Objective To investigate the elfects of some class Ⅰ antiarrhythmic agents on QT dispersion and compared with those of amiodarone. Methods Group I was composed of 30 cases, they were all treated with class Ⅰ agents....Objective To investigate the elfects of some class Ⅰ antiarrhythmic agents on QT dispersion and compared with those of amiodarone. Methods Group I was composed of 30 cases, they were all treated with class Ⅰ agents. The drugs used include: mexiletine (8 cases), moricizine (9), propafenone (12) and apridine (1). GrouP Ⅱ was composed of other 30 patients, and were all treated with amiodarone. The ddlerences of QT intervals between ECG leads (QTd and QTcd) were measured belore and aler medication. Results Before medication, the QTmax and QTcmax in group Ⅱ were signilicantly longer than those of group Ⅰ, resulting in greater QTd and QTcd in grouP Ⅱ (QTd:66± 14ms vs 31± 16ms, P<0.01; QTcd:71±36ms vs 44± 18ms, P<0.01). Alter medication, QTmax and QTcmax of group Ⅰ were prolonged, leading to the lengthening of QTd (from 31±16ms to 45±17ms, P<0.01) and QTcd (from 44± 18 ms to 58± 21ms, P<0.05), indicating the increase of inhomogeneity of myocardial repolarization after the treatment of class Ⅰ agents. Alter amiodarone treatment, QTmin and QTmax in grouP Ⅱ were both prolonged, with a greater amplitude of QTmin prolongation, resulting in decreased QTd and QTcd in group Ⅱ (QTd /rom 66± 14ms to 36±22ms, P<0.01, QTcd from 71±36ms to 45±27ms, P<0.01). The signifcant dofference of QTd and QTcd between two groups disappeared aler medication. Conclusion The results of the present study may relect the opposite effects of amiodarone and these class Ⅰ agents on myocardial repolarization.展开更多
文摘Objective To investigate the elfects of some class Ⅰ antiarrhythmic agents on QT dispersion and compared with those of amiodarone. Methods Group I was composed of 30 cases, they were all treated with class Ⅰ agents. The drugs used include: mexiletine (8 cases), moricizine (9), propafenone (12) and apridine (1). GrouP Ⅱ was composed of other 30 patients, and were all treated with amiodarone. The ddlerences of QT intervals between ECG leads (QTd and QTcd) were measured belore and aler medication. Results Before medication, the QTmax and QTcmax in group Ⅱ were signilicantly longer than those of group Ⅰ, resulting in greater QTd and QTcd in grouP Ⅱ (QTd:66± 14ms vs 31± 16ms, P<0.01; QTcd:71±36ms vs 44± 18ms, P<0.01). Alter medication, QTmax and QTcmax of group Ⅰ were prolonged, leading to the lengthening of QTd (from 31±16ms to 45±17ms, P<0.01) and QTcd (from 44± 18 ms to 58± 21ms, P<0.05), indicating the increase of inhomogeneity of myocardial repolarization after the treatment of class Ⅰ agents. Alter amiodarone treatment, QTmin and QTmax in grouP Ⅱ were both prolonged, with a greater amplitude of QTmin prolongation, resulting in decreased QTd and QTcd in group Ⅱ (QTd /rom 66± 14ms to 36±22ms, P<0.01, QTcd from 71±36ms to 45±27ms, P<0.01). The signifcant dofference of QTd and QTcd between two groups disappeared aler medication. Conclusion The results of the present study may relect the opposite effects of amiodarone and these class Ⅰ agents on myocardial repolarization.