Preliminary Simulation Study Of The Electrophysiological Mechanisms Of Short QT Syndrome

For many years, major advances have been made in the understanding of the clinical substrates of inherited arrhythmogenic diseases sudden cardiac death (SCD) with structurally normal heart and to find new and more effective therapeutic and diagnostic strategies. Since 1960, Many simulation studies for ventricular myocardium cell are based on varies channels in the ionic mechanisms underlying cardiac excitation, such as Hodgkin-Huxley model, Beele-r-Reuter model and Luo-Rudy model. These Models argue for a detailed understanding of the ionic mechanisms that promote the molecular and genetic feat-Wures of the heart electrophysiological.In recent years, several syndromes potentially responsible for arrhythmic sudden death have been described. Most of them have been primarily identified from abnormal baseline ECG patterns in patients with aborted sudden cardiac death and their relatives. In 2000, Gussak reported a family with paroxysmal atrial fibrillation and constantly shortened QT intervals was identified. From then on, a high familial risk for sudden cardiac death associated with a short QT interval was demonstrated by many reports. Furthermore, episodes of atrial fibrillation were documented in patients with a short QT syndrome at different ages even in adolescents. It must nowadays be considered in the evaluation of patients with syncope, aborted sudden cardiac death, atrial fibrillation, ventricular fibrillation and/or a positive family history for syncope and sudden death.It is unclear and remains to be answered in the future the total mechanisms for shortened QT intervals, It has been shown that three type mutations in genes at least that encode different ion channels could underlie alterations in the action potential (AP) morphology and Short QT interval leading to an increased risk of ventricular arrhythmias and SCD.Several antiarrhythmic drugs such as ibutilide, sotalol, and flecainide have been demonstrated to be ineffective in prolongation of the QT interval.Some researches show that QUINDINE will be an effective drug. Facing the high risk for ventricular tachyarrhythmias, the implantable cardioverter defibrillator is to date the therapy of choice in patients with a short QT syndrome. At present, therapy of choice in the prevention of sudden cardiac death is the implantable cardioverter defibrillator.In this article, we firstly address a mathematical model of the action potential of human ventricular cells Based on Luo-Rudy2000 model and Tusscher model, then we use this model to Simulate and Study the electrophysiological mechanisms of SQTS1, SQTS2 and SQTS3.According to the result of Computer simulations, we analysis that more outward current would stabilize reentry by accelerating ventricular repolarization, thus causing a shortening of the terminal phase of the cardiac action potential. Wavebreaks and rotation in SQTS would lead to a high probability ventricular fibrillation and sudden cardiac death.This is definitely an exciting era in which channelopathies are being described in the clinic whilst models that faithfully reproduce the clinical symptoms. This may pave the way for the development of new and more effective therapeutic and diagnostic strategies in the not too distant future.