Novel Invasive And Noninvasive Autonomic Nervous System Intervention In Preventing Atrial And Ventricular Arrhythmia

OBJECTIVE Previous study has shown that spinal cord stimulation(SCS)may suppress atrial fibrillation(AF)inducibility,but the mechanism is elusive.To determine whether SCS could inhibit AF inducibility by suppressing autonomic remodeling in rapid atrial pacing(RAP)-induced AF canine model.Methods:Eighteen canines were randomly divided into RAP group(RAP,n=9)and RAP+SCS group(RAP combined with SCS,n=9).Effective refractory period(ERP),window of vulnerability(WOV),AF inducibility,autonomic neural function and activity from anterior right ganglionated plexus(ARGP)and left stellate ganglion(LSG)were measured at baseline,3-hour RAP and 6-hour RAP.Then,ARGP and LSG were excised for western blot and mRNA analysis.In another 4 dogs(Control group,receive sham RAP and sham SCS),tissues were also excised for analysis.Results:In RAP group,RAP resulted in significant(1)decrease in ERP and increase in ERP dispersion,?WOV and AF inducibility;(2)activation of ARGP and LSG versus baseline.In RAP+SCS group,however,these changes were significantly attenuated by SCS.Compared with Control group,c-fos and nerve growth factor(NGF)were significantly up-regulated and small conductance calcium-activated potassium channels type 2(SK2)was significantly down-regulated in RAP group.In RAP+SCS group,however,c-fos,NGF and SK2 kept at a normal level as compared to Control group.Conclusions:SCS may suppress RAP-induced AF by inhibithing autonomic remodeling and the underlying mechanism of the salutary effect of SCS might partly contribute to modulating the expression of c-fos,NGF and SK2.BACKGROUND Previous studies have shown that spinal cord stimulation(SCS)may reduce ventricular arrhythmias(VAs)induced by acute myocardial infarction(AMI).Furthermore,activation of left stellate ganglion(LSG)appears to facilitate VAs after AMI.OBJECTIVES To investigate whether pretreatment with SCS could protect against VAs by reducing the LSG neural activity in an AMI canine model.METHODS Thirty dogs were anesthetized and randomly divided into SCS group(with SCS,n=15)and Sham group(sham operation without SCS,n=15).SCS was performed for 1 hour before AMI.Heart rate variability(HRV),ventricular effective refractory period(ERP),serum norepinephrine level,LSG function measured by blood pressure increases in response to LSG stimulation and LSG neural activity were measured for 1 minute at baseline and 1 hour after SCS.AMI was induced by left anterior descending coronary artery ligation and then HRV,LSG neural activity and VAs were measured.RESULTS In comparison with baseline,SCS for 1 hour significantly prolonged ventricular ERP,increased HRV and attenuated LSG function and LSG activity in the SCS group,whereas no significant change was shown in the Sham group.AMI resulted in significant diminish in HRV and increase in LSG neural activity in the Sham group,which were attenuated in the SCS group(Frequency:99134 impulses/min vs 62±22 impulses/min;Amplitude:0.41±0.12 mV vs 0.18±0.05 mV;both P<0.05).The incidence of VAs was significantly lower in the SCS group than that in the Sham group.Conclusions SCS may prevent AMI induced VAs,possibly by suppressing LSG activity.BACKGROUND Vagal nerve stimulation(VNS)has been shown to provide a protective effect against ischemia/reperfusion(I/R)-related arrhythmias by preventing the loss of Connexin43(Cx43).Our previous studies showed that atrial epicardial ganglionated plexus stimulation(GPS)might exert a VNS-like effect on ventricular electrophysiology.OBJECTIVES To investigate whether GPS could preserve Cx43 and reduce I/R induced ventricular arrhythmia.METHODS Sixteen dogs were randomly divided into GPS group(N=8,receiving GPS)and Sham group(N=8,receiving sham GPS).Ventricular effective refractory period(ERP)and heart rate variability(HRV)were measured at baseline and 1 h after GPS.Myocardial I/R was then performed.Ventricular arrhythmia occurred