| Atrial fibrillation(AF)is currently the most common sustained clinical arrhythmia, with an incidence about 0.5% in the population. AF becomes increasingly common with age, having an incidence reaching 8.8% in patients at the age of eighties. In China, one of the most common etioloy of AF is mitral diseases in rheumatic heart diseases. AF is one of causes of ischemic stroke and doubles mortality in hospital.The Incidence of AF in rheumatic heart diseases is very high, nearly up to 80% in mitral diseases with AF. AF is very harmful to human health so that the research about its etiology, mechanism of onset, prophylaxis and treatment has become one of focal points and hot spots in cardiovascular research field. There is few study on molecular mechanism of onset of AF in rheumatic heart diseases in domestic and in aboard. Ocurrence and development of AF are very complicated process accompanied by many mechanisms in them. Post study on AF with rheumatic heart diseases mainly focused on ion-channel protein, connexin of myocardial cells and related molecules. Many current studies showed that calcium overload is one of mechanism of AF onset. Calcium overload can activate many signal transduction systems in cells, one of the obvious points in that is the changes of Calpain I. Calpain I is a member of Calpain family and it is one of calcium dependent neutral proteases. Calpain I is widely present in many organs and tissues and participate in many pathophysiologic process. Recent research showed that activated Calpain I can degrade contraction protein partially, and lead to low contractive function and changes of structure and channel protein of myocardial cells which are closely related to electrophysiologic reconstruction and structural reconstruction. Recently there is no report on Calpain I changes and its mechanism in AF patients with rheumatic heart diseases and there is also no report on relationship between Calpain I changes and clinic electrophysiologic characters during AF in rheumatic heart diseases. Based on AForementioned research background, this study construcrted on electrophysiologic mapping and Calpain I changes of [Foundation] This project is supported by National Natural Science Fundation of China(30070749)AF patients with rheumatic heart diseases, focusing on electrophysiologic character and Calpain I changes in different AF. This study detected on Calpain I changing character and effecting mechanism in different levels in AF patients with rheumatic heart diseases, and elucidated correlaton between microcosmic molecule changing and electrophysiologic parameters of macroscopic epicardial mapping in AF patients with rheumatic heart diseases.This study broke through obstacles between medical basic research and clinic study, combined molecular mechanism which belong to basic research with clinic epicardial mapping in AF patients with rheumatic heart diseases. Following research work having been done in this field, this study further elucidate onset and developping mechanism and characters of AF in patients with rheumatic heart diseases. Methods and results of this study as follows:This study includes five parts. All the subjects suffered from mitral diseases. Subjects in the first two parts were divided into four groups by different kinds of diseases and AF types: Group A(n=12): Sinus rhythm group with non-rheumatic heart diseases; Group B(n=13): Sinus rhythm group with rheumatic heart diseases; Group C(n=14): Paroxysmal AF group with rheumatic heart diseases; Group D(n=16): Persistent AF group with rheumatic heart diseases. In the first part, epicardial mapping to left atrium and right atrium was performed before intra-cardiac operation, and electrophysiologic mechanism of AF with rheumatic heart diseases was analyzed by the result of epicardial mapping. In the second part, myocardial specimens of right atrial incision in the four groups were acquired for detecting Calpain I activity and Calpain II activity and performing immunohistochemistry study. Three groups was divided in other three p... |
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