Changes Of HCN2 Gene Protein Of Atrial Myocytes In Rheumatic Valvular Heart Disease

Objective:By comparing the rheumatic valvular heart disease, rheumatic patients with atrial fibrillation with and without atrial fibrillation (sinus rhythm) in patients with atrial muscle hyperpolarization activated cyclic nucleotide gating cation channels-2 (HCN-2) subtype protein expression, and explains the adult atrial muscle cells in vitro tissue in vitro culture method and the appraisal, explore its correlation with rheumatic atrial fibrillation occurred.Methods:According to the symptoms and signs and ecg heart colour to exceed and other auxiliary examination in patients with rheumatic heart disease with mitral stenosis, and 40 cases of patients with operation indications, always, if there is a history of atrial fibrillation is divided into:22 cases of atrial fibrillation (AF) group, atrial fibrillation (SR) of 18 cases, conventional surgery to remove the right auricle tissue, application identified by immunofluorescence atrial myocyte, flow cytometry detection in patients with rheumatic engineered gene protein expression, and CCK 8 method is applied to detect the atrial muscle cells proliferation.Results:By immunofluorescence method appraisal result in tissue explant culture of primary cell into The atrial muscle cells, flow cytometry test results, the AF group and SR in engineered gene protein expression were 86.73±4.05% and 69.5 ±4.61% of patients with AF group into The atrial muscle cells engineered protein expression significantly higher amount of SR group (t= 12.53, P< 0.05), the results showed that patients with rheumatic heart disease associated with atrial fibrillation atrial muscle engineered gene expression in the muscle cell protein increased significantly.Conclusion:Rheumatic heart disease patients with atrial fibrillation with atrial muscle engineered gene protein expression in quantity is obviously higher than that of without atrial fibrillation group, prompt engineered gene expression of the protein may be involved in the development process of rheumatic heart disease atrial fibrillation.