The Suppressive Effect And Relative Mechanism Of Propofol On Ventricular Arrhythmia

ObjectiveTo evaluate the propofol induced response of premature ventricular contractions(PVCs)originating from different regions and discover the possible mechanism in non-structural heart disease patients.Methods30 consecutive patients with frequent PVCs without diurnal rhythm character referred for catheter ablation were enrolled in this study.Propofol was injected by anesthetist via peripheric vein(1mg/kg)before the radiofrenquency ablation.Electrocardiogram,blood pressure,heart rate(HR)and oxygen saturation were continuously monitored and recorded.PVCs burden,the level of renin,angiotensin,and aldosterone of blood were evaluated before and after the use of the propofol infusion.Thereafter,PVCs were mapped and ablated under ENSITE NAVX system.Patients were divided into three groups based on the change of PVCs burden within 30 seconds:positive response group(PVCs decreasing from 51% to 100%),weakly positive response group(PVCs decreasing from 20% to 50%),and negative response group(PVCs decreasing lower than20%),respectively.ResultsOf all patients enrolled in our study,the mean age was 49.10±15.77(18-73)years old,13(43.3% patients)were males.The PVCs in 29 of 30 patients were defined as idiopathic ventricular arrhythmias(IVAs).The number of patients with positive response,weakly positive response and negative response were 11(36.7%),9(30.0%),10(33.3%),respectively.The mean heart rate(HR)of patients was significantly decreasing from 69.6±6.21 to 68.37±6.4 beats per minute after the induction of propofol(T=2.413,P=0.022).The level of renin decreased from 10.8 u IU/ml to9.3 u IU/ml,after the utility of propofol,so as the level of angiotensin,decreasing from47.15±14.74 pg/ml to 45.63±11.58 pg/ml,and the level of aldosterone,decreasing from 12.9±3.32ng/dl to 5.63±3.37 ng/dl,after the application of propofol.But there was no significant difference in the level of renin(Z=-1.070,P=0.285),angiotensin(T=0.733,P=0.469),and aldosterone(T=-0.296,P=0.77)of blood between before and after the use of propofol.No significant difference in change of HR among 3 response groups was observed(F=1.548,P=0.231),as well as for the change of renin(F=0.604,P=0.554),angiotensin(F=0.663,P=0.524),and aldosterone(F=2.719,P=0.085).IVAs originating from right ventricular outflow tract-pulmonary sinus cusps(RVOTPSCs)were more likely to response to propofol,while IVAs originating from non-RVOT-PASC were not.The disparate responses of propofol in RVOT-PSCs group and non-RVOT-PSCs group were statistically significantly different(Z=2.796,P=0.003).ConclusionsPropofol can restrain IVAs,and this effect is associated with the arrhythmogenic focus.IVAs originating from RVOT-PSCs spot can be suppressed by propofol.The cardioversion effect of propofol for IVAs is not related to autonomous nervous system.