RFCA is widely used to manage VT associated with structural heart disease when implantable cardioverter defibrillator (ICDs) or antiarrhythmic drugs have failed, and it is usually the sole treatment for idiopathic VT[5]. However, the effect is still unsatisfactory. Some studies have showed that one-year success rate after catheter ablation is 70%[6], and the 5-year recurrence rate is still as high as 46%[7]. In this retrospective study, 101 patients who with intractable VT and operated under general anesthesia were included. Among them, 29 patients(28.7%) experienced VT no induction during operation, and 26 patients (25.7%) relapsed within one year. This study also demonstrated that the lower BIS value < 40 was one risk factor for VT no induction, what’s more, the recurrence rate of VT was significantly higher in group N than group I (51.7% vs 15.3%), which shows VT no induction was an independent predictor of VT recurrence within one year.
Currently, wake-state or MAC is the most commonly used anesthetic method for RFCA. However, for more complex VT and unstable patients, general anesthesia is still required. Regular mechanical ventilation can reduce the interference of breathing on RFCA, improve the success rate of operation, shorten the operation time, reduce the recurrence rate and adverse reactions[8]. Unfortunately, clinical practice has shown that general anesthesia may cause VT induced failure or hemodynamic instability. The inducibility of arrhythmia is important, much ablation for ventricular arrhythmia targets symptomatic focal PVCs rather than sustained VT. Furthermore, activation and entrainment mapping, and searching for the earliest PP are still the most widely used techniques[9–10], which can only be used when VT induced stability. Therefore, for those patients who cannot be induced, it is often difficult to map the ablation target, thus affecting the success rate of ablation.
Many anesthetics (such as inhaled anesthetics, propofol and dexmedetomidine, etc.) have been shown their potential effects on cardiac conduction and interfere with the clinical induction of VT, whatsmore, some types of VT (such as outflow tract VT caused by ARVC) are extremely sensitive to sedation[3]. Therefore, to control the depth of anesthesia and to ensure the induction of arrhythmia and hemodynamic stability plays a very important role in the outcome of VT treatment.
Propofol is widely used during the induction and maintenance of anesthesia. Apart from these anesthetic properties, propofol has additional antiarrhythmic and proarrhythmic effects. At clinically relevant concentrations, the incidence of arrhythmia is relatively low, but the effect of arrhythmia inhibition is more significant. Studies have demonstrated that propofol has a protective effect on myocardial ischemia and arrhythmia which are caused by ischemia-reperfusion injury[11–12]. Propofol also has been shown to terminate atrial fibrillation and VT storm[13–14]. This effect may be due to the fact that the electrical storms are often caused by adrenergic stimulation, what's more, propofol can reduce the sympathetic tension by mediated GABA receptor, and inhibit sympathetic activity and cardiac electrical storm[15–16]. In addition, propofol can also shorten the Q-T interval of long Q-T syndrome; therefore, it may have the potential to prevent episodes of VT which are caused by Q-T interval dispersion[17].
Similarly, sevoflurane may also affect the induction of VT, which mainly produces a cascade reaction through a variety of signal transduction pathways such as protein kinase C, tyrosine protein kinase, etc., changing the gene expression of cardiomyocytes, and producing a variety of anti-injury factors. Furthermore, sevoflurane also prevents intracellular calcium overload through KATP channels, reduces ischemia-reperfusion injury and produces cellular protection[12], so as to decrease the occurrence of ventricular arrhythmias. In addition, sevoflurane and other volatile anesthetics can also delay atrioventricular repolarization and reduce the possibility of inducing ventricular arrhythmia in vitro by prolonging the duration of the action potential, but its clinical significance is not clear.
Recently, some experts have suggested that monitored anesthesia care (MAC) can be used to replace traditional general anesthesia in RFCA, which can effectively reduce the use of anesthetics that may affect VT induction and ensure the hemodynamics stability. However, MAC also has its limitations, which may increase the risk of respiratory depression and hypoxia. Therefore, the choice of the ideal anesthesia program still needs to weigh the pros and cons.
Our study has several limitations. First, this study is a retrospective study, in which only BIS values were used as the evaluation index for anesthesia depth. It is difficult to track the real-time blood concentration of various anesthetics, and it is impossible to determine which drug is the main factor that causes non-inducible of VT. Our team will conduct a prospective group analysis of the influence factors in the follow-up prospective research. Second, the number of cases in this study is small and it is a single-center study, which may lead to the bias of results and a large 95% CI.
In conclusion, we have reported that patients with VT who experience RFCA under general anesthesia, with the increase of anesthesia depth, may increase the risk of VT no induction, which in turn affects postoperative outcomes. Anesthesiologists need to have a deeper understanding of the effects of anesthesia methods and drugs on RFCA, so as to choose the ideal anesthesia management strategy and anesthesia depth to ensure the patient safety while improving the success rate of surgery.