Important Innovation in Atrial Fibrillation Ablation Using a New Energy Source Called Electroporation or Pulse Field Ablation (PFA)
Atrial fibrillation is the most common cardiac arrhythmia in clinical practice and can significantly impact a patient’s quality of life. Characterized by chaotic and irregular electrical activity in the atria, this condition can cause debilitating symptoms such as palpitations, fatigue, and a reduced ability to perform daily activities. Additionally, it is associated with an increased risk of serious complications, including stroke and heart failure. For these reasons, effective and safe treatment is essential to improve the management of this arrhythmia and reduce related risks.
In our Center, we have adopted one of the most advanced techniques for treating atrial fibrillation: Pulsed Field Ablation (PFA). This innovative method represents a significant shift from traditional ablative techniques, offering a combination of high precision and safety.
PFA is based on a completely different approach from thermal methods such as radiofrequency (heat) and cryoenergy (cold). This modern technology uses very short, high-intensity electrical pulses to generate a phenomenon known as electroporation. In practical terms, this technology creates microscopic pores in the membranes of the heart cells responsible for the arrhythmia, leading to their selective death. The most significant aspect of this technique is its ability to preserve surrounding tissues, such as the oesophagus, phrenic nerves, and pulmonary veins, effectively eliminating the risk of severe complications often associated with traditional ablative methods.
To ensure the best results, our Canter uses two different types of catheters, each with specific characteristics that allow us to customize the approach based on the patient’s needs. The variable loop catheter (Varipulse™, Biosense Webster, Irvine, CA, USA; Figure 1) is particularly suitable for precisely adapting to the anatomy of the pulmonary veins, making it ideal for more complex cases.
(VaripulseTM, BiosenseWebster, Irvine, CA, USA; figura 1)
The modulable configuration catheter (Farapulse™, Marlborough, MA, USA; Figure 2), on the other hand, allows for uniform treatment of larger areas, ensuring effective isolation of target structures. This technological flexibility enables us to address a wide range of clinical situations, customizing each procedure based on the patient’s anatomical and clinical characteristics.
(FarapulseTM, Marlborough, MA, USA; figura 2)
Our Center is among the first to have adopted this technology using the variable loop catheter (Varipulse™), which is demonstrating promising results comparable to those obtained with the modulable configuration catheter (Farapulse™). Both solutions expand our therapeutic possibilities, demonstrating that both approaches offer equal efficacy in meeting the diverse needs of patients with different forms of atrial fibrillation.
Another advantage of PFA is the speed and precision of the procedure. The ability to create effective lesions without requiring rigid contact between the catheter and the treated tissue not only accelerates procedure times but also improves the patient’s experience.
Clinical studies have shown that PFA offers comparable, if not superior, efficacy to traditional techniques, with high success rates in the complete isolation of the pulmonary veins, a crucial phase for the treatment of atrial fibrillation. Additionally, thanks to the reduced risk of complications, this method stands out as a highly safe option for patients.
The adoption of this advanced technology, along with the expertise of our team, allows us to offer innovative, safe, and effective treatment, keeping pace with the latest developments in modern cardiology.
The state of the art of ablation of atrial fibrillation
The poor success of drug therapy for atrial fibrillation (FA) has encouraged many researchers to explore alternative strategies (1-9). Recent randomized studies have shown that the ablative strategy is superior to therapy with antiarrhythmic drugs in patients with paroxysmal / persistent AF (10-12), and more recently also in patients with “chronic” AF (13). However, further studies are required to confirm these results. In recent years, the number of AF ablation procedures has grown worldwide with increasingly shorter procedure times, thus allowing the inclusion of patients with structural heart disease and long-standing / permanent AF. Due to the excellent success rates reported by the pioneering groups and the attractive possibility of a definitive cure for AF, many patients have started to seek this curative approach, as many electrophysiologists and centers offer it in accordance with the new guidelines. From 1999 to 2007, we carried out more than 15,000 AF ablation procedures in our Electrophysiology Laboratory with a total long-term success rate of > 90% in patients with paroxysmal / persistent AF and 80% in permanent AF, reporting a low incidence of major complications. Despite the development of more and more new technologies and tools, the mechanisms of AF are manifold and many still remain unknown. Three years ago, we demonstrated for the first time the advantage of vagal denervation in patients with paroxysmal AF who underwent ablation and these observations are still a milestone today for understanding the pathophysiology and treatment of AF. Currently, however, we need to have more information on the pathophysiology of permanent AF to measure or limit ablation targets, since patients with long-lasting or permanent AF require extensive ablation and repeat procedures.
