Genetically Determined Response to Atenolol in Patients With Persistent Atrial Fibrillation
Status:
Completed
Trial end date:
2016-09-01
Target enrollment:
Participant gender:
Summary
Atrial fibrillation (AF), the most common sustained heart rhythm disorder, is becoming
increasingly prevalent in the Western world. The number of people with AF in the United
States is projected to roughly double by the year 2050, to an estimated 6-12 million. For
many patients with AF, rate control with atrioventricular (AV) node blockers is a widely
accepted therapeutic strategy. These agents control heart rate, thus preventing symptoms and
systolic heart failure associated with tachycardia due to a rapid ventricular response to AF.
Beta-blockers are widely accepted as first line agents for rate control in AF, especially
when patients have concomitant hypertension (HTN), coronary artery disease, cardiomyopathies,
or heart failure (HF). As a class, beta-blockers are among the most commonly prescribed
cardiovascular medications.
Among patients with AF treated with beta-blockers, the heart rate (HR) response varies
substantially. Sometimes, adequate rate control can be achieved by titration of the
beta-blocker dose; but frequently, additional AV nodal blockers and/or digoxin are necessary.
In some cases, adequate rate control cannot be achieved even with the simultaneous use of
multiple AV nodal blockers, necessitating mechanical ablation of the AV node and permanent
pacemaker implantation.
Patient-specific variables that influence the response to beta-blockers include comorbid
conditions, weight, age, and level of physical activity. Ethnic differences in the response
to beta-blockers for the treatment of HTN and HF are well-described. However, the
contribution of genetic variants to beta-blocker efficacy in AF is unknown. We propose to
study whether the ADRB1 Gly389Asp SNP reduces response to beta-blockade in subjects with
permanent AF.
Phase:
N/A
Details
Lead Sponsor:
Vanderbilt University Vanderbilt University Medical Center