Ventricular tachycardia (VT) is caused by abnormal electrical circuits originating from diseased areas of the ventricular myocardium. It usually results in a rapid heartbeat, preventing effective ventricular refill and adequate cardiac output. Untreated VT is usually life-threatening.
Depending on the type, VT may be managed by antiarrhythmic drugs. People who have recurrent VT episodes may need an implantable cardiac defibrillator (ICD) or endocardial catheter ablation to destroy diseased areas of the ventricular myocardium and interrupt the abnormal electrical circuits.
The procedure is carried out with the patient under sedation or general anaesthesia. The pericardial space is accessed by a subxiphoid needle puncture under fluoroscopic guidance. A guidewire is introduced through the needle and a sheath is advanced over the guidewire so that the tip is placed inside the pericardial sac. The sheath is aspirated to check for bleeding. A radiofrequency catheter is inserted into the sheath. After electrophysiological mapping to determine target sites for ablation, radiofrequency energy pulses are applied to the epicardium.
During the procedure, catheter position is monitored with a three-dimensional mapping system to avoid collateral damage. Saline is placed in the pericardial space to reduce the risk of oesophageal injury, and steroids are administered to reduce the risk of pericarditis.
Patients can have a combined procedure that includes electrophysiological mapping and ablation by both endocardial and epicardial approaches.
Sections 2.3 and 2.4 describe efficacy and safety outcomes which were available in the published literature and which the Committee considered as part of the evidence about this procedure. For more detailed information on the evidence, see the overview.
In a case series of 48 patients with VT, of whom 18 had epicardial ablation, the procedure eliminated VT-inducing circuits in 94% (17 out of 18) of patients (mean follow-up 25 months). In a case series of 14 patients, an epicardial VT circuit was mapped in 7 patients and was successfully terminated with epicardial ablation in all patients (mean follow-up 14 months). In a case series of 10 patients, VT-inducing circuits were eliminated in 8 (there were no episodes of syncope at 18-month follow-up).
The Specialist Advisers stated that key efficacy outcomes included termination of VT (acutely and making it non-inducible), lack of VT recurrence, and reduction in the need for ICDs.
No deaths directly attributable to the procedure have been reported in the literature. There were three deaths because of progression of severe heart failure. One patient in a case series of 48 patients died from decompensated congestive heart failure several weeks after successful epicardial ablation. Two patients in a case series of 20 patients died because of progressive heart failure during follow-up (mean 12 months).
In a case series of 20 patients, one patient developed arteriovenous fistula formation needing surgical repair. In the same study, another patient developed an atrioventricular block.
In a case series of 10 patients, one patient developed haemopericardium needing drainage. In the same study three patients developed pericardial friction rub without haemopericardium.
In a case series of 48 patients, three patients developed transient pericarditis that resolved within 1 week. In a second case series of 10 patients, two patients reported acute thoracic pain needing analgesia.
In a case series of 10 patients, five patients were in heart failure during the procedure, and one of these needed urgent heart transplantation after the procedure.
The Specialist Advisers considered that potential safety concerns included myocardial puncture; pericarditis; coronary artery damage; perforation of the right ventricle; damage to the oesophagus, bronchi and phrenic nerve; gastric puncture and damage to abdominal vessels and organs when accessing the pericardial space.