Clinical Trials Logo

Platelet Function clinical trials

View clinical trials related to Platelet Function.

Filter by:

NCT ID: NCT04456608 Terminated - Platelet Function Clinical Trials

Genetic and Dietary Predictors of Anti-platelet Response

Start date: August 1, 2016
Phase: Phase 4
Study type: Interventional

This study will investigate differences in platelet aggregation under basal and aspirin-treated conditions in American Indian and Alaska Native people who have extreme levels (low and high) of n-3 polyunsaturated fatty acids (n-3 PUFAs, EPA and DHA) in red blood cell membranes. The study will also determine whether or not platelet aggregation under the different conditions is modified by CYP4A11, CYP4F2, CYP4F11, PEAR1, and ACTN1 gene variation.

NCT ID: NCT03149250 Not yet recruiting - Platelet Function Clinical Trials

Characteristics of Primary and Plasmatic Hemostasis in Preeclampsia

Start date: September 1, 2017
Phase: N/A
Study type: Observational

The study aims to investigate the impact of preeclampsia on hemostasis.

NCT ID: NCT03125681 Completed - Platelet Function Clinical Trials

Remote Ischemic Conditioning and Platelet Dysfunction

Start date: May 11, 2017
Phase: N/A
Study type: Interventional

The purpose of this study is to evaluate the effects of remote ischemic conditioning on platelet function during off-pump coronary artery bypass surgery.

NCT ID: NCT02997111 Completed - Thrombosis Clinical Trials

PFA-100 Responsive to Effect of Energy Drinks on Platelet Function

Start date: February 14, 2017
Phase: N/A
Study type: Interventional

This study evaluates the responsiveness of the Platelet Function Analyzer (PFA-100) to the effect of energy drinks on platelet function. Participants' will have blood drawn prior to and 60 minutes after ingesting 250ml of a commercially available sugar-free energy drink.

NCT ID: NCT02594345 Completed - Platelet Function Clinical Trials

Effect of Exosomes Derived From Red Blood Cell Units on Platelet Function and Blood Coagulation

Start date: October 2015
Phase: N/A
Study type: Interventional

This study is designed to analyze the effect exosomes derived from red blood cell units have on blood coagulation and platelet function. It is an in vitro study using healthy volunteers' blood.

NCT ID: NCT02215993 Completed - Clinical trials for Acute Coronary Syndrome

Sampling P2Y12 Receptor Inhibition With Prasugrel and Ticagrelor in Patients Submitted to Thrombolysis

SAMPA
Start date: July 2013
Phase: Phase 4
Study type: Interventional

Introduction: Platelet aggregation plays an important role in ischemic complications in patients undergoing to percutaneous coronary intervention (PCI). The addition of clopidogrel, as a second antiplatelet agent, to acetylsalicylic acid (ASA) was effective in reducing major cardiovascular events in patients with acute coronary syndrome (ACS). However, approximately 30% of ACS patients are resistant to clopidogrel, representing a population of medically vulnerable and high risk for major cardiovascular events, including myocardial infarction (MI), stent thrombosis and death. In the randomized trial TRITON, prasugrel compared to clopidogrel was more effective in significantly reducing the rates of MI (7.4% vs. 9.4%) and stent thrombosis (2.4% vs .1,1%) in patients with ACS, however, patients treated with prasugrel showed higher rates of bleeding (2.4 vs. 1.8%) and no difference in mortality. Upon analysis of subgroups is not recommended its use in patients with a history of stroke in those older than 75 years and weighing less than 60 kg. The latest class of inhibitors of the P2Y12 receptor is the cyclopentyl-triazolopyrimidines represented by ticagrelor. Unlike the thienopyridines, ticagrelor interacts with the platelet receptors in a reversible way and has a beginning and peak of action faster. The efficacy and safety of ticagrelor were evaluated in the study PLATO, where 18.624 patients with ACS were randomized to receive clopidogrel (75mg/day, with a loading dose of 300 to 600mg) or ticagrelor (90mg 2x/day with a loading dose of 180mg) The primary combined endpoint (mortality from vascular causes, MI or stroke) at 12 months was significantly lower in the ticagrelor (9.8% vs. 11.7%). There was no significant difference in the rates of major bleeding in both groups. Moreover, the isolated analysis of the rates of MI, vascular mortality and mortality from all causes showed statistically significant reduction in the ticagrelor users. In this study, the main adverse effects were dyspnea and bradycardia. The assessment of platelet reactivity may allow the individualization of antiplatelet therapy. However, simply increasing the dose of clopidogrel in patients who persisted with high platelet reactivity was not able to reduce the combined endpoint of cardiovascular death, nonfatal myocardial infarction and stent thrombosis in six months. In a population of patients with stable coronary artery disease, the substitution of clopidogrel for ticagrelor showed a rapid and persistent decrease in platelet aggregation measured by different laboratory methods. However, in patients with ACS subjected to PCI, the assessment of platelet aggregation after the replacement of clopidogrel for prasugrel or ticagrelor still requires evidence. Objectives: To evaluate the platelet response to ticagrelor and prasugrel in ACS patients with ST-segment elevation submitted to thrombolysis. To evaluate security in follow up of 30 days. Methods: The study will be a prospective, randomized, single-center (São Paulo Hospital - Federal University of São Paulo), single-blind. The investigators will select 50 patients admitted with ACS with ST-segment elevation submitted to thrombolysis and who underwent cardiac catheterization between 3 to 24 hours in the case of reperfusion or immediately for rescue angioplasty. Blood sample for analysis of platelet aggregation through the system VerifyNow ®, shall be obtained immediately after the procedure on patients on clopidogrel for at least seven days in maintenance dose of 75mg or after 8 to 6 hours after the dose of 300mg and 600mg respectively. Patients will be randomized in a 1:1 ratio to receive ticagrelor the dose of 180mg and maintained dose of 90 mg twice a day for thirty days or prasugrel dose of 60mg and maintained for thirty days at a daily dose of 10mg. A new blood sample and analysis of platelet aggregation will be repeated after 2, 6 and 24 hours. The demographic and clinical data of this population will be collected in specific form and stored in databases for later analysis

