Electrophysiologic Study Of Crista Terminalis And Pulmonary Vein

Background: According to many clinical researches, more than 90% of the ectopical starting points which can cause focal atrial fibrillation are focus on the wall of pulmonary veins (PV).But there is still lack of reasonable explaination on the reason why pulmonary veins can become the focus parts which can cause focal atrial fibrillation (AF).It was suggested that perhaps they were related to the increasing of the local myocardial tissue spontaneous activities, triggered activity or the micro back-turning circle, And still, there was short of foundational researches of morphological study to interpret all these mechanisms. Crista terminalis (CT) is endocardial hunches in the right atrium, which arising from the right appendage, reaching to the lateral and inferior walls and connected with Eustachian ridge. Pectinate muscles (PM) originate from the crest in varying angles and extend along the wall of the appendage. CT marks the junction of the venous part and rough zones. With the development of radiofrenquency ablation of focal atrial tachycardia especially focal atrial fibrillation, the implications of CT in the initiation and maintenance of atrial tachycardia (AT) arose widespread attention. CT is the rare site of focal AF and most common site of focal AT. It is the anatomic basis of atrial flutter and inappropriate sinus tachycardia. Kalman named it as "Cristal tachycardias". Knowledge about the reason why CT become arrhythmogenic and their implications for the atrial tachycardiais is limited. The underlying anatomic and electrophysiologic properties remain unclear. In spite of the ripid progress of radiofrequency catheter ablation, anti-arrhythmia drug remain very important.Our study contained three parts of investigation. The purpose of this study was to investigate the morphological, electrophysiological and electropharmacologic characteristics of the crista terminalis and left atrial-pulmonary vein (LA-PV), and their implicationsfor the atrial tachycardia especially atrial fibrillation.Materials and Methods: 40 health adult rabbits weighing from 1500 to 2500 g, regardless of sexual distinction. 10 for histochemical dyeing to observe by optical microscope. Obtain 7 sample of hearts with lung , fix and dissect to demonstrate CT, left atrium and focal atria fibrillation are focus on the wall of PV. Observing the anatomical situation of these pulmonary veins. Got pulmonary veins, 20's for embedding with paraffin wax, then HE dye after slicing. Observe by optical microscope. Other 30 rabbits for investigating the electrophysiologic properties of LA-PV and and the electropharmacologic property of Nifekalant, a novel classâ…¢antiarrhythmic drug. By using standard glass microelectrode technique, cellular action potentials (APs) of CT and LA-PV were recorded in normal Tyroid's perfusion and Tyroid's perfusion with 1 u mol/L isoproterenol, 5.5 u mol/L acetylcholine and 2.13mg/L nifekalant respectively.Result: The middle and/or inferior segments of CT were so flat that there were no endocardial hunches at all. The pectinate muscles (PM) originate from the crest in varying angles and extend along the wall of the appendage toward the vestibule of tricuspid valve. They formed "ridge-like" or "bridge-like" structure. Most PM have non-uniform arrangement with abundant interlacing trabeculations between them. The perimysium enveloped groups of paralled myocardium of the crest. Pulmonary veins have myocytes twist in their outer layer from the orifices of them. These myocytes are focus and spread on the roots of the pulmonary veins, varied in their directions disorderly, but extend and stretch toward the far end of these pulmonary veins at some particular part of their walls. Pulmonary vein cardiomyocytes had smaller resting membrane potential (RMP), action potential amplitude (APA), action potential duration(APD) and maximum phase 0 upstroke velocity (Vmax) than that of left atrium. All displayed fast-response action potentials under the well-controlled experimental condition. No spontaneous pacemaking activities, early or delayed afterdepolarisations were observed. No electrophysiological inhomogeneity between the distal and the proximal part of the pulmonary veins was observed. Infusion of 5.5 uM acetylcholine (ACH) shortens APD and abbreviates the effective refractory period (ERP) of left atrium and proximal part of PV, Infusion of 1 u M of Isoprenaline (ISO) also abbreviates the ERP of left atrium and proximal part of PV, and may induce early afterdepolarisations, But ACH and ISO have little effect on distal part of PV. Nifekalant significantly increase atrial and PV' s APD, and there was a tandency of prolonging the ERP of atrium and PV.Conclution: The anatomic and histological properties of CT and its junctional area may provide the morphologic basis which may be the origin of arrhythmia. The disorderly arrangement of myocytes located in the root of pulmonary vein's wall provides the basis by which pulmonary veins can form the rapid back-turning circle which can trigger atrial fibrillation. PV cardiomyocytes have discrete action potential properties, so PV may be a privileged site for atrial reentry, especially in the presence of ACH. Electrophysiological effects of nifekalant are attenuated in the remodeled atrium, and may be effective in the prevention of AF.