Antiplatelet Therapy Effect on Extracellular Vesicles in Acute Myocardial Infarction
- Registration Number
- NCT02931045
- Lead Sponsor
- Medical University of Warsaw
- Brief Summary
Platelet activation and aggregation leads to myocardial infarction. Platelet P2Y12 receptors are essential for platelet activation. Antagonists against the P2Y12 receptor, which are established in secondary prevention of myocardial infarction, have unexplained anti-inflammatory effects. A novel P2Y12 receptor antagonist ticagrelor reduced infection-related mortality compared to clopidogrel, previous standard treatment for patients with myocardial infarction. Activated platelets release pro-inflammatory and procoagulant platelet extracellular vesicles. The investigators assume that decrease in infection-related mortality in patients treated with ticagrelor may be explained by greater inhibition of the release of platelet vesicles by ticagrelor, compared to clopidogrel. This study is expected to identify an additional mechanism of action of ticagrelor, which might contribute to the observed clinical benefits in patients treated with ticagrelor.
- Detailed Description
Not available
Recruitment & Eligibility
- Status
- COMPLETED
- Sex
- All
- Target Recruitment
- 60
- Age > 18 years
- Informed consent to participate in the study
- Percutaneous coronary intervention with stent implantation due to first S T elevation myocardial infarction, or first non S T -elevation myocardial infarction
- Administration of a loading dose of clopidogrel
- Known coagulopathy
- Known history of bleeding disorder
- Suspicion of intracranial haemorrhage
- Need for oral anticoagulation therapy
- Administration of glycoprotein (GP) II b - III a antagonists
- Cardiogenic shock
- Severe chronic renal failure (estimated glomerular filtration rate < 30 mL/min)
- Severe liver insufficiency
- Chronic dyspnea
- Increased risk of bradycardia
- Autoimmune disease
- Infectious disease
- Neoplasms
- Pregnancy
- Study drug intolerance
- Co-administration of ticagrelor or clopidogrel with strong CYP3A4 inhibitors
- Participation in any previous study with ticagrelor or clopidogrel
Study & Design
- Study Type
- INTERVENTIONAL
- Study Design
- PARALLEL
- Arm && Interventions
Group Intervention Description Ticagrelor Ticagrelor Ticagrelor: oral, 180 mg once (loading dose) followed by 90 mg twice daily (maintenance dose) Clopidogrel Clopidogrel Clopidogrel: oral, 300 mg or 600 mg once (loading dose) followed by 75 mg once daily (maintenance dose)
- Primary Outcome Measures
Name Time Method Concentration of Platelet Extracellular Vesicles/ml 6 months following the beginning of antiplatelet therapy Concentration of platelet extracellular vesicles/ml measured with flow cytometry
- Secondary Outcome Measures
Name Time Method Concentration of Extracellular Vesicles From Leukocytes 6 months Concentration of extracellular vesicles from leukocytes/ ml measured with flow cytometry
Concentration of Extracellular Vesicles Exposing Phosphatidylserine 6 months Concentration of extracellular vesicles exposing phosphatidylserine/ml measured with flow cytometry
Concentration of Extracellular Vesicles Exposing Fibrinogen 6 months Concentration of extracellular vesicles exposing fibrinogen/ ml measured with flow cytometry
Concentration of Extracellular Vesicles From Endothelial Cells 6 months The concentrations of extracellular vesicles from endothelial cells/ ml measured with flow cytometry
Trial Locations
- Locations (2)
Laboratory of Experimental Clinical Chemistry, Academic Medical Centre of the University of Amsterdam
🇳🇱Amsterdam, Netherlands
1st Chair and Department of Cardiology, Medical University of Warsaw
🇵🇱Warsaw, Poland