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Action of the Vidaza on the Atrial Fibrillation (AVIFA)

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.
 
ClinicalTrials.gov Identifier: NCT03298321
Recruitment Status : Unknown
Verified October 2019 by Hospices Civils de Lyon.
Recruitment status was:  Recruiting
First Posted : October 2, 2017
Last Update Posted : October 16, 2019
Sponsor:
Information provided by (Responsible Party):
Hospices Civils de Lyon

Brief Summary:
Genomic studies on atrial fibrillation patients have identified polymorphisms in regions surrounding the PITX2 gene, suggesting it could be the locus responsible for atrial fibrillation. The PITX2 gene is essential for establishing the asymmetry between systemic and pulmonary blood flow, which is absolutely required for proper heart functions. In addition, PITX2 is required for the development the atrium myocardium. Investigators have performed transcriptomic analysis on left atrium tissues from atrial fibrillation patients and identify genes whose expression is altered in atrial fibrillation. Among affected genes, PITX2 expression is strongly decreased in the left atrium of atrial fibrillation patients. Moreover, investigators observed that the PITX2 promoter region is hypermethylated in atrial fibrillation patients. Interestingly, DNA methylation is a key actor of gene expression and directly regulates RNA transcription either by directly modulating transcription factor (TF) binding to gene promoters or by modifying local chromatin structures, therefore limiting access of TFs to DNA. These epigenetic modifications are reversible and therefore represent an interesting therapeutic target. Hence, many compounds that inhibit DNA methyl-transferase are currently tested in different disease models. Recently-designed hypomethylating molecules are available, such as the 5'azacytidine (Vidaza®, Celgen Inc.) or the 5-aza-2'-deoxycytidine (Decitabine) (Dacogen®, Janssen Cilag). Investigators have performed preliminary studies on the effect of Decitabine on DNA methylation and proper cardiac function recovering in a SHR model. Results indicate that the chronic delivery of Decitabine improves the arrhythmia profile by reducing tachyarrhythmia, fibrosis, as well as the oxidative stress in SHR left atrium submitted Acute Leukemia is a rare pathology with an incidence of 4 per 100,000 in France. Azacytidine, which is closely related to Decitabine, is commonly used for treating Acute Leukemia and possesses anti-neoplastic effect through multiple mechanisms, including direct cytotoxicity of blood cancer cells and DNA hypomethylation. The goal of this study is to evaluate the effects of azacytidine on arrhythmia and left atrium fibrosis as well, which are the two mains phenotypic manifestation of atrial fibrillation in humans. Investigators hypothesize that azacytidine decreases PITX2 promoter methylation and increases PITX2 expression. Hence, investigators expect to ameliorate the duration of atrium action potential and to observe a decrease of atrium fibrosis.

Condition or disease Intervention/treatment
Atrial Fibrillation Acute Leukemia Other: Effect of Vidaza treatment

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Study Type : Observational
Estimated Enrollment : 14 participants
Observational Model: Cohort
Time Perspective: Prospective
Official Title: Action of the Vidaza on the Atrial Fibrillation
Actual Study Start Date : December 20, 2018
Estimated Primary Completion Date : December 20, 2021
Estimated Study Completion Date : December 20, 2021


Group/Cohort Intervention/treatment
Vidaza patients
This study will be performed on adults with Acute Myeloid Leukemia and atrial fibrillation. Only patients treated for the first time with vidaza® within an hospital hematology unit will be included.
Other: Effect of Vidaza treatment
The goal of this study is to evaluate the effects of azacytidine on arrhythmia and left atrium fibrosis.




Primary Outcome Measures :
  1. Evolution of atrial arrhythmic events [ Time Frame: Maximum 12 months ]
    Evolution of the atrial arrhythmic events observed in the inclusion, 6 months or 12 months (according to the frequency of follow-up of the atrial fibrillation) after the beginning of the cure by Holter-ECG.


Secondary Outcome Measures :
  1. Evolution of the morphology and the fibrosis atrial [ Time Frame: Maximum 12 months ]
    Evolution of the morphology and the fibrosis atrial observed in the inclusion, 6 months or 12 months (according to the frequency of follow-up of the atrial fibrillation) after the beginning of the cure by transthoracic echocardiography.



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Ages Eligible for Study:   18 Years and older   (Adult, Older Adult)
Sexes Eligible for Study:   All
Accepts Healthy Volunteers:   No
Sampling Method:   Non-Probability Sample
Study Population
This study will be performed on adults with Acute Myeloid Leukemia and atrial fibrillation. Only patients treated for the first time with vidaza® within an hospital hematology unit will be included.
Criteria

Inclusion Criteria:

  • Age ≥ 18 years old
  • Patient with history of paroxysmal atrial fibrillation, and /or presenting a dilatation of the left atrium.
  • Patient selected for a first Vidaza® treatment
  • Non-opposition of the patient to participate in the study

Exclusion Criteria:

  • Age < 18 years old
  • No paroxysmal atrial fibrillation
  • Patients with previous history of Vidaza® treatment

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): NCT03298321


Contacts
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Contact: Philippe CHEVALIER, MD 04 72 35 76 89 ext +33 philippe.chavalier@chu-lyon.fr
Contact: Camille VALLA 04 27 85 62 69 ext +33 camille.valla@chu-lyon.fr

Locations
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France
Service de rythmologie - GH Est-Hôpital Louis Pradel - CHU de Lyon HCL Recruiting
Bron, France, 69229
Contact: Philippe CHEVALIER, MD    04 72 35 76 89 ext +33    philippe.chavalier@chu-lyon.fr   
Contact: Camille VALLA    04 27 85 62 69 ext +33    camille.valla@chu-lyon.fr   
Principal Investigator: Philippe CHEVALIER, MD         
Centre Léon Berard Recruiting
Lyon, France, 69008
Contact: Anne-Sophie Michallet, MD, PhD    04.78.78.26.41 ext +33    anne-sophie.michallet@lyon.unicancer.fr   
Principal Investigator: Anne-Sophie Michallet, MD, PhD         
Hopital Lyon Sud Recruiting
Pierre-Bénite, France, 69310
Contact: Pierre-Yves COURAND, MD, PhD    04.78.86.57.37 ext +33    pierre-yves.courand@chu-lyon.fr   
Contact: Fiorenza Barraco, MD, PhD    04.78.86.43.40 ext +33    fiorenza.barraco@chu-lyon.fr   
Principal Investigator: Pierre-Yves COURAND, MD, PhD         
Sub-Investigator: Fiorenza Barraco, MD, PhD         
Sponsors and Collaborators
Hospices Civils de Lyon
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Responsible Party: Hospices Civils de Lyon
ClinicalTrials.gov Identifier: NCT03298321    
Other Study ID Numbers: 69HCL17_0114
First Posted: October 2, 2017    Key Record Dates
Last Update Posted: October 16, 2019
Last Verified: October 2019
Individual Participant Data (IPD) Sharing Statement:
Plan to Share IPD: No

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Studies a U.S. FDA-regulated Drug Product: No
Studies a U.S. FDA-regulated Device Product: No
Additional relevant MeSH terms:
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Atrial Fibrillation
Arrhythmias, Cardiac
Heart Diseases
Cardiovascular Diseases
Pathologic Processes
Azacitidine
Antimetabolites, Antineoplastic
Antimetabolites
Molecular Mechanisms of Pharmacological Action
Antineoplastic Agents
Enzyme Inhibitors