View clinical trials related to Platelet Reactivity.
Filter by:Patients with Chronic Coronary Syndrome (CCS) undergoing with elective percutaneous coronary intervention (PCI) are treated with dual antiplatelet therapy (DAPT), consisting of aspirin combined with clopidogrel for 6 months. The aim of DAPT is to prevent recurrent thrombotic events, i.e. death, stent thrombosis and/ or myocardial infarction (MI). However, the trade-off of thrombotic prevention by DAPT is an increased risk of bleeding. Multiple strategies to reduce bleeding risk and optimize outcomes have been proposed. On one hand the bleeding risk can be reduced by shortening the duration of DAPT and omitting aspirin. This has been proven effective in patients with acute coronary syndromes (ACS) compared to standard DAPT, without a significant difference in thrombotic events. On the other hand, personalized medicine by means of genotyping to ensure that a patient is treated with an, for them, effective drug, can be a strategy to optimize patients outcomes. In CCS patients the preferred P2Y12-inhibitor is clopidogrel. However, clopidogrel must first be activated by the CYP2C19 enzyme in the liver. Only then can clopidogrel inhibit the P2Y12-receptor and prevent platelet activation. Almost thirty percent of patients has a genetic variation of the gene encoding this CYP2C19 enzyme. In these patients, clopidogrel is not or hardly activated, putting them at a higher risk of thrombotic events than patients who do not have this gene variation. By determining the CYP2C19 genotype, it is possible to estimate whether clopidogrel will be effective or not. In this trial the investigators evaluate the pharmacodynamic effects of genotype guided P2Y12-inhibitor monotherapy in patients with CCS undergoing PCI. In the intervention arm the CYP2C19 genotype will be assessed using a point-of-care test device on the cardiology ward, which can be performed by (research) nurses. Patients with a CYP2C19 loss-of-function (LOF) allel will be treated with monotherapy ticagrelor or prasugrel. Patients who are non-carrier of a LOF allel will receive clopidogrel. The control arm will be treated with the current standard-of-care, which is DAPT, consisting of aspirin combined with clopidogrel for 6 months. The main goals is to assess the antithrombotic effects of individualized P2Y12 monotherapy strategy versus clopidogrel plus aspirin in elective PCI patients.
Extreme body weights (BW) or body mass index (BMI) affect the pharmacokinetics of antithrombotic drugs and consequently may affect cardiovascular risk during treatment. The goal of this clinical trial is to establish if clopidogrel treatment can be optimized in patients with a low or high BW compared to patients with a normal BW by adjusting the dosage of clopidogrel and evaluating platelet reactivity. Participants are stratified into three groups based on their BW (Low BW: BW <60kg; normal BW: 60-100kg; High BW: >100 kg) Clopidogrel dosage will then be adjusted to the BW, as follows: - Low BW: >10 days clopidogrel 50mg 1dd1, followed by >10 days clopidogrel 25mg 1dd1. - Normal BW: Clopidogrel 75mg 1dd1. - High BW: >10 days clopidogrel 150mg 1dd1 followed by >10 days prasugrel 10mg 1dd1. The primary endpoint of the study is P2Y12 Reaction Units (PRU) and platelet inhibition measured using the VerifyNow measured before starting new treatment regimen (at the end of 10 days of treatment).
The goal is to determine whether fentanyl and morphine have similar effects in reducing aspirin's effect upon platelets in emergency department patients with chest discomfort. Morphine has been shown to worsen outcomes in heart attack patients due to reduction of oral anti-platelet agent effectiveness and so many providers have switches to using fentanyl. However, it is largely unknown whether fentanyl has similar effects.
Dual antiplatelet therapy (DAPT) with aspirin and a P2Y12 inhibitor reduces thrombotic events in patients with coronary artery disease, but these benefits come at the expense of increased risk of bleeding when compared with aspirin monotherapy. Increased evidence showed that P2Y12 inhibitor monotherapy still maintain antiischemic efficacy while reducing the bleeding risk compared with DAPT. Therefore, the investigators performed this study to observe the efficacy of ticagrelor in comparison to clopidogrel in Chinese patients with stable CAD.
Ticagrelor has been demonstrated to provide a more rapid and more powerful inhibition of platelet aggregation compared with clopidogrel in coronary artery disease (CAD) patients. However, current guidelines recommend ticagrelor 90 mg twice daily might not be suitable for patients of Chinese. Therefore, the investigators performed this study to observe the efficacy of 60-mg ticagrelor in comparison to 75-mg clopidogrel in Chinese patients with stable CAD.