during the first hour after reperfusion was measured and myocardial tissue from the peri-infarct zone was excised for immunohistological analysis.In another 4 dogs(Control group,receiving sham GPS and sham I/R),myocardial tissue from the corresponding area was also excised.RESULTS Compared with the Sham group,GPS caused a significant increase in ventricular ERP and HRV,and a significant decrease in I/R-induced ventricular arrhythmias.Western blotting revealed a marked reduction in the amount of phosphorylated Cx43 and total Cx43 in the Sham group,whereas no significant change was observed in the GPS group compared with the Control group.Immunohistochemistry results confirmed that the myocardial I/R-induced loss of phosphorylated Cx43 from the intercellular junctions was prevented by GPS.Conclusion:GPS protects against I/R induced ventricular arrhythmias,accompanied by preserving Cx43.Objectives:To investigate the effect of selective ablation of the ligament of Marshall(LOM)on ventricular arrhythmias(VAs).Background:Previous studies have demonstrated that selective stimulation of sympathetic elements of the LOM,the distal segment of the LOM that extends beyond the left superior pulmonary vein(LOMLSPV),might induce VAs.Methods:In Protocol 1,the blood pressure(BP)and ventricular effective refractory period(ERP)changes as response to LOMLSPV stimulation and left stellate ganglion(LSG)stimulation were measured before and after LOMLSPV ablation in 8 anesthetized dogs.In Protocol 2,24 dogs were randomly divided into Group 1(received cesium alone,n=8),Group 2(cesium combined with LSG stimulation,n=8)and Group 3(cesium combined with LSG stimulation after LOMLSPV ablation,n=8).Early after-depolarization(EAD)amplitude,VA prevalence and the tachycardia threshold(measured according to the dose of cesium administered)were compared among the groups.Results:In Protocol 1,both LOMLSPV stimulation and LSG stimulation significantly increased BP and shortened the ventricular ERP,both of which were significantly attenuated by LOMLSPV ablation.In Protocol 2,compared with Group 1,the prevalence of the VAs and the EAD amplitudes were significantly augmented in Group 2 and were maintained at a comparable level in Group 3.Furthermore,the tachycardia threshold in Group 2(0.625 mmol/kg)was significantly lower than that noted in Groups 1 and 3(both 1.000 mmol/kg,P<0.05).Conclusions:LOMLSPV ablation reduced the prevalence of the VAs induced by cesium in combination with LSG stimulation,and the antiarrhythmic effect may involve the blockade of the sympathetic conduit between the LSG and the ventricles.Background Previous studies have shown that exposure the vagal nerve or the chest to the low-frequency electromagnetic field(LF-EMF)might suppress atrial fibrillation by mediating the cardiac autonomic nervous system.In the present study,we hypothesized that the use of LF-EMF to the left stellate ganglion(LSG)might also modulate LSG neural activity,thereby affecting the ventricular arrhythmia in an acute myocardial infarction canine model.Methods and Results Sixteen dogs were randomly divided into LF-EMF group(n=8,with LF-EMF stimulation)and Control group(n=8,with sham LF-EMF stimulation).LF-EMF(1HZ;stimulation time 8s;interstimulus interval,5s)was delivered to the surface area of LSG for 90 minutes.At baseline,LSG stimulation resulted in a significant increase in blood pressure,which was significantly attenuated at both 30min and 90min after LF-EMF in LF-EMF group and kept at a comparable level at both times in the Control group.As compared to group baseline,both 30min and 90min LF-EMF stimulation resulted in a significant decrease in LSG neural activity,whereas no significant change was caused by sham LF-EMF.When compared to the Control group,the AMI induced activation of LSG and ventricular arrhythmia was significantly attenuated in the LF-EMF group.Conclusions:Noninvasive LF-EMF stimulation can suppress LSG neural activity,thereby reducing ventricular arrhythmia in AMI canine model.