Recent data from our laboratory indicate that the progression from the initial paroxysmal form to the persistent or permanent form of AF is relatively rapid and can be predicted by clinical variables (14). As a result, the identification of subjects with a high risk of progression is useful for optimal timing in performing the ablation, avoiding a late procedure when the AF has become permanent. Currently, ablative strategies for patients with permanent AF and associated structural heart disease are complex, long lasting, less effective, and are associated with a high risk of complications. Over the past two years, pioneering groups have confirmed our previous results, even in patients with permanent AF using a gradual approach, which includes the sequential addition of additional targets of ablation through repeated ablative procedures, so as to limit or modify the anatomical substrates, electrophysiological and / or autonomic (15). If the elimination of the substrate is really crucial for the result, the mapping and navigation systems should be able to accurately visualize the complexity of the anatomy of the left atrium, in order to precisely place the lesions, avoiding unnecessary and dangerous radio frequency (RF) applications (Figure 1).
Fig. 1 Pre-and post-ablation color-coded voltage maps of the left atrium by CARTO (Panel A) and NavX (Panel B) systems with typical circumferential lesions as performed by CPVA are shown in the postero-anterior anatomic view. Note that inside encircled areas no voltage gradients are evident (red color).
What does circumferential ablation of the pulmonary veins (or CPVA) consist of?
Circumferential ablation of the pulmonary veins (or CPVA) is currently the standard procedure performed in our electrophysiology laboratory. The procedure is performed using manual catheters or remotely with soft magnetic catheters, with faster times than other approaches (16). The CPVA consists of large circumferential lines of injury performed point by point, so as to allow the disconnection of all pulmonary veins (PV), vagal denervation and the non-inducibility of both AF and atrial tachycardia (AT) at the end of the procedure. The data accumulated by our laboratory indicate that, in patients with paroxysmal / persistent AF without atrial magnification, CPVA alone is associated with excellent results, while in patients with long-lasting / persistent or permanent AF and with dilated atria, further linear lesions are necessary to achieve the non-inducibility of arrhythmias.
Objectives of the CPVA
The purpose of transcatheter ablation is to eliminate the trigger and modify the substrate with the least amount of lesions possible. The restoration of the stable sinus rhythm and the non-inducibility at the end of the procedure of both AF and AT is the gold standard of the CPVA. However, many patients with long-lasting / permanent AF, after achieving the sinus rhythm at the end of the procedure, are still susceptible to the induction of sustained AF / AT, requiring additional linear lesions in the left atrium (LA) to achieve non-inducibility. The end points of the standard CPVA procedure include the electrical disconnection of the PVs, vagal denervation, posterior lesion lines and the mitral isthmus line; further linear lesions, including coronary sinus disconnection (CS), are the latest targets. The objectives are achieved with a single mapping / scaler catheter. At present, we do not use the pebble technology since our approach is not limited to disconnecting the PV and since the achievement of multiple objectives precludes its use. In addition, PV have anatomies that vary widely from patient to patient, with a wide range of diameters, and the frequent presence of common ostia in over 30% of patients make it difficult to use this technology.
