Ventricular arrhythmias are an important cause of morbidity and mortality and come in a variety of forms, from single premature ventricular complexes to sustained ventricular tachycardia and fibrillation. Rapid developments have taken place over the past decade in our understanding of these arrhythmias and in our ability to diagnose and treat them. The field of catheter ablation has progressed with the development of new methods and tools, and with the publication of large clinical trials. Therefore, global cardiac electrophysiology professional societies undertook to outline recommendations and best practices for these procedures in a document that will update and replace the 2009 EHRA/HRS Expert Consensus on Catheter Ablation of Ventricular Arrhythmias. An expert writing group, after reviewing and discussing the literature, including a systematic review and meta-analysis published in conjunction with this document, and drawing on their own experience, drafted and voted on recommendations and summarized current knowledge and practice in the field. Each recommendation is presented in knowledge byte format and is accompanied by supportive text and references. Further sections provide a practical synopsis of the various techniques and of the specific ventricular arrhythmia sites and substrates encountered in the electrophysiology lab. The purpose of this document is to help electrophysiologists around the world to appropriately select patients for catheter ablation, to perform procedures in a safe and efficacious manner, and to provide follow-up and adjunctive care in order to obtain the best possible outcomes for patients with ventricular arrhythmias.

Retrograde coronary venous infusions of ethanol using a balloon-tipped infusion catheter were effective in ablating ventricular myocardium. Retrograde chemical ablation did not itself result in inducible VT or adversely affect hemodynamic measurements or coronary arteries. Transmural myocardial necrosis, necessary in the ablation of VT associated with coronary artery disease, can be produced by higher infusion volumes.

Catheter ablation of the AV conduction system and permanent pacemaker implantation were associated with improved quality of life and left ventricular function in this population of highly symptomatic patients with atrial fibrillation refractory to medical therapy.

Accufix pacing leads pose a low, ongoing risk of injury. Extraction is associated with substantially higher risks, and a conservative management approach is indicated for most patients.

Conduction block usually occurred when continuous transmural necrosis was present, and conduction usually persisted when continuous transmural necrosis was absent. However, important exceptions were observed, including block when the ablation zone was wide but nontransmural, and conduction despite a thin line of continuous transmural necrosis.

Mixed venous oxy-hemoglobin saturation (MVO2) is a physiological variable with several features that might be desirable as a control parameter for rate adaptive pacing. Despite these desirable characteristics, the long-term reliability of the MVO2 sensor in vivo is uncertain. We, therefore, designed a study to prospectively evaluate the long-term performance of a permanently implanted MVO2 saturation sensor in patients requiring VVIR pacing. Under an FDA approved feasibility study, eight patients were implanted with a VVIR pulse generator and a right ventricular pacing lead incorporating an MVO2 sensor. In order to accurately assess long-term stability of the sensor, patients underwent submaximal treadmill exercise using the Chronotropic Assessment Exercise Protocol (CAEP) at 2 weeks, 6 weeks, and 3, 6, 9, 12, 18, and 24 months following pacemaker implantation. Paired maximal exercise testing using the CAEP was also performed with the pacing system programmed to the VVI and VVIR modes in randomized sequence with measurement of expired gas exchange after 6 weeks and 12 months of follow-up. During maximal treadmill exercise the peak exercise heart rate (132 +/- 9 vs 71.5 +/- 5 beats/min, P < 0.00001) and maximal rate of oxygen consumption (1,704 +/- 633 vs 1382 +/- 407 mL/min, P = 0.01) were significantly greater in the VVIR than in the VVI pacing mode. Similarly, the duration of exercise was greater in the VVIR than the VVI pacing mode (8.9 +/- 3.6 min vs 7.6 +/- 3.7 min, P = 0.04). The resting MVO2 and the MVO2 at peak exercise were similar in the VVI and VVIR pacing modes (P = NS). However, the MVO2 at each comparable treadmill exercise stage was significantly higher in the VVIR mode than in the VVI mode (CAEP stage 1 (P = 0.005), stage 2 (P = 0.04), stage 3 (P = 0.008), and stage 4 (P = 0.04). The correlation between MVO2 and oxygen consumption (VO2) was excellent (r = -0.93). Telemetry of the reflectance of red and infrared light and MVO2 in the right ventricle during identical exercise workloads revealed no significant change over the first 12 months of follow-up (ANOVA, P = NS). The chronotropic response to exercise remained proportional to VO2 in all patients over the first 12 months of follow-up. The time course of change in MVO2 during maximal exercise was significantly faster than for VO2. At the 18- and 24-month follow-up exercise tests, a significant deterioration of the sensor signal with attenuation of chronotropic response was noted for 4 of the 8 subjects with replacement of the pacing system required in one patient because of lack of appropriate rate modulation. Rate modulated VVIR pacing controlled by right ventricular MVO2 provides a chronotropic response that is highly correlated with VO2. This parameter responds rapidly to changes in workload with kinetics that are more rapid than those of VO2. Appropriate rate modulation provides a higher MVO2 at identical workloads than does VVI pacing. Although the MVO2 sensor remains stable and accurate over the first year following implantation, significa...

Endocardial recordings from a patient with both sustained ventricular tachycardia and AV nodal reentrant tachycardia are presented that demonstrate spontaneous transient entrainment of ventricular tachycardia by AV nodal reentrant tachycardia. During electrophysiological catheterization, there were repeated episodes of spontaneous conversion from a wide to a narrow QRS morphology following the induction of ventricular tachycardia. With conversion from the wide to the narrow QRS, the ventricular deflection in the coronary sinus electrograms demonstrated an abrupt change in morphology, indicating a change in activation sequence at this site from the wavefront of depolarization emerging from the ventricular tachycardia circuit to a wavefront conducting over the His‐Purkinje system. However, the right ventricular apex electrogram demonstrated a constant morphology with a decrease in cycle length equal to that of the other intracardiac electrograms, indicating a constant direction of activation from the ventricular tachycardia circuit, and that ventricular tachycardia had been transiently entrained by AV nodal reentrant tachycardia. In addition, rapid atrial pacing during ventricular tachycardia narrowed the QRS and demonstrated transient entrainment of the right ventricular apex electrogram. Although transient entrainment of a tachycardia is evidence supporting reentry with an excitable gap as the probable mechanism, its demonstration has required the use of rapid pacing techniques. This case is a spontaneously occurring example of transient entrainment of one tachycardia circuit by another, a phenomenon that has not been previously described.

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