View clinical trials related to Platelet Reactivity.
Filter by: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.
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.
Clopidogrel administration is commonly prescribed in patients undergoing percutaneous coronary intervention, in patients with previous stroke and in patients under chronic hemodialysis via fistulae. Patients with chronic renal failure present lower clopidogrel response compared to those with normal renal function. Ticagrelor is a new oral direct-acting antagonist, which provides greater platelet inhibition in both clopidogrel responders and non-responders. It has also been shown that in patients with chronic kidney disease (creatinine clearance <60 mL/min)ticagrelor achieved an absolute risk reduction of cardiovascular death, myocardial infarction, and stroke greater than that of patients with normal renal function. Clopidogrel resistant patients as assessed by VerifyNow P2Y12(Accumetrics)will be administered after informed consent ticagrelor 90 mg twice daily for 15 days. Platelet reactivity will be determined at the end of the treatment period. Bleeding events, major adverse cardiac events and any side effects until Day 15 will be reported in a descriptive manner.
This is a single-center, randomized, single-blind, investigator-initiated, pharmacodynamic study with a parallel design. Patients with ST elevation myocardial infarction, undergoing primary percutaneous coronary intervention will be randomized after informed consent, in a 1:1 ratio to the following treatment groups: Group Α: Ticagrelor 180mg loading dose (LD), followed by a 90mg x2 maintenance dose (MD)starting 12±6 hours post LD, until Day 5 (5 days after randomization) Group Β: Prasugrel 60 mg LD followed by 10mg x1 MD starting 24 hours post LD, until Day 5 (5 days after randomization). Platelet reactivity assessment will be performed at randomization (Hour 0) and at 1, 2, 6, 24 hours after randomization, and on Day 5. Documentation of major adverse cardiac events (death, myocardial infarction, stroke, revascularization procedure with PCI or CABG)and serious adverse events (bleeding, other adverse events)will be performed until Day 5.
The use of dual antiplatelet therapy is considered standard of care in patients post percutaneous coronary intervention (PCI) with stenting. However, a significant proportion of patients is considered clopidogrel resistant and this resistance is shown to be accompanied by future adverse events. The aim of the study is to define in consecutive patients with acute coronary syndrome (ACS) undergoing PCI, those aged>75years and/or weighted<60 Kg with high on-clopidogrel platelet reactivity (Platelet Reactivity Units-PRU≥235) as estimated 24 hours post PCI with the VerifyNow assay. Those patients will be randomized after informed concent in 1:1 fashion to prasugrel 5 mg or clopidogrel 150mg daily. Platelet reactivity will be assessed at day 15 and then treatment crossover will be performed. At day 30 platelet reactivity will be determined as well.
The PHP study aims to delineate gene products involved in high on-treatment platelet reactivity in aspirin-treated cardiovascular patients.
Platelets are a major component of clot formation which can lead to clotting events such as heart attack. During treatment for a heart attack, doctors try to remove this blockage as quickly as possible so that the heart can recover and start to work properly again. The standard of care at the Heart Institute for patients having a heart attack is a procedure called a Percutaneous Coronary Angioplasty. A drug called Clopidogrel (Plavix) is routinely used prior to the angioplasty to prevent blood clots. Patients usually remain on Clopidogrel for at least one year following the angioplasty. Clopidogrel works by preventing the blood from forming sticky substances called platelets, which clump together to form clots. Despite the routine use of Clopidogrel, some patients still return to the hospital with another heart attack, or with more chest pain. There is a growing body of evidence that recurrence of these complications may be attributed to some patients having a poor response to Clopidogrel. This pilot study will examine how platelets react to different doses of Clopidogrel given to patients having a heart attack.