MMP-9 in Myocardial Fibrosis and Structural Remodeling in Rheumatic Heart Disease Patients with Atrial Fibrillation: A Single-center Prospective Case-control Study
Abstract Background: Atrial fibrillation (AF) is a common arrhythmia that induces disability or death; however, the underlying pathogenesis is yet unclear. This study aimed to investigate the expression of matrix metalloproteinase-9 (MMP-9) in rheumatic valvular heart disease (RVHD) and its value in predicting AF.Methods: In this single-center, prospective case-control study, 30 patients who received valve replacement for the treatment of RVHD in the Cardiac and Major Vascular Department, Yue Bei People’s Hospital between August 2012 and January 2015 were included in this study. The patients were categorized equally into two groups according to the electrocardiogram characteristics: sinus rhythm (SR) group and chronic atrial fibrillation (AF) group. In patients hospitalized for RVHD, the fasting serum was collected on the following day in the morning, and the tissues of right auricle were collected during the operation. Hematoxylin and eosin staining and Masson staining were performed to assess the pathological structures of myocardial tissues and changes in collagen fibers. Enzyme-linked immunosorbent assay was used to measure the level of MMP-9 in serum, and the distribution of the protein in myocardial tissues was assessed by immunohistochemistry. Echocardiography was performed before the surgery to measure the left atrial diameter and ejection fraction.Results: The MMP-9 expression was significantly higher in the AF group than the SR group (4.2281 ± 0.9165 ng/mg vs. 2.7613 ± 1.2166 ng/mg, p < 0.05). The MMP-9 levels were positively associated with left atrial diameter (LAD) (p < 0.01) and collagen volume fraction (CVF) (p < 0.05).Conclusions: MMP-9 expression is elevated in AF patients and could be one of the major factors involved in the remodeling of atrial structures in AF. MMP-9 influences the metabolism of collagen and promotes the fibrosis of the myocardium, participates in cardiac structural remodeling, and plays a role in the onset and maintenance of AF.