人类中缓慢性心律失常依赖性长QT综合征与丙吡胺所致QT间期延长之间的关系。

Relation between bradycardia dependent long QT syndrome and QT prolongation by disopyramide in humans.

作者信息

Furushima H, Niwano S, Chinushi M, Ohhira K, Abe A, Aizawa Y

机构信息

First Department of Internal Medicine, Niigata University School of Medicine, Japan.

出版信息

Heart. 1998 Jan;79(1):56-8. doi: 10.1136/hrt.79.1.56.

DOI:10.1136/hrt.79.1.56

PMID:9505920

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1728587/

Abstract

BACKGROUND

Recent molecular biological investigations have identified abnormal genes in familial forms of long QT syndrome, but in bradycardia dependent acquired long QT syndrome, no such genetic abnormality has yet been identified.

OBJECTIVE

To investigate the relation between the responses of QT interval to pacing change and to disopyramide.

METHODS

This study included 13 patients with bradyarrhythmia who had undergone pacemaker implantation. The patients were divided into two groups: group I (n = 8), patients with QT prolongation (QT interval > or = 500 ms) during bradycardia; group II (n = 5), patients without QT prolongation (QT interval < 500 ms) during bradycardia. The responses of QT interval caused by the change of pacing rate were determined and compared with the changes of the QT interval after disopyramide administration.

RESULTS

The QT interval in group I was significantly longer than that in group II when the pacing rate was decreased from 110 to 50 beats/min: mean (SD) 451 (16) v 416 (17) ms at 90 beats/min (p = 0.0033), and 490 (19) v 432 (18) ms at 70 beats/min (p = 0.0002), respectively. The QT interval was prolonged significantly by disopyramide in both groups, but the change was more pronounced in group I than in group II: 78 (33) v 35 (10) ms (p < 0.05).

CONCLUSIONS

This study suggests that the patients showing bradycardia dependent QT prolongation are also more markedly affected by disopyramide and that abnormal potassium channel may be the underlying mechanism.

摘要

背景

近期分子生物学研究已在家族性长QT综合征中鉴定出异常基因，但在心动过缓依赖性获得性长QT综合征中，尚未发现此类基因异常。

目的

研究QT间期对起搏变化和丙吡胺的反应之间的关系。

方法

本研究纳入了13例植入起搏器的缓慢性心律失常患者。患者分为两组：I组（n = 8），心动过缓时QT间期延长（QT间期≥500 ms）的患者；II组（n = 5），心动过缓时QT间期未延长（QT间期<500 ms）的患者。测定起搏频率变化引起的QT间期反应，并与给予丙吡胺后QT间期的变化进行比较。

结果

当起搏频率从110次/分钟降至50次/分钟时，I组的QT间期明显长于II组：90次/分钟时平均（标准差）为451（16）对416（17）ms（p = 0.0033），70次/分钟时为490（19）对432（18）ms（p = 0.0002）。两组患者丙吡胺均使QT间期显著延长，但I组的变化比II组更明显：78（33）对35（10）ms（p < 0.05）。