Obesity Mediates Response to Antiarrhythmic Drugs in A-Fib

Obesity may cause a differential response to antiarrhythmic drugs (AADs) used to suppress atrial fibrillation (AF), according to a study published online in JAMA Cardiology.

Aylin Ornelas-Loredo, from the University of Illinois at Chicago, and colleagues conducted an observational study involving 311 patients enrolled in a clinical-genetic registry to examine whether obesity differentially mediates response to AADs in symptomatic AF. In addition, mice fed a high-fat diet for 10 weeks were assessed.

The researchers found that nonresponse to class I AADs was less in patients with versus those without obesity (30 versus 6 percent). Similar symptomatic response to a potassium channel blocker was seen for both groups. Significant indicators of the probability of failure to respond to AADs included obesity, AAD class (class I versus III AAD [obese] odds ratio, 4.54), female versus male sex (odds ratio, 2.31), and hyperthyroidism (odds ratio, 4.95). Pacing induced AF in 100 and 30 percent of diet-induced obesity (DIO) mice and controls, respectively. When treated with sotalol versus flecainide, DIO mice showed a greater reduction in AF burden (85 versus 25 percent).

"Our study not only suggests that obesity mediates response to AADs for AF, but also that there is reduced therapeutic effectiveness of sodium channel compared with potassium channel blocker AADs," the authors write. "Our findings may have important implications for the management of AF in patients with obesity."

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