Disconnection of the pulmonary vein
The circumferential lines are located in the atrial tissue outside the ostia of the PV, an area often called the antrum (Figure 1). The lesions are designed to surround the left and right PVs individually or in pairs. Validation of electrical insulation with the catheter for circular mapping is not performed in our laboratory, since we have performed a real distal electrical insulation through the reduction of potential reduction (reduction > 90% of the electrogram amplitude), even within the surrounded areas (electrogram amplitude < 0.1 mV). Disconnection of the PVs is obtained with the optimal stability of the catheter and the contact with the wall that remains in a rapid attenuation of the atrial electrograms during each delivery of RF until their complete elimination (Figure 2).
Fig. 2 During RF applications local atrial potentialson the lesionlines and within encircled areas become wider andlower (black),completely disappearing (light blue) within 20-50seconds.
Signals in partially ablated areas require additional RF applications before moving on to the next ablation site.
Autonomic objectives of vagal denervation
Whenever possible, the elimination of vagal reflexes in innervation sites during the procedure is one of the most important objectives, since vagal denervation is a strong predictor for the long-term success of the ablation procedure (Figure 3). We first demonstrated that CPVA induces not long-term, but transient, vagal denervation, which in any case increases its long-term efficacy (8). These results have been confirmed by many other authors with different ablative approaches, and now vagal denervation constitutes a fascinating new strategy for AF ablation. Our results on changes in HRV after ablation add new insights for understanding the mechanisms of AF and its treatment. While standard CPVA lesions are practiced, RF deliveries evoke vagal reflexes in approximately 30% of patients. Sinus bradycardia (HR < 40 beats per minute), asystole, AV block, and hypotension occurring within seconds of the start of RF application should be counted as vagal reflexes (Figure 3).
Fig. 3 At beginning of RF applications around theleft superior PV(ablation site on the pre-ablation voltage map) avagal reflex iselicited (RF1), attenuated (RF2), and then abolished(RF3). Of note,the ablation site at which the vagal reflex was evokedis included inthe standard lesion set (post-ablation voltage map).As shown, thereflex resulted in hypotension and high degree AVblock.
If a reflex of this type is evoked, RF energy is supplied until such reflexes are abolished, or up to a maximum of 30 seconds. The purpose of ablation in these sites is the cessation of the reflex, followed by sinus tachycardia or AF. Failure to reproduce reflexes with repeated RF applications is considered a confirmation of denervation. Based on our experience, we have always tried to stimulate, and therefore ablate, these sites for vagal denervation. We have reported a detailed “autonomic map” of the left atrium as an ablation target, showing that like the left upper pulmonary vein, the septal region is also richly innervated (8).
Ablation of the posterior line and mitral isthmus
In the standard CPVA procedure, additional ablation lines are practiced along the posterior wall and the roof of the LA between the two series of lesions that connect the upper and lower PVs and the mitral annulus (Figure 1). The mitral isthmus line is used to prevent post-ablation atrial tachycardia (5,16,17) and to further reduce the arrhythmic substrate (Figure 3). The completeness of the mitral isthmus line is an important electrophysiological goal and is validated during epicardial stimulation from the coronary sinus (CS) and during mapping of the coronary sinus, looking for double potentials along the block line, and confirmed by differential pacing (5). The minimum interval between double potentials in the mitral isthmus during pacing from CS after block is about 150 ms, depending on the atrial size and the extent of the scars and lesions (5).
Ablation of the tricuspid hollow isthmus line
Patients with AF and a history of common atrial flutter or patients with permanent AF undergo ablation of the cavotricuspidal isthmus line. If all endpoints are reached at the end of the standard CPVA and the patient is in sinus rhythm, the non-inducibility of AF / AT is the ultimate goal.
Additional linear lesions and disconnection of the coronary sinus
If the inducibility of AF and AT persists even after cardioversion, we carefully review the lesion lines and the ablated areas to verify potential residues and apply radio frequency when needed. If necessary, additional ablation lines are performed (usually roof, septum or LA base) before isolation of the CS, which is the ultimate goal (Figure 4).
