The ablation of ventricular tachycardias is an intervention that consists of the selective destruction (ablation) of the cardiac tissue where the circuits responsible for initiating and maintaining these arrhythmias are found.
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The term ventricular tachycardia (VT) means an accelerated rhythm of the heart with a frequency equal to or greater than 120 beats / minute that originates in the ventricular chambers.
Ventricular tachycardias are defined as non-sustained ventricular tachycardias (NSVT) if they last less than 30 seconds, and sustained ventricular tachycardias (SVT) if they last longer or must be interrupted because they cause hemodynamic collapse.
From a clinical point of view, the most important element of these tachycardias is that which divides them into:
This diagnostic element has an important meaning in pathophysiological and prognostic terms, in fact:
The ablation of ventricular tachycardias is an intervention that consists of the selective destruction (ablation) of the cardiac tissue where the circuits responsible for initiating and maintaining these arrhythmias are found.
The ablation of ventricular tachycardias has different aspects, depending on the classification of the VTs.
In the preparation for ablation surgery, it is extremely important, where possible, to have 12-lead electrocardiographic recordings of the clinical episodes of ventricular tachycardia.
This enables the guidance of the ablation procedure with greater precision, because the analysis of the electrocardiogram identifies in advance the most likely site of origin of the ventricular tachycardia.
Idiopathic ventricular tachycardias have some common sites of origin:
The ablation procedure of idiopathic VTs is generally performed with mild sedation, using local anesthesia for the acquisition of the vascular accesses necessary for the positioning of the intracardiac catheters.
These vascular accesses consist of the right femoral vein and the right femoral artery (in the forms of tachycardia originating in the left heart).
Once the necessary vascular accesses are obtained, a stimulating catheter is placed in the right ventricle. Using this catheter, the heart is electrically stimulated so that ventricular tachycardia appears (is induced).
At this point, a catheter capable of navigating inside the heart is introduced into the appropriate location, and the tachycardia mapping phase begins, i.e. identification of the site of origin of the tachycardia.
This phase is assisted by the use of radioscopic techniques and three-dimensional electroanatomical mapping of the heart.
With this instrumentation, it is possible to accurately reconstruct the three-dimensional anatomy of the cardiac region of interest and create maps of origin and propagation of the tachycardia circuit.
Once this circuit has been identified, it is ablated using a particular form of electric current (radio frequency), capable of selectively destroying only the cardiac tissue responsible for the arrhythmia.
Once this phase of the procedure is performed, the heart undergoes a programmed cardiac stimulation (electrophysiological study) to confirm that the procedure has been successful.
Also in this case, it is of great importance to be able to have, whenever possible, 12-lead electrocardiographic traces of the arrhythmic episodes. Above all, in these patients, these traces constitute a fundamental guide in the conduct of the ablative procedure.
A precise pre-procedural clinical framework of the patient is also essential, in order to be able to prepare all the diagnostic and therapeutic measures necessary to perform the ablation procedure in the safest and most effective way possible.
In particular, the patient’s need for hemodynamic support during the procedure must be assessed, and all the therapeutic devices indicated by the particular clinical conditions of the individual patient must be prepared.
The ablation procedure of ventricular tachycardias associated with structural heart disease are usually performed under general anesthesia, with intensive cardio-respiratory monitoring.
Vascular accesses are similar to those of ablation of idiopathic ventricular tachycardias, but percutaneous epicardial access is often necessary, when there is reason to believe that the origin of tachycardia is at the epicardial level.
The ablation of these forms of tachycardia invariably presupposes the use of three-dimensional electroanatomical mapping systems.
It is possible to distinguish two basic types of ablation strategy in VTs associated with structural heart disease:
The ventricular tachycardia ablation procedure involves a series of different and successive stages:
What are the problems and critical issues of ablation of ventricular tachycardias?
Particular problems of ablation of ventricular tachycardias include:
Is the cardiac defibrillator always required after ablation?
The ablation of ventricular tachycardias is still a complementary treatment to the ICD implant, and is generally offered to those patients who have experienced one or more relapses of sustained ventricular tachycardias. The primary purpose of ablation of VTs is to reduce arrhythmic burden and the consequent need for ICD interventions, and therefore improve the patient’s quality of life and survival.
The use of tachycardia ablation has become increasingly widespread thanks to the improvement of mapping techniques and thanks to the availability of new substrate targets (such as late potentials). Thanks to the electrophysiological study, the risk of recurrence of arrhythmias can be better predicted.
In general, especially in patients with ventricular tachycardias associated with structural heart disease, the ICD is always maintained even after effective ablation. Hemodynamically tolerated idiopathic or monomorphic VT patients may have a lower risk of sudden death, particularly in the absence of structural heart disease, or if heart function is only moderately reduced. It may not be necessary to maintain the cardiac defibrillator in such patients, although this has not yet been fully investigated. However, the possibility of performing ever more effective and specific ablations could eventually result in patients at lower risk having this procedure as an alternative therapy to the ICD.
What are the risks of ablation of ventricular tachycardias?
Transcatheter radiofrequency ablation of ventricular tachycardias presents, like all invasive procedures, a risk of complications. The most frequent complications are local ones that include a small hematoma at the site of introduction of the catheters, while, much rarer are the lesions affecting the blood vessels or nerves that run in the vicinity of the vessels. Injuries to the vessels in the vicinity of the heart or in the heart itself occur with an extremely low frequency. More frequently the complications are transient (mild self-absorption hematoma, transient chest pain) or correctable.
Then there are more serious and much rarer complications, such as the induction of hemodynamically unstable arrhythmias, which require support of the circulation (through ECMO) and cardiopulmonary resuscitation maneuvers. In very rare cases, a perforation of the heart may occur, with a collection of blood in the pericardium (hemopericardium), which may require drainage (pericardiocentesis) or even more rarely cardiac surgery. Of course, the risk of adverse events is higher in patients with structural heart disease than in patients without structural heart disease, given the different basic clinical risk of these patients.
In any case, in our center, during the ablation of ventricular tachycardia, in addition to electrophysiologists, there are also specialist anesthesiologists, and the procedure is generally carried out in a hybrid room (i.e. a room specifically equipped in case it is necessary to intervene with ECMO or with a cardiac surgery procedure).
In summary, the risk associated with ablation of ventricular tachycardia is low compared to the risks of the arrhythmia itself, and the advantage derived from its use for the patient is very high, since these procedures are often life-saving, and are conducted in patients no longer responsive to drug therapies.