RESEARCH ARTICLE Increased expression of N t Q

Atrial fibrillation (AF) is the most common cardiac arrhythmia in clinical practice [1,2]. Valvular heart dis-ease (VHD), which comprises pathological changes in the mitral or aortic valves, causes AF. Valvular surgery is an option to prevent heart failure in serious VHD patients [3,4]. AF is self-perpetuating because tachyarrhythmia causes electrophysiological and structural changes that exacerbate or maintain AF [5]. This structural remodel-ing can contribute to both the development and mainten-ance of AF [6,7]. Several factors associated with atrial structural remodeling have been identified [8], of which atrial fibrosis and myocyte hypertrophy are considered key [9]. Atrial fibrosis is a hallmark of arrhythmogenic struc-tural remodeling [10,11]. Cardiac fibrosis is defined as a detrimental process causing imbalanced extracellular matrix deposition and heart degradation. Cardiac fibrosis causes excessive fibroblast proliferation and accumu