| BACKGROUND AND OBJECTIVE:Ventricular arrhythmia and sudden cardiac death usually occur in early stage of acute myocardial infarction (AMI), and are related to the increased unsuitability of cardiac electricity after myocardial infarction. Many studies have shown that the increase of QT dispersion (QTd) has related to increased heterogeneity of myocardial refractoriness and to occurrence of clinically maligment ventricular arrhythmia. It is important to treat and prevent malignant ventricular arrhythmia after AMI. In recent decades, beta-blocker plays an important role in reducing the mortality rate and preventing sudden cardiac death. Therefore, in our study, we use sotalol to evaluate the effects of the QTd and ventricular arrhythmia of patients with AMIMETHODS:60 patients of AMI were divided into case group (n=30) and the control group (n=30)with random, single-blind and respective way. The corrected QT (QTc) and the QTd are measured at admission and ten days after hospitalization with the treatment of sotalol (80-160mg/d). Simultaneously, ventricular arrhythmia is observed in successive 24 hours and then compared with the control group.RESULTS:At admission, there was no difference of QTc and QTd between the two groups (417.4±14.3ms vs 413.2±14.6ms P>0.05; 66.2±11.6ms vs 67.4±14.3ms P>0.05).In the case group, the QTc was longer than those control group after two days of sotalol application, while the QTd was decreased more than the control group. (437.8±17.7ms vs 429.6±16.4ms P<0.05; 68.9±11.7ms vs 78.1±21.1ms P<0.05). After 7 days, the QTd was significantly reduced (48.2±14.7ms vs 59.1±13ms P<0.01).After four days of thromblytic, the QTd among the patients with thrombosis melted was obviously decreased (P<0.05), while the QTd in the case group was shorter than the control group(P<0.05). On the seventh day, the difference was the biggist(P<0.01),and the arrhythmia of reperfusion was disappear in case group. Out of the 60 patients with AMI, there were 18 cases with maligment ventricular arrhythmia, whose QTd was distinctly longer than those without arrhythmia (92.2±19.2ms vs 65.2±19.4ms P<0.01). Within two weeks of sotalol treatment, the occurrence of ventricular arrhythmia was significantly less in the case group than in the control group (16.6% vs 43.3% P<0.05). CONCLUSION:It is obvious that the increased QTd is closely related to the occurrence of ventricular arrhythmia. As to the patients with AMI, the early use of sotalol can decrease the QTd, change its natural evolution and reduce the occurrence of maligment ventricular arrhythmia. It indicates that sotalol can effectively minimize dispersion of myocardial refractoriness, and also it can stabilic the activity of cardiac electricity ,as well as it can reduce the risk of sudden death and improve prognosis. |