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Impact of Dabigatran and Phenprocoumon on Clopidogrel Mediated ADP Induced Platelet Aggregation in Patients With Atrial Fibrillation (Dabi-ADP-2)

This study has been terminated.
(Slow recruitment; Study was terminated for futility reasons)
Sponsor:
ClinicalTrials.gov Identifier:
NCT01352702
First Posted: May 12, 2011
Last Update Posted: February 5, 2015
The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. Listing a study does not mean it has been evaluated by the U.S. Federal Government. Read our disclaimer for details.
Information provided by (Responsible Party):
Deutsches Herzzentrum Muenchen
  Purpose
The aim of this study is to evaluate whether dabigatran reduces clopidogrel mediated ADP induced platelet aggregation measured by MEA as compared to phenprocoumon after a two-week treatment with either agent.

Condition Intervention Phase
Coronary Heart Disease Atrial Fibrillation Acute Coronary Syndrome Atherosclerosis Drug: Dabigatran Drug: Phenprocoumon Phase 4

Study Type: Interventional
Study Design: Allocation: Randomized
Intervention Model: Parallel Assignment
Masking: None (Open Label)
Primary Purpose: Treatment
Official Title: Impact of Dabigatran and Phenprocoumon on Clopidogrel Mediated ADP Induced Platelet Aggregation in Patients With Atrial Fibrillation

Resource links provided by NLM:


Further study details as provided by Deutsches Herzzentrum Muenchen:

Primary Outcome Measures:
  • ADP induced platelet aggregation [ Time Frame: 2 weeks ]
    To determine whether there are differences in ADP induced platelet aggregation after 2 weeks in patients receiving dabigatran or phenprocoumon.


Secondary Outcome Measures:
  • Platelet function tests [ Time Frame: 2 weeks ]
    ADPtest HS (MEA) , TRAP, Collagen

  • Coagulation parameters [ Time Frame: 2 weeks ]
    aPTT, INR, Thrombin coagulation time


Enrollment: 46
Study Start Date: May 2011
Study Completion Date: May 2014
Primary Completion Date: May 2014 (Final data collection date for primary outcome measure)
Arms Assigned Interventions
Experimental: Arm 1
Dabigatran Therapy
Drug: Dabigatran
Patients assigned to this group will receive Dabigatran
Other Name: Pradaxa
Active Comparator: Arm 2
Phenprocoumon Therapy
Drug: Phenprocoumon
Patients assigned to this group will receive Phenprocoumon
Other Name: Marcumar

Detailed Description:

Oral anticoagulation with vitamin K antagonists (OAC) is the standard care for reducing stroke in patients with atrial fibrillation. Just recently the direct, competitive thrombin inhibitor dabigatran has been approved by the FDA for stroke prevention in patients with atrial fibrillation. In a large multicenter trial it was shown that dabigatran was at least as effective as Vitamin K antagonists in the prevention of stroke without an increase of major hemorrhage.

Approximately 6 % of patients who undergo coronary stenting and need DAT with aspirin and clopidogrel need in addition OAC for the reduction of cardiac, cerebral and systemic thromboembolic events5. These patients will therefore need triple therapy, a therapy which is associated with increased bleeding complications. Although phenprocoumon given solely without clopidogrel has no impact on ADP induced platelet aggregation, it has been shown that phenprocoumon significantly attenuates the antiplatelet effects of clopidogrel.

ADP induced platelet aggregation measured with multiple electrode platelet aggregometry (MEA) is a marker for the efficacy of the clopidogrel therapy and (i) a low response (AUC ≥ 468) to clopidogrel has been associated with an increase of ischemic events such as stent thrombosis and (ii) patients with an enhanced response to clopidogrel (AUC ≤ 188) have higher bleeding rates.

It is therefore crucial to evaluate whether an additional antithrombotic therapy such as dabigatran alters clopidogrel mediated ADP induced platelet aggregation. While it has been shown that intravenous administration of the direct thrombin inhibitor bivalirudin further reduces ADP induced platelet aggregation in patients on clopidogrel therapy, it is unknown whether dabigatran has also an impact on ADP induced platelet aggregation.

To evaluate the impact of dabigatran on ADP induced platelet aggregation we will randomize patients with atrial fibrillation and the need for oral anticoagulation and current clopidogrel therapy for a two-week treatment with either dabigatran or phenprocoumon and we hypothesize that dabigatran is superior to phenprocoumon in the reduction of ADP induced platelet aggregation. Patients who are not concomitantly treated with clopidogrel are being studied in a different trial with a similar study design (Dabi ADP-1).

  Eligibility

Information from the National Library of Medicine

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Ages Eligible for Study:   18 Years and older   (Adult, Senior)
Sexes Eligible for Study:   All
Accepts Healthy Volunteers:   No
Criteria

Key Inclusion Criteria:

  • Patients with atrial fibrillation and an indication for oral anticoagulation (CHA2DS2-VASc score≥ 1).
  • Current clopidogrel treatment
  • Informed, written consent by the patient or her/his legally-authorized representative for participation in the study.

Key Exclusion Criteria:

  • Age ≤18 years
  • Cardiogenic shock
  • Current therapy with dabigatran
  • Patients with a recent thromboembolic event and high thromboembolic risk requiring bridging therapy with either unfractionated heparin or LMWH
  • Contraindication for oral anticoagulation
  • Active bleeding
  • Known allergy or intolerance to the study medications: dabigatran, phenprocoumon
  Contacts and Locations
Information from the National Library of Medicine

To learn more about this study, you or your doctor may contact the study research staff using the contact information provided by the sponsor.

Please refer to this study by its ClinicalTrials.gov identifier (NCT number): NCT01352702


Locations
Germany
Deutsches Herzzentrum Muenchen
Munich, Germany, 80636
Sponsors and Collaborators
Deutsches Herzzentrum Muenchen
Investigators
Principal Investigator: Julinda Mehilli, MD Deutsches Herzzentrum München, Klinik für Herz- und Kreislauferkrankungen
  More Information

Responsible Party: Deutsches Herzzentrum Muenchen
ClinicalTrials.gov Identifier: NCT01352702     History of Changes
Other Study ID Numbers: GE IDE No. A01711
2011-000504-18 ( EudraCT Number )
First Submitted: May 11, 2011
First Posted: May 12, 2011
Last Update Posted: February 5, 2015
Last Verified: February 2015

Additional relevant MeSH terms:
Atrial Fibrillation
Heart Diseases
Atherosclerosis
Acute Coronary Syndrome
Coronary Disease
Coronary Artery Disease
Myocardial Ischemia
Arrhythmias, Cardiac
Cardiovascular Diseases
Pathologic Processes
Arteriosclerosis
Arterial Occlusive Diseases
Vascular Diseases
Clopidogrel
Dabigatran
Phenprocoumon
Platelet Aggregation Inhibitors
Purinergic P2Y Receptor Antagonists
Purinergic P2 Receptor Antagonists
Purinergic Antagonists
Purinergic Agents
Neurotransmitter Agents
Molecular Mechanisms of Pharmacological Action
Physiological Effects of Drugs
Antithrombins
Serine Proteinase Inhibitors
Protease Inhibitors
Enzyme Inhibitors
Anticoagulants