Certain People With Atrial Fibrillation May Have Changes on Ecg When Given Procainamide That May be Related to a Genetic Difference

This study is currently recruiting participants. (see Contacts and Locations)
Verified December 2013 by Vanderbilt University
Sponsor:
Information provided by (Responsible Party):
Dawood Darbar, Vanderbilt University
ClinicalTrials.gov Identifier:
NCT01205529
First received: September 17, 2010
Last updated: December 16, 2013
Last verified: December 2013

September 17, 2010
December 16, 2013
November 2010
October 2015   (final data collection date for primary outcome measure)
ST segment elevation ≥ 1 mm in the right precordial leads (V1-V3), either at baseline or manifested after Na+ channel block with intravenous procainamide [ Time Frame: During (5, 10, 15, 20, 25, 30 minutes after initiating) or up to 15 minutes after completion of intravenous procainamide infusion ] [ Designated as safety issue: No ]
ST segment elevation ≥ 1 mm in the right precordial leads (V1-V3), either at baseline or manifested after Na+ channel block with intravenous procainamide [ Time Frame: During (5, 10, 15 miutes after initiating) or up to 30 minutes after initiation of intravenous procainamide infusion ] [ Designated as safety issue: No ]
Complete list of historical versions of study NCT01205529 on ClinicalTrials.gov Archive Site
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Certain People With Atrial Fibrillation May Have Changes on Ecg When Given Procainamide That May be Related to a Genetic Difference
Prospective Evaluation of a Potential Sodium Channel-Related Endophenotype

The purpose of this study is to look for a similarity in people's genes that may help understand which people could benefit from certain drugs for the treatment of atrial fibrillation.

Current drug therapies to suppress AF are incompletely and unpredictably effective and carry significant (albeit generally small) risks of serious adverse effects, including drug-induced long QT syndrome (diLQTS), other forms of proarrhythmia, increased mortality through uncertain mechanisms, and extracardiac toxicity. Identification of clinical and genetic subtypes of AF will permit stratification of therapeutic approaches and thereby facilitate the practice of personalized medicine. Furthermore, limited success of drug therapy and increase in drug toxicity in AF is probably because the arrhythmia represents a final common pathway of multiple initiating mechanisms, including those some that are genetically-defined.

Identifying specific intermediate phenotypes ("endophenotypes") associated with defined clinical courses in AF represents a potential method to systematically subtype patients by underlying mechanism and represents a much-needed clinical advance. Clinical endophenotypes that have been studied include atrial fibrillatory rate, prolonged signal-averaged P-wave duration, and biomarker profiles. The endophenotype we will study here is right precordial ST segment elevation, seen not only in Brugada syndrome (BrS) (where it is unmasked by sodium channel blocking drugs) but also commonly in lone AF and in patients with AF-associated rare variants in genes encoding the cardiac sodium channel α- or β-subunits. Taken together these data suggest the hypothesis to be tested in this study, that variants in multiple genes can culminate in a similar AF-prone substrate by reducing sodium current that can be identified by screening for baseline or manifest right precordial ST segment elevation endophenotype after sodium channel block with intravenous procainamide.

Interventional
Not Provided
Endpoint Classification: Safety Study
Intervention Model: Single Group Assignment
Masking: Open Label
Primary Purpose: Diagnostic
Atrial Fibrillation
Drug: Procainamide
One time intravenous infusion of Procainamide administered over 30 minutes. Dosage is calculated as 10mg/kg based on subject's ideal body weight.
Atrial Fibrillation with ST changes on electrocardiogram
Those patients with ST segment or J Point elevation on electrocardiogram. Can be on initial screening electrocardiogram or on electrocardiograms during procainamide infusion. These subjects will also have SCN5A mutation.
Intervention: Drug: Procainamide
Not Provided

*   Includes publications given by the data provider as well as publications identified by ClinicalTrials.gov Identifier (NCT Number) in Medline.
 
Recruiting
750
October 2015
October 2015   (final data collection date for primary outcome measure)

Inclusion Criteria:

  • 18 years of age or older
  • Undergoing AF ablation at Vanderbilt or MGH

Exclusion Criteria:

  • Patients taking membrane active anti-arrhythmic drugs with sodium channel blocking properties (amiodarone, dronedarone, flecainide, propafenone) at the time of the ablation
  • Patients with a history of Brugada syndrome or type 1 Brugada ECG pattern on the baseline ECG
  • Patients with a history of drug-induced torsades de pointes
  • Patients with a known history of hypersensitivity to procainamide, procaine or related drugs
  • Patients with a history of systemic lupus erythematosus and myasthenia gravis
  • Patients with a history of second degree AV block (Mobitz type II) or third degree AV block
  • Women of child-bearing potential unless post-menopausal, surgically sterile, or have a negative pregnancy test day on the day of procedure
  • Patients with dual chamber pacemakers or implantable defibrillators requiring ventricular pacing (uninterpretable ECG)
  • Patients unable to give informed consent
Both
18 Years and older
Yes
Contact: Gayle Kucera, RN 615-936-6069 gayle.a.kucera@vanderbilt.edu
United States
 
NCT01205529
IRB # 100800, U19HL065962
Yes
Dawood Darbar, Vanderbilt University
Vanderbilt University
Not Provided
Principal Investigator: Dawood Darbar, MD, PhD Vanderbilt University
Vanderbilt University
December 2013

ICMJE     Data element required by the International Committee of Medical Journal Editors and the World Health Organization ICTRP