ST-segment Elevation as an AF Endophenotype (Proc)
|ClinicalTrials.gov Identifier: NCT01205529|
Recruitment Status : Completed
First Posted : September 20, 2010
Results First Posted : May 2, 2018
Last Update Posted : May 2, 2018
|Condition or disease||Intervention/treatment||Phase|
|Atrial Fibrillation||Drug: Procainamide||Not Applicable|
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 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 early-onset ('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.
|Study Type :||Interventional (Clinical Trial)|
|Actual Enrollment :||161 participants|
|Intervention Model:||Single Group Assignment|
|Masking:||None (Open Label)|
|Masking Description:||All participants and investigators were blinded to the genetic sequencing results at the time of outcome ascertainment|
|Official Title:||ST-segment Elevation With Procainamide as an ECG Endophenotype of AF|
|Study Start Date :||November 2010|
|Actual Primary Completion Date :||June 2015|
|Actual Study Completion Date :||June 2015|
AF with ST changes on ECG
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 harbor cardiac sodium channel gene variants.
One time intravenous infusion of Procainamide administered over 30 minutes. Dosage is calculated as 10mg/kg based on subject's ideal body weight.
- ST Segment Elevation ≥ 1.5 mm in the Right Precordial Leads (V1-V3), Either at Baseline or Manifested After Sodium 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 ]Number of participants who demonstrated ST-segment elevation >1.5mm in the right precordial leads (V1-V3) either at baseline or after sodium channel block with intravenous procainamide infusion.
Please refer to this study by its ClinicalTrials.gov identifier (NCT number): NCT01205529
|United States, Tennessee|
|Vanderbilt University Medical Center|
|Nashville, Tennessee, United States, 37232|
|Principal Investigator:||Dawood Darbar, MD, PhD||Vanderbilt University|