Fig. 4 Anatomical map reconstructed by NavX guidance in a patientwith permanent AF. After completing the standard CPVA lesion set,atrial fibrillation becomes more organized and slower resemblingan AT (cycle length 540 ms) which after coronary sinus disconnectionpromptly converts to sinus rhythm (cycle length 660 ms). On themap CS geometry is depicted in red and RF applications are taggedin green.
The compartmentalization is assessed by the presence of a “corridor” of double potentials and by the demonstration of activation towards the block line on both sides. A complete LA roof line can be demonstrated by progressive caudocranial activation on the posterior wall during LA stimulation. Fervent atrial activity from the CS musculature can be a conductor for long-lasting or permanent AF. The electrical disconnection of the coronary sinus from the atrium is performed with ablation at the endocardial or epicardial level (or both). The total elimination of the electrical activity of the coronary sinus is the ideal goal, but the organization of the electrical activity of the CS and / or the slowing down of the local frequency with dissociation between the activity potential of the CS and LA is also considered as proof of CS isolation. Endocardial and / or epicardial CS sites are frequent ablation targets in patients with permanent AF and dilated atria.
Post-ablation remapping
Once the non-inducibility of the AF / AT has been obtained, the LA is re-mapped, and the pre-ablation and post-ablation activation maps are compared (Figure 1). In patients in sinus rhythm, LA post-ablation remapping is done using the pre-ablation map for the acquisition of new points to compare the pre- and post-ablation bipolar voltage maps. In AF patients, after restoration of the sinus rhythm, post-ablation mapping is carried out using the anatomical map acquired during AF to validate the accuracy of the lesions. The incomplete block is revealed by the propagation of the impulse throughout the ablative line and requires further RF applications to complete the line despite the non-inducibility.
What are the patient selection criteria for the atrial fibrillation ablative procedure?
In recent years, the indications for the ablation of AF through CPVA have expanded widely, based on the results of numerous clinical trials. The procedure is primarily indicated in symptomatic patients with atrial fibrillation refractory to antiarrhythmic drug therapy. Currently the procedure is recommended at an early stage of the disease, independently of the refractoriness of antiarrhythmic drugs. In recent years, the indication has also extended to patients with heart failure and valvulopathies, and also in older subjects, in subjects with permanent AF and / or mitral or aortic mechanical valve prostheses. A low ejection fraction of the left ventricle does not represent an absolute contraindication to CPVA. Indeed studies, such as CASTLE-AF, have shown that these patients also benefit from ablation. Recent studies have highlighted the usefulness of continuing antiarrhythmic therapy after ablation. Therefore therapy with antiarrhythmic drugs is generally continued after ablation, and dosages are generally progressively reduced. Anticoagulant therapy is also generally continued after ablation, and is suspended on a case-by-case basis after AF ablation.
Pre-procedure preparation
The transesophageal echocardiogram (TEE) is the examination of choice to exclude the presence of thrombi in the left atrium or auricle, which are considered an absolute contraindication to the ablative procedure, which is postponed until the presence of cardiac thrombi is excluded from a new TEE during anticoagulant therapy (both with DOAC and Dicumarolic drugs). At discharge, a transthoracic echocardiogram is usually performed. Three days before the procedure, patients taking oral anticoagulant therapy stop it. The night before ablation, heparin infusion is started to reach ACT values between 200 and 250 seconds; heparin is stopped only 2 hours before the procedure to safely perform transseptal puncture. A weight-dependent infusion dose of narcotic, such as remifentanil (0.025-0.05 mcg / kg / minute) is also used. Cardiac surgery is readily accessible to perform emergency surgical procedures when needed. An echocardiography in the electrophysiology laboratory is available primarily for the diagnosis of pericardial tamponade.
