Patanè Salvatore, Marte Filippo, Di Bella Gianluca, Currò Alessio, Coglitore Sebastiano
Int J Cardiol. 2008 Nov 12;130(2):e71-3. doi: 10.1016/j.ijcard.2007.11.070. Epub 2008 Feb 5.
Torsade de pointes is a form of polymorphic ventricular tachycardia occurring in a setting of prolonged QT interval on surface electrocardiogram. Several non-antiarrhythmic drugs including antibiotic and antipsychotic agents have been shown to prolong cardiac repolarization predisposing to torsade de pointes ventricular tachycardia. Blockade of the delayed rectifier (repolarising) potassium current and drug interactions with inhibitors of the cytochromes P450 (CYP)-mediated metabolism are the most common underlying mechanisms. Many antiarrhythmic drugs have been also implicated in prolonging QT interval and triggering torsades de pointes, especially during chronic therapy or in case of acute high dose toxicity. Progressive renal disease is associated from the earliest stages with increased QT interval and dispersal and with an increased risk of cardiovascular death, specifically sudden death. It has also been reported that cCorrected QT (QTc) interval prolongation and torsade de pointes are associated with end-stage renal disease (ESRD) and that they can be a cause of sudden death in ESRD. We present a case of torsade de pointes in a 82-year-old Italian woman with chronic renal failure.
尖端扭转型室速是一种多形性室性心动过速，发生于体表心电图QT间期延长的情况下。包括抗生素和抗精神病药物在内的几种非抗心律失常药物已被证明可延长心脏复极，易引发尖端扭转型室性心动过速。延迟整流（复极化）钾电流的阻断以及药物与细胞色素P450（CYP）介导代谢的抑制剂之间的药物相互作用是最常见的潜在机制。许多抗心律失常药物也与QT间期延长和触发尖端扭转型室速有关，尤其是在长期治疗期间或急性高剂量中毒的情况下。进展性肾病从最早阶段就与QT间期延长和离散增加以及心血管死亡风险增加有关，特别是猝死。也有报道称，校正QT（QTc）间期延长和尖端扭转型室速与终末期肾病（ESRD）有关，并且它们可能是ESRD猝死的原因。我们报告一例82岁患有慢性肾衰竭的意大利女性发生尖端扭转型室速的病例。
