Investigation On Expression Of Cx40 And Cx43 In Patients With Rheumatic Heart Disease And Atrial Fibrillation

Background and Objective: Atrial fibrillation (AF) is the most prevalent permanent arrhythmia ,and do harm to human beings' health.But its cause isn't clear. 1914,Garrey performed innovative experiments that implicated reentry as the mechanism of fibrillation.He further proposed that persistence of fibrillationis directly proportioned to the size of the tissue mass involved.This marked a start of the mechanism of atrial fibrillation in modern times.Since then,a series of hypothesis on the mechanism of fibrillation was brought forward in succession.At present,a wealth of data suggests that reentry is the primary mechanism of atrial fibrillation. It was reported four models of reentry,inclucing leading circle model ,spiral wave reentry, ring model and figure-of-eight model.If they fundtion, ring model must has anatomical barrier,but the other three model have just only functional barrier.The change of single ion channel just alter the excitability of single cell,so gap junction(GJ) is the basis of cardiac integrated electrical current.That whole heart can be synchronous excitation.Animal models of the atrial fibrillation and operative samples suggested that connexins constituted GJ related to the initiation and perpetuation of the atrial fibrillation .So far five connexins have been identified,i.e. Cx40,Cx43,Cx45,Cx37 and Cx46.Among them Cx40,Cx43,Cx45 is relatively abundant in cardiac muscle,Cx37 distributing to wall of cardiac vascular,a small quantity of Cx37 and Cx46 distributing to atrium or ventricle.Except sinus node,atrioventricular node,some...