Heart patients prone to emotionally triggered atrial fibrillation are less likely to experience an arrhythmia if they’re taking beta-blockers, according to a June 3 study published in Heart Rhythm.
Just like heart attacks or ventricular arrhythmias, AFib is a CV condition that can be aggravated or triggered by psychosocial stress and negative emotions, lead investigator Rachel Lampert, MD, and colleagues at the Yale School of Medicine said in the journal. Those kinds of stressors increase activity in the sympathetic nervous system and decrease vagal activity, leaving patients vulnerable to heart irregularities.
“Catecholamines increase and heart rate variability decreases with anger recall and other stress-inducing laboratory protocols, which in turn alter electrophysiological properties of the atrium, likely pathways from stress to AFib,” Lampert, a professor of internal medicine at Yale, and co-authors said. “Sympathetic activation may precede AFib, and sympathomimetic drugs are profibrillatory, used to purposefully induce AFib in patients undergoing ablation, supporting the concept that other adrenergic stimuli could also promote AFib.”
Beta-blockers have seen success in mitigating the autonomic and hemodynamic effects of psychosocial stress in heart patients, in one case attenuating stress-induced arrhythmias in an animal model. In an effort to replicate those results in humans, Lampert and her team studied 95 patients with a history of AFib who presented to Yale New Haven Hospital or the Hospital of Saint Raphael between 2004 and 2008.
For a year, study participants carried an electronic diary with them and recorded the emotions they were experiencing before AFib episodes struck. They also captured their heart rhythm on a handheld monitor whenever they developed symptomatic AFib for five minutes or more and were asked to record their emotions while wearing an ambulatory Holter monitor for 24 hours once every month.
Around half of patients were receiving preventive treatment with beta-blockers, while the other half abstained from additional therapy. Lampert et al. reported participants taking beta-blockers were just as likely to experience anger or stress than their counterparts, but the emotional episodes only raised their odds of AFib by four times, compared to 20 times in patients not taking beta-blockers.
“The mechanisms underlying the protective effects of beta-blockers likely involve influences on both central and peripheral systems,” the authors wrote. “In this study, lipophilic beta-blockers exerted a stronger effect, suggesting central influences may predominate, although this finding should be interpreted with caution as numbers are small.”
In the study, Lampert and colleagues said the effect of beta-blockers was strongest in those taking drugs without antiarrhythmic properties.
“Excluding those on sotalol, the effect of beta-blockers was even stronger, completely countering the triggering effects of anger or stress,” the team said. “While the effect of beta-blockers on the overall prevalence of AFib could not be evaluated in this nonrandomized study, they did reduce the ability of anger or stress to trigger AFib. Identifying patients with AFib prone to emotional triggering may be one strategy to target beta-blockers to those most likely to benefit.”