Home About us Contact
|
Home About us Contact | ||
|
|
||
Long QT (long + qt)
Terms modified by Long QT Selected AbstractsSex Modulates the Arrhythmogenic Substrate in Prepubertal Rabbit Hearts with Long QT 2JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 5 2005Ph.D., TONG LIU M.D. Females have a greater susceptibility to Torsade de Pointes in congenital and drug-induced long QT syndrome (LQTS) that has been attributed to the modulation of ion channel expression by sex hormones. However, little is known regarding sex differences in pre-puberty, that is, before the surge of sexual hormones. In patients with congenital LQTS types 1 and 2, male children tend to have a greater occurrence of adverse events, especially in 10,15 year olds, than their female counterpart. To evaluate whether the rabbit model of drug-acquired LQTS exhibits similar age dependences, hearts of prepubertal rabbits were perfused, mapped optically to record action potentials (APs) and treated with an IKr blocker, E4031 to elicit LQTS2. As expected, AP durations (APD) were significantly longer in female (n = 18) than male hearts (n = 10), at long cycle length. Surprisingly, E4031 (50,250 nM) induced a greater prolongation of APDs in male than in female hearts, and in both genders reversed the direction of repolarization (apex , base to base , apex), enhancing dispersions of repolarization. Furthermore, in male hearts, E4031 (0.5 ,M) elicited early afterdepolarizations (EADs) that progressed to polymorphic ventricular tachycardia (PVT) (n = 7/10) and were interrupted by isoproterenol (40 nM) and prevented by propranolol (0.5,2.5 ,M). In female hearts, E4031 (0.5 ,M) produced marked prolongations of APDs yet few EADs with no progression to PVT (n = 16/18). Thus, sex differences are opposite in prepubertal versus adult rabbits with respect to E4031-induced APD prolongation, EADs and PVT, underscoring the fact that APD prolongation alone is insufficient to predict arrhythmia susceptibility. [source] Concomitant-Acquired Long QT and Brugada Syndromes Associated with Indapamide-Induced Hypokalemia and HyponatremiaPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 6 2008NGAI-SHING MOK M.B.B.S. Electrolyte disturbances are known to cause acquired Long QT syndrome (LQTS) and Brugada syndrome. While a reduction in INa due to SCN5A mutation is implicated as the underlying mechanism in Brugada syndrome, hyponatremia, which can give rise to a reduced INa, has never been reported in literature as a cause or precipitating factor in this syndrome. We detailed a case in which concomitant-acquired LQTS and Brugada syndrome were associated with severe hypokalemia and hyponatremia following indapamide use for treatment of hypertension and highlighted the potential role of hyponatremia in the pathogenesis of the acquired form of Brugada syndrome. [source] Dofetilide-Induced Long QT and Torsades de PointesANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 3 2007Mehmet K. Aktas M.D. Dofetilide, a new class III antiarrhythmic agent, has been approved as an antiarrhythmic agent for the treatment of atrial fibrillation and atrial flutter. Dofetilide selectively inhibits the rapid component of the delayed rectifier potassium current resulting in a prolongation of the effective refractory period. Like other drugs that affect potassium currents, the prolonged QT interval occurring in the patients treated with dofetilide can be complicated by torsades de pointes. We report four cases of dofetilide-induced QT prolongation and torsades de pointes. We discuss the risk factors for the development of dofetilide-induced long QT and torsades de pointes and review the current literature. [source] What is more dangerous in long QT 3 syndrome?ACTA PHYSIOLOGICA, Issue 4 2008Arrhythmogenic trigger or substrate? No abstract is available for this article. [source] Modelling and imaging cardiac repolarization abnormalitiesJOURNAL OF INTERNAL MEDICINE, Issue 1 2006Y. RUDY Abstract. Repolarization abnormalities, including those induced by the congenital or acquired long QT (LQT) syndrome, provide a substrate for life-threatening cardiac arrhythmias. In this article, we use computational biology to link HERG mutations mechanistically to the resulting abnormalities of the whole-cell action potential. We study how the kinetic properties of IKs (the slow delayed rectifier) that are conferred by molecular subunit interactions, facilitate its role in repolarization and ,repolarization reserve'. A new noninvasive imaging modality (electrocardiographic imaging) is shown to image cardiac repolarization on the epicardial surface, suggesting its possible role in risk stratification, diagnosis and treatment of LQT syndrome. [source] Right ventricular noncompaction associated with long QT in a fetus with right ventricular hypertrophy and cardiac arrhythmiasPRENATAL DIAGNOSIS, Issue 6 2008Ruben J. Acherman No abstract is available for this article. [source] Dofetilide-Induced Long QT and Torsades de PointesANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 3 2007Mehmet K. Aktas M.D. Dofetilide, a new class III antiarrhythmic agent, has been approved as an antiarrhythmic agent for the treatment of atrial fibrillation and atrial flutter. Dofetilide selectively inhibits the rapid component of the delayed rectifier potassium current resulting in a prolongation of the effective refractory period. Like other drugs that affect potassium currents, the prolonged QT interval occurring in the patients treated with dofetilide can be complicated by torsades de pointes. We report four cases of dofetilide-induced QT prolongation and torsades de pointes. We discuss the risk factors for the development of dofetilide-induced long QT and torsades de pointes and review the current literature. [source] | |||||||||||||