The study sought to observe the effects of optimal dose of ticagrelor（90 mg qd）ticagrelor and double standard-dose clopidogrel on platelet reactivity in coronary heart disease patients with high on-treatment platelet reactivity (HTPR) while on clopidogrel. HTPR with clopidogrel administration in coronary heart disease (CHD) patients has associated with an increased risk of adverse events. Newer P2Y12 inhibitors ticagrelor (90mg BID) provide stronger platelet inhibition compared with clopidogrel, but a low-dose of ticagrelor (90mg QD) has not been previously studied in Chinese CHD patients with HTPR.
Platelet function testing has been considered for DAPT strategy adjustments to reduce the patient's risk of ischemia and bleeding. Although several previous RCT studies did not find any benefit in the detection of platelet function， the previous studies were mostly low-risk populations, and the P2Y12 receptor antagonists were simply clopidogrel, and the detection methods were relatively simple. Therefore, the need for platelet monitoring in high-risk ACS patients receiving new potent P2Y12 inhibitor ticagrelor, as well as the diagnostic threshold for different platelet function assays needs further study. In addition, due to the differences on the response to anti-platelet drugs between the East and the West, it is not appropriate to simply refer to the conclusion of the other party. However, as of now, there is no large sample randomized controlled study systematically focused on the applicability and status of platelet function tests in East Asian populations, especially Chinese populations.
to assess whether cessation of 12 months DAPT regimen containing Ticagrelor results in a hyperreactive phase of platelet function
In the PLATO substudy referring to patients presenting with an ST-elevation Myocardial Infarction(STEMI), out of the 4201 who received ticagrelor, 1326 had been pre-treated with a 600mg clopidogrel loading dose (LD) within 24 hours prior to randomization. It is a logical assumption, that patients who are being reloaded with ticagrelor will demonstrate reduced platelet reactivity (PR) at 24 hours, in comparison to those who were initially loaded with ticagrelor, due to the synergistic antiplatelet effect. Single loading with ticagrelor though, will possibly be accompanied by a smaller bleeding potency compared to reloading with ticagrelor. Therefore, we assume that single loading with ticagrelor is non-inferior to reloading with ticagrelor, in terms of platelet reactivity. P2Y12 inhibitor naive patients with STEMI, they will be randomized immediately after coronary angiography (Hour 0) in receiving either Ticagrelor 180mg LD or Clopidogrel 600mg LD and 2 hours later reloading with Ticagrelor 180mg, after written informed consent. PR will be measured, using the VerifyNow assay at randomization (Hour 0) and at 2, 4, 6 and 24 hours post randomization. In addition, a 12-lead ECG will be performed before randomization, 90 and 180 minutes after the first balloon inflation, as well as on the exit day. Troponin I and CK-MB will be assessed at randomization and at hour 4, 12, 24, 48 and 72 after randomization. Non inferiority of Ticagrelor LD versus Ticagrelor re-LD would be accepted if the upper bound of the 2-sided 95% CI around the estimated LS mean difference (Ticagrelor LD minus Ticagrelor re-LD) in the primary end point (PR at 24 hours) would lie bellow Δ=35 PRU. This non-inferiority margin (Δ) represents the upper bound of the LS mean difference in PR between Ticagrelor and Prasugrel arm at 24 hours after LD in a pharmacodynamic study of 55 STEMI patients. Considering previous studies PR at 24 hours post randomization was estimated at 47±40 PRU and 41±35 PRU for Ticagrelor only LD and Ticagrelor re-LD group respectively. To obtain 85% statistical power with a 2-sided alpha=0.05, approximately 32 patients in each treatment group (64 in total) would be needed to establish the primary hypothesis using the abovementioned non-inferiority margin of 35 PRU. Anticipating a 5% dropout rate, enrollment was set to at least 68 patients. The primary endpoint, as well as PR at all the other time points of the study will be analyzed separately via a mixed effect model with treatment as fixed effect, patient as a random intercept and PR at baseline as a covariate. Least squares estimates of the mean difference will be presented, with 95% confidence intervals and a two-sided p-value for the treatment effect. P values for secondary endpoints will be reported for two-tailed tests of superiority.
This is a prospective, multi-center, non-randomized, controlled study in 2 sequential groups of P2Y12 inhibitor-naive consecutive STEMI patients undergoing primary PCI. Following aspirin 325 mg LD, patients will receive 60 mg or 100 mg of prasugrel, respectively. Platelet reactivity (PR)will be assessed at Hour 0 (before prasugrel's administration immediately prior to PCI) and at Hours 0.5, 1, 2, 4 thereafter. Platelet function testing (in PRU) will be performed with the VerifyNow (Accumetrics Inc., San Diego, CA, USA) P2Y12 function assay.