长QT综合征地抗心律失常药物.pptVIP

Acquired Long QT Syndrome by Antiarrhythmic Drugs Chen Liying MD – Cardiology Department An Zhen Hospital Beijing CHINA. NASPE-Heart Rhythm Association International fellow. Bologna 2004. Franco Naccarella MD – Cardiology Department Azienda USL Città di Bologna ITALY Stefano Sdringola Maranga MD – Cardiology Division Hermann Memorial Hospital Houston TX USA CHINA 1-16/11/2005 CARDIOSTIM 2004 – June 16-19 Nice, France Genetic characterization of congenital LQT syndrome Mechanims of Drug-induced QT Prolongation and TdP 1 The blockade of Ikr current by antiarrhythmic drugs that are capable of prolonging the action potential duration is at least in part responsible for their proarrhythmic effect. It is interesting to note that many other drugs that cause the development of early afterdepolarizations and TdP block the Ikr channel. The incidence of TdP remain low, however, and not all drugs that block Ikr have the same arrhythmogenic potential. The precise reason for the different effects of Ikr blocker is unknown. Mechanims of Drug-induced QT Prolongation and TdP 2 Thus, in an ordinary situation, the administration of an Ikr blocker might not prolong the QT interval. However in the presence of an otherwise subclinical lesion in the repolarization mechanisms (i.e. reduced repolarization reserve), the same Ikr blocker may precipitate marked QT prolongation and TdP. Mechanims of Drug-induced QT Prolongation and TdP 3 The causes for these lesions may be acquired (e.g. myocardial infarction, congestive heart failre, ischemia, etc.) or congenital (formes frustes of congenital long QT syndrome). The extent of QT prolongation and risk of TdP associated with a given drug may not be linearly related to the dose of plasma level of the drug, because patient and metabolic factors are also important (e.g. gender, electrolyte levels, etc) There is not a simple relationship of drug-induced QT prolongation and the likelihood of the development of TdP which can sometimes occur w