When and Where Does the Reentry Start in Long-QT Syndrome? - A Computer Simulation Study | IEEE Conference Publication | IEEE Xplore

When and Where Does the Reentry Start in Long-QT Syndrome? - A Computer Simulation Study


Abstract:

Reentry is the main form of arrhythmia. To know when and where the reentry starts in Long QT Syndromes (LQTS) and its relation with M cells distribution, the Luo-Rudy dyn...Show More

Abstract:

Reentry is the main form of arrhythmia. To know when and where the reentry starts in Long QT Syndromes (LQTS) and its relation with M cells distribution, the Luo-Rudy dynamic ionic model (LRdOO) of the mammalian ventricular action potential (AP) was used in a two dimensional transmural tissue sheets simulation. LQTS was simulated by reducing the membrane conductance of IKs for LQT1 and IKr for LQT2, and by altering the steady-state inactivation of the fast sodium current INa for LQT3. The endocardium was paced 10 times at a constant basic cycle length (BCL) of 500 ms (S1), and following a 2000 ms pause, a S2 stimulus was applied, or also a S3 stimulus was applied. The simulation was processed by changing shape, size and position of M cell domain, and S2S3 interval. We found that pause induced early after depolarization (EAD) started reentry near the boundary between endocardial domain and M cells domain. Only S3 stimulus that located in vulnerable windows could form reentry. The started position of the reentry depended upon the distribution of island of M cells and the position of extrasystole.
Date of Conference: 11-13 June 2009
Date Added to IEEE Xplore: 14 July 2009
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Conference Location: Beijing, China

I. Introduction

The long-QT syndrome (LQTS) characterized by the appearance of long QT intervals and wide T waves in the electrocardiogram (ECG) is associated with an atypical type of polymorphic ventricular tachycardia (VT) that may lead to sudden cardiac death [1]. Reentry is the main form of arrhythmia. The presence of ring road of conductance route, unidirectional conduction block and slow conduction velocity are the conditions for producing reentrant excitation. The heterogeneity of repolarization is the source of reentry. Optical mapping experiments showed that the unique topographical distribution of mid-myocardial cells (M cells) caused unidirectional block and reentrant excitation. By using optical mapping, Akar's group studied the distribution of M cells across the transmural surface [2]. Their experiments showed that M cells exhibited an island-like distribution but not sandwich-like. The island-like distribution of M cells extended toward endocardial or epicardial surfaces. M cells exhibited the longest APDs, but epicardial cells exhibited the shortest APDs. The distribution of APDs is the substrate of the heterogeneity of repolarization. The genetic mutations of LQTS result in a loss of ionic channel function with slow action potential repolarization and prolonged APDs[3]. It is important that M cell has many unique electrophysiological properties. M cells have a steeper APD-rate relation and a longer action potential duration (APD) than epicardial or endocardial cells. M cells display greater responsiveness to interventions that prolong APD (eg, agents with class III antiarrhythmic action) and a higher susceptibility to the development of early afterdepolarizations (EADs). These properties suggest that M cells play an important role in arrhythmias associated with abnormal repolarization in the congenital or acquired long-QT syndrome (LQTS) [4].

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