Could plugging the oxidation-mediated Ca2+ leak stem the tide of the atrial fibrillation epidemic?

As the most common sustained arrhythmia, atrial fibrillation (AF) afflicts 2 million patients in the United States alone, and this number is predicted to double by the year 2050.1 Although AF is not life-threatening, it is linked to a 2-fold increase in mortality when present as a comorbidity in heart disease patients.2,3 AF can have devastating consequences, such as stroke, impaired cardiac performance, and promotion of cardiomyopathy. The treatment of AF can also produce life-threatening side effects, such as ventricular arrhythmias and hemorrhage. AF patients are generally classified as paroxysmal (episodes lasting 7 days), persistent (lasting 7 days but treated to restore sinus rhythm), or permanent (no attempt to restore sinus rhythm).2,3 AF is usually secondary to other conditions such as hypertension, heart failure, valvular disease, sleep apnea, hyperthyroidism, and diabetes. Most of these AF-inducing conditions are associated with elevated atrial pressure and atrial stretch, as well as increased oxidative stress and inflammation, which lead to structural and electric changes (remodeling) that create a substrate for supporting AF induction and maintenance.4,5