficiency of therapy or rather the assessment of the impairment of hemostasis is of vital importance.
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This was a retrospective study of 368 patients admitted in 2002 and 420 patients admitted in 2005 for ACS (with and without ST-segment elevation). We analyzed clinical characteristics and treatment strategies.
There was no significant difference in primary end point between the 2 randomization arms (8.8% in-lab vs. 10.3% pre-load; p = 0.72); this was mainly driven by periprocedural MI (8.8% vs. 9.3%, p = 0.99). No increased risk of bleeding or vascular complications was observed in the pre-load arm (5.4% vs. 7.8%; p = 0.42). As determined by the VerifyNow assay (Accumetrics, San Diego, California), patients in the in-lab group showed higher platelet reactivity during PCI and 2 h after intervention versus those in the pre-load arm (p < or = 0.043).
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A total of 95 patients with acute NCIS were recruited. Phosphorylation of the vasodilator stimulated phosphoprotein (VASP) was detected using flow cytometry, and genes(CYP2C19,CYP3A4) were detected using the Sanger method. The baseline of platelet reactivity index (BPRI) before clopidogrel treatment and the platelet reactivity index with clopidogrel treatment (CPRI) for 7 days were measured. Laboratory clopidogrel resistance (LCR) was defined as CPRI of ≥ 50%. Clinical clopidogrel resistance (CCR) was defined as the presence of progressive stroke during hospitalization, stroke recurrence or occurrence of other ischemic vascular events within 6 months.
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Patients with minor ischemic stroke (MIS) are at high risk of recurrent ischemic stroke (RIS). The aim of this study was to evaluate the effects of platelet receptor gene (P2Y12, P2Y1) and glycoprotein gene (GPIIIa) polymorphisms, as well as their interactions, on antiplatelet drug responsiveness and clinical outcomes in patients with acute MIS.
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As the population ages, an increasing number of trauma patients are taking antiplatelet and anticoagulant medications (ACAP) prior to their injuries. These medications increase their risk of hemorrhagic complications, particularly intracerebral hemorrhage. Clopidogrel and warfarin are common and their mechanisms well understood, but optimal reversal methods continue to evolve. The novel direct thrombin and factor Xa inhibitors are less well described and do not have existing antidotes.
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Among 2,401 patients who underwent TAVR and survived to 30 days, MLBCs occurred in 142 (5.9%) at a median time of 132 days (interquartile range: 71 to 230 days) after the index procedure. Gastrointestinal complications (n = 58 [40.8%]), neurological complications (n = 22 [15.5%]), and traumatic falls (n = 11 [7.8%]) were identified as the most frequent types of MLBCs. Independent predictors of MLBCs were the presence of low hemoglobin at baseline, atrial fibrillation or flutter at baseline or 30 days, the presence of moderate or severe paravalvular leak at 30 days, and greater left ventricular mass at 30 days. MLBCs were identified as a strong independent predictor of mortality between 30 days and 1 year (adjusted hazard ratio: 3.91; 95% confidence interval: 2.67 to 5.71; p < 0.001).
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The incremental cost-effectiveness of newer antithrombotic treatments for secondary stroke prevention, compared with aspirin or warfarin, remains to be established.