NCT ID: NCT01881698 Recruiting - Pregnancy Clinical Trials

Evaluation of Platelet Function in Pregnancy With Multiple Electrode Aggregometry

MULPP
Start date: October 2013
Phase: N/A
Study type: Observational [Patient Registry]

Establishment of a range of normal values in pregnancy with the Multiple Electrode Aggregometry (Multiplate@) device, a device that allows measurement of not only platelet count but platelet function. This has not been studied in ths special patient group. Results from this trial will be used as a basis for further investigation of abnormal platelet function in pregnancy.

NCT ID: NCT01837758 Completed - Platelet Function Clinical Trials

Monitoring Platelet Function During Continuous Hemodialysis

Start date: December 2012
Phase: N/A
Study type: Observational

Aim of the study is a description of changes in platelet function during continuous veno-venous hemodialysis or hemofiltration in patients on an intensive care unit using the Multiplate system.

NCT ID: NCT01428102 Terminated - Coagulation Clinical Trials

RapidTEG MA Validation

R-TEG MA
Start date: July 2011
Phase: N/A
Study type: Observational

During normal physiological conditions hemostasis (the ability of blood to clot) is kept in homeostatic balance by feedback mechanisms. These mechanisms involve an extremely complex series of steps on both sides of the coagulation cascade including cellular components (i.e. clot formation and breakdown). However, should this homeostatic balance be upset, normal hemostasis is affected resulting in pathological clotting (vessel blockage) or bleeding (hemorrhage). In instances that include acquired or congenital abnormalities of the hemostatic system it is clinically important to diagnose, monitor and manage the patient to optimize therapeutic intervention. Moreover, it is important to regulate the hemostasis system in the post-surgical outpatient who receives oral anticoagulant therapy to maintain the homeostatic balance. The TEG® analyzer, using a small whole blood sample, documents the interaction of platelets with the protein coagulation cascade from the time of placing the blood in the analyzer until initial fibrin formation, clot rate strengthening and fibrin-platelet bonding via GPIIb/IIIa, through eventual clot lysis. It displays both qualitatively and quantitatively the two distinct parts of hemostasis - the part that produces the clot and the part that causes the breakdown of the clot. It shows the balance or degree of imbalance in the patient's hemostasis system, highlights any areas of deficiency or excess, and offers a precise view of the patient's hemostasis condition. If the system is not in balance, one can see where the imbalance lies. If a patient is bleeding, it is crucial to determine the cause of bleeding as soon as possible in order to start the proper treatment. By utilizing a kaolin/tissue factor activator (RapidTEG™), the TEG® system can measure the interaction and simultaneous contribution of the intrinsic and extrinsic coagulation pathways which initiate and result in clot formation. This RapidTEG™ reagent can deliver results faster than activating with Kaolin alone. This protocol will specifically assess one algorithm called MA. MA is a direct function of the maximum dynamic properties of fibrin and platelet bonding via GPIIb/IIIa that represents the ultimate strength of the fibrin clot. This represents platelet function. The objective of the study is to demonstrate the substantial equivalence of MA RapidTEG vs. MA Kaolin.

NCT ID: NCT01352923 Recruiting - Platelet Function Clinical Trials

Study of Polymorphisms in pear1 Gene Link to Platelet Activation and Signaling Pathway Variations

Start date: May 2011
Phase: N/A
Study type: Interventional

In this study PEAR1 polymorphisms effects will be analyze in blood platelets to determine how PEAR1 regulates platelet activation.