Characterizing the global changes in miRNA expression in human atrial appendages with persistent atrial fibrillation.

Atrial fibrillation (AF), the most common cardiac rhythm disorder, is a major cause of cardiovascular morbidity and mortality. AF is characterized by the rapid and irregular activation of the atrium with diverse abnormalities, including electrical, structural, metabolic, neurohormonal, or molecular alterations.3 Although the pathophysiology of AF is complex, it has traditionally been treated with antiarrhythmic drugs that control the rhythm by altering cardiac electrical properties, principally by modulating ion channel function. However, treatments of AF with antiarrhythmic drugs have mostly failed to control the heart rhythm, because the electrical characteristics of atrial cardiomyocytes are eventually altered or remodeled during the course of AF. The aims of this study were to characterize the global changes in miRNA expression in human atrial appendages and to identify the target ion channel(s) responsible for electrical remodeling in AF. In this study, we performed a comprehensive analysis of miRNA microarrays, using a strict selection for human samples. Human atrial right appendages were collected from patients who had received open-heart surgery at Oita University Hospital; 10 samples were from patients with persistent AF (AF group) and 11 samples from patients with normal sinus rhythm (NSR group). The samples were only from male (60–79 years old) patients, and excluded those with chronic heart failure, diabetes, inflammatory diseases, endocrine diseases, metabolic diseases, kidney diseases requiring hemodialysis, history of steroid treatment, and paroxysmal AF. The AF group included patients with a documented record of sustained AF for 6 months or longer. The NSR group included patients with no documented history of AF.