Author + information
- Flavia Bittar Britto Arantes,
- Fernando Menezes,
- Andre Franci,
- Carlos Barbosa,
- Talia F. Dalçoquio,
- Carlos K. Nakashima,
- Aline Ferrari,
- Marco Scanavini Filho,
- Remo Furtado,
- Luciano Baracioli,
- Jose Ramires,
- Roberto Kalil-Filho and
- Jose Nicolau
Background: The interaction between anticoagulants and platelet function is complex. Previous laboratory data have shown that dabigatran increases urinary thromboxane metabolite excretion, indicating platelet-activating effect. Thereafter, data from RELY trial suggested that dabigatran 150mg could enhance the risk of myocardial infarction in atrial fibrillation patients.
Methods: Prospective interventional study conducted in chronic coronary artery disease (CAD) patients on aspirin. Patients (n=29, mean age 64 y., 69% male) were assigned to dabigatran 150mg bid for 5 days followed by a washout period of 30 days, then enoxaparin 1mg/kg bid for 5 days. Platelet function tests were performed at baseline and after both treatments using multiple electrode aggregometry (MEA, AUC unit) with arachidonic acid (ASPItest) and TRAP stimuli. Additionally, ELISA for plasma quantitative determination of thromboxane B2 (pg/ml) was also executed.
Results: The main results are depicted in the figure. As can be seen, in comparison with baseline, dabigratan increased platelet aggregation, and enoxaparin decreased it. Similar pattern was obtained for thromboxane B2. There was no difference between the drugs, as assessed by MEA-TRAP.
Conclusions: Dabigatran increases platelet activation and aggregation promoted by thromboxane in patients with coronary artery disease on aspirin when compared to enoxaparin.
Poster Hall, Hall C
Saturday, March 18, 2017, 3:45 p.m.-4:30 p.m.
Session Title: Antithrombotic Therapy in Ischemic Heart Disease
Abstract Category: 3. Acute and Stable Ischemic Heart Disease: Therapy
Presentation Number: 1252-308
- 2017 American College of Cardiology Foundation