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
Acute myocardial infarction （AMI） is an acute cardiovascular emergency. This study was undertaken to assess the effect of tumor necrosis factor-a （TNF-a） on ventricular arrhythmias induced byAMI in rats in vivo. ...Acute myocardial infarction （AMI） is an acute cardiovascular emergency. This study was undertaken to assess the effect of tumor necrosis factor-a （TNF-a） on ventricular arrhythmias induced byAMI in rats in vivo. Two hundred and forty male Wistar rats were randomized into a sham- operation group, an AMI group, and a recombinant human tumor necrosis factor receptor：Fc fusion protein（rhTNFR：Fc） group. Acute anterior wall myocardial infarction was produced in the AMI group by ligating the left anterior descending coronary artery （LAD）, and there was no ligation but operation in the sham-operation group. The rhTNFR：Fc group was treated with rhTNFR：Fc（10 mg/kg）, a TNF-a antagonist, 24 hours before LAD ligation. The spontaneous and induced programmed electrical stimulation ventricular arrhythmias were recorded at baseline and 10 minutes, 20 minutes, 30 minutes, 60 minutes, 3 hours, 6 hours and 12 hours after ligation. At the same time the protein and mRNA expression levels of TNF-a among different groups were detected by histochemistry and real-time fluorescent quantitative PCR. Expression of TNF-a increased markedly from 10 minutes after infarction, peaked at 20-30 minutes, and returned to baseline gradually in the AMI group and rhTNFR：Fc group. The time- windows of spontaneous and induced ventricular arrhythmias were similar. Compared with the AMI group, the rhTNFR：Fc group showed a lesser expression of TNF-a protein and a lower incidence of ventricular arrhythmias （P〈0.05）. There was no obvious change in the sham-operation group. The expression of TNF-a induced by AMI could contribute to the onset of ventricular arrhythmias.展开更多
BACKGROUND： Ventricular arrhythmia （VA） is one of the most common complications of myocardial infarction （MI）, and ventricular tachycardia and fibrillation are the main causes for sudden cardiac death. This study...BACKGROUND： Ventricular arrhythmia （VA） is one of the most common complications of myocardial infarction （MI）, and ventricular tachycardia and fibrillation are the main causes for sudden cardiac death. This study aimed to explore the effect of ramipril on the occurrence of VA and its mechanism after MI in rabbits. METHODS： Twenty-four New Zealand rabbits purchased from the Wuhan Laboratory Animal Research Center were divided into three groups： sham-operated （SHAM） group （n=8）, MI group （n=8） and MI with ramipril （RAM） group （n=8）. Rabbits in the SHAM group received a median sternotomy without ligation of the left ventricular coronary artery. Rabbits in the MI and RAM groups received a median sternotomy followed by ligation of the left coronary artery. The successful anterior MI was confirmed by elevation of the ST segment with more than 0.2 mV in lead II and II1. After MI, rabbits in the RAM group were fed with intragastric ramipril （1 mg/kg per day ） for 12 weeks. Before and 12 weeks after MI in the three groups, ventricular tachycardia or fibrillation （VT/VF） episodes and MAP in cadiocytes of the epicardium, mid-myocardium and endocardium were recorded by a multichannel physiograph. Student＇s t test and ANOVA were used for statistical analysis. RESULTS： VT/VF episodes were decreased more markedly in the RAM group than in the MI group after 12 weeks （2.6±0.8 vs. 12.±＋2.9, P〈0.05）. Twelve weeks after MI, the duration of repolarization for 90% （APD90） of three-tier ventricular myocytes in the MI group was longer than that before MI （258.2±21.1 vs. 230.1±23.2,278.0±23.8 vs. 245.8±25.4,242.6±22.7 vs. 227.0±21.7, P〈0.05）. However, the APD90 was not significantly different at 12 weeks before and after MI in the RAM group （P〉0.05）. Moreover, the transmural dispersion of repolarization （TDR） was increased more markedly 12 weeks after MI in the MI group than in the SHAM and RAM groups （36.2±10.2 vs. 18.7±6.2, 24.9±8.7, P〈0.05）. But the TDR was not significantly different between the RAM and SHAM groups （18.7±6.2 vs. 24.9±8.7, P〉0.05）. CONCLUSION： Ramipril may reduce the incidence of malignant ventricular arrhythmia via mprovement of transmembrance repolarization heterogeneity after MI.