BACKGROUND Myocardial ischemia and ST-elevation myocardial infarction(STEMI)increase QT dispersion(QTD)and corrected QT dispersion(QTcD),and are also associated with ventricular arrhythmia.AIM To evaluate the effects ...BACKGROUND Myocardial ischemia and ST-elevation myocardial infarction(STEMI)increase QT dispersion(QTD)and corrected QT dispersion(QTcD),and are also associated with ventricular arrhythmia.AIM To evaluate the effects of reperfusion strategy[primary percutaneous coronary intervention(PPCI)or fibrinolytic therapy]on QTD and QTcD in STEMI patients and assess the impact of the chosen strategy on the occurrence of in-hospital arrhythmia.METHODS This prospective,observational,multicenter study included 240 patients admitted with STEMI who were treated with either PPCI(group I)or fibrinolytic therapy(group II).QTD and QTcD were measured on admission and 24 hr after reperfusion,and patients were observed to detect in-hospital arrhythmia.RESULTS There were significant reductions in QTD and QTcD from admission to 24 hr in both group I and group II patients.QTD and QTcD were found to be shorter in group I patients at 24 hr than those in group II(53±19 msec vs 60±18 msec,P=0.005 and 60±21 msec vs 69+22 msec,P=0.003,respectively).The occurrence of in-hospital arrhythmia was significantly more frequent in group II than in group I(25 patients,20.8%vs 8 patients,6.7%,P=0.001).Furthermore,QTD and QTcD were higher in patients with in-hospital arrhythmia than those without(P=0.001 and P=0.02,respectively).CONCLUSION In STEMI patients,PPCI and fibrinolytic therapy effectively reduced QTD and QTcD,with a higher observed reduction using PPCI.PPCI was associated with a lower incidence of in-hospital arrhythmia than fibrinolytic therapy.In addition,QTD and QTcD were shorter in patients not experiencing in-hospital arrhythmia than those with arrhythmia.展开更多
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BACKGROUND Myocardial ischemia and ST-elevation myocardial infarction(STEMI)increase QT dispersion(QTD)and corrected QT dispersion(QTcD),and are also associated with ventricular arrhythmia.AIM To evaluate the effects of reperfusion strategy[primary percutaneous coronary intervention(PPCI)or fibrinolytic therapy]on QTD and QTcD in STEMI patients and assess the impact of the chosen strategy on the occurrence of in-hospital arrhythmia.METHODS This prospective,observational,multicenter study included 240 patients admitted with STEMI who were treated with either PPCI(group I)or fibrinolytic therapy(group II).QTD and QTcD were measured on admission and 24 hr after reperfusion,and patients were observed to detect in-hospital arrhythmia.RESULTS There were significant reductions in QTD and QTcD from admission to 24 hr in both group I and group II patients.QTD and QTcD were found to be shorter in group I patients at 24 hr than those in group II(53±19 msec vs 60±18 msec,P=0.005 and 60±21 msec vs 69+22 msec,P=0.003,respectively).The occurrence of in-hospital arrhythmia was significantly more frequent in group II than in group I(25 patients,20.8%vs 8 patients,6.7%,P=0.001).Furthermore,QTD and QTcD were higher in patients with in-hospital arrhythmia than those without(P=0.001 and P=0.02,respectively).CONCLUSION In STEMI patients,PPCI and fibrinolytic therapy effectively reduced QTD and QTcD,with a higher observed reduction using PPCI.PPCI was associated with a lower incidence of in-hospital arrhythmia than fibrinolytic therapy.In addition,QTD and QTcD were shorter in patients not experiencing in-hospital arrhythmia than those with arrhythmia.
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.