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Acute myocardial infarction （AMI） is an acute cardiovascular emergency. This study was undertaken to assess the effect of tumor necrosis factor-a （TNF-a） on ventricular arrhythmias induced byAMI in rats in vivo. Two hundred and forty male Wistar rats were randomized into a sham- operation group, an AMI group, and a recombinant human tumor necrosis factor receptor：Fc fusion protein（rhTNFR：Fc） group. Acute anterior wall myocardial infarction was produced in the AMI group by ligating the left anterior descending coronary artery （LAD）, and there was no ligation but operation in the sham-operation group. The rhTNFR：Fc group was treated with rhTNFR：Fc（10 mg/kg）, a TNF-a antagonist, 24 hours before LAD ligation. The spontaneous and induced programmed electrical stimulation ventricular arrhythmias were recorded at baseline and 10 minutes, 20 minutes, 30 minutes, 60 minutes, 3 hours, 6 hours and 12 hours after ligation. At the same time the protein and mRNA expression levels of TNF-a among different groups were detected by histochemistry and real-time fluorescent quantitative PCR. Expression of TNF-a increased markedly from 10 minutes after infarction, peaked at 20-30 minutes, and returned to baseline gradually in the AMI group and rhTNFR：Fc group. The time- windows of spontaneous and induced ventricular arrhythmias were similar. Compared with the AMI group, the rhTNFR：Fc group showed a lesser expression of TNF-a protein and a lower incidence of ventricular arrhythmias （P〈0.05）. There was no obvious change in the sham-operation group. The expression of TNF-a induced by AMI could contribute to the onset of ventricular arrhythmias.
基金supported by a grant from the Natural Science Foundation of Hubei(2007ABA288)
文摘BACKGROUND： Ventricular arrhythmia （VA） is one of the most common complications of myocardial infarction （MI）, and ventricular tachycardia and fibrillation are the main causes for sudden cardiac death. This study aimed to explore the effect of ramipril on the occurrence of VA and its mechanism after MI in rabbits. METHODS： Twenty-four New Zealand rabbits purchased from the Wuhan Laboratory Animal Research Center were divided into three groups： sham-operated （SHAM） group （n=8）, MI group （n=8） and MI with ramipril （RAM） group （n=8）. Rabbits in the SHAM group received a median sternotomy without ligation of the left ventricular coronary artery. Rabbits in the MI and RAM groups received a median sternotomy followed by ligation of the left coronary artery. The successful anterior MI was confirmed by elevation of the ST segment with more than 0.2 mV in lead II and II1. After MI, rabbits in the RAM group were fed with intragastric ramipril （1 mg/kg per day ） for 12 weeks. Before and 12 weeks after MI in the three groups, ventricular tachycardia or fibrillation （VT/VF） episodes and MAP in cadiocytes of the epicardium, mid-myocardium and endocardium were recorded by a multichannel physiograph. Student＇s t test and ANOVA were used for statistical analysis. RESULTS： VT/VF episodes were decreased more markedly in the RAM group than in the MI group after 12 weeks （2.6±0.8 vs. 12.±＋2.9, P〈0.05）. Twelve weeks after MI, the duration of repolarization for 90% （APD90） of three-tier ventricular myocytes in the MI group was longer than that before MI （258.2±21.1 vs. 230.1±23.2,278.0±23.8 vs. 245.8±25.4,242.6±22.7 vs. 227.0±21.7, P〈0.05）. However, the APD90 was not significantly different at 12 weeks before and after MI in the RAM group （P〉0.05）. Moreover, the transmural dispersion of repolarization （TDR） was increased more markedly 12 weeks after MI in the MI group than in the SHAM and RAM groups （36.2±10.2 vs. 18.7±6.2, 24.9±8.7, P〈0.05）. But the TDR was not significantly different between the RAM and SHAM groups （18.7±6.2 vs. 24.9±8.7, P〉0.05）. CONCLUSION： Ramipril may reduce the incidence of malignant ventricular arrhythmia via mprovement of transmembrance repolarization heterogeneity after MI.