The transseptal puncture
Usually, before the transseptal puncture, a catheter is inserted into the coronary sinus to map the left atrial activity, and a multipolar catheter is placed in the right atrium to map the electrical activity of the right atrium. CPVA requires a single transseptal puncture for the mapping / ablation catheter. After transseptal access, a single bolus of heparin is administered intravenously, and two blood samples are taken every 15 minutes to check the ACT, which must be maintained > 250 s or more.
Identification of ablation targets
An accurate identification of the targets and a relatively short ablation are required to avoid major complications and successfully achieve all the objectives. Currently, this is facilitated by the use of 3-D navigation and mapping systems that provide precise orientation from the anatomical and electrophysiological point of view. CPVA is performed in about 1 hour, but it can be longer (up to 3 hours) in patients with permanent AF with dilated atria to achieve all objectives including disconnection of CS and non-inducibility of AF / AT. We do not routinely use intracardiac echocardiography and the Lasso catheter.
Electroanatomical mapping
Usually in our Electrophysiology laboratory, we use the CARTO mapping systems (BiosenseWebster, Diamond Bar, CA, USA) and the EnSiteNavX (St. Jude Medical, St. Paul, MN, USA), which have significantly shortened the time of fluoroscopy, improving the safety profile of the procedure (figure 1). The early adoption by our group of the CARTO mapping system has allowed an accurate reconstruction of the complex left atrial anatomy and is now accepted by the entire electrophysiology community that performs AF ablation (2). The CARTO system continuously locates the position of the catheter using three very low magnetic fields, while the NavX system is based on electric fields generated by three pairs of skin electrodes orthogonal in three axes: X, Y, and Z. (Figure 1). Unlike the CARTO, the new NavX allows to obtain a 3-D reconstruction of both the tip and the body of the catheter, which is particularly useful in “difficult” areas, such as the ostia of the PV, the crest, the mitral annulus and the septal area. The monitoring of the catheter with the NavX system is obtained by a proximity indicator which, based on the color intensity of the tip of the catheter, allows the operator to check the optimal contact of the ablation catheter, a contact that when associated with the abatement of the atrial potential indicates achievement of the goal (Figure 1). During RF applications, cardiac movement, pain and breathing are all factors that affect the stability of the positioning of the catheter, but NavX software allows to minimize the amount of target movement, as well as respiratory artifacts. When the posterior wall is ablated, which is a vulnerable area at greater risk of cardiac perforation, the presence of pain can cause changes in the respiratory rate, and respiratory compensation by the NavX is useful for maintaining catheter stability. Furthermore, Navx technology is able to create separately any desired anatomy for each ablation target which results in a more accurate ablation, in particular of difficult targets, such as the ostia of the PVs, their cavern, the posterior wall, and the CS (figures 4 and 5).
Fig. 5 Post-ablation anatomic maps under NavX guidance of the leftatrium with simultaneous intracardiac recordings. The coronarysinus geometry is represented in red. Note the shape of 2 catheters,of which one is inside the coronary sinus (yellow) as referencecatheter and the other around the right PV ostium (white with greentip) for mapping and ablation. After ablation local atrial potentialsaround the right superior PV are dissociated from LA or completelyabsent indicating PV disconnection (Panels A and B).
Although the NavX Ensite system allows you to collect many points quickly and sequentially, in difficult areas, it is preferred to acquire points manually as in the CARTO system. Another important advantage of the NavX system, compared to the CARTO, is that the patient’s movements during the procedure do not concern the reconstruction of the map, as the reference catheter also moves due to the presence of patches attached to the patient’s body. As for the CARTO system, after ablation, a voltage map is shown by a colorimetric gradient to verify the complete elimination of potentials along and within the lesion lines (Figure 1). Currently, with both electroanatomical systems, in a few minutes we are able to reconstruct the anatomy of the LA and the ablation targets. The reconstruction of the PVs and their hosts represents the first step and is confirmed by the simultaneous use of fluoroscopy, electrograms, and impedance gradients. Typically and simultaneously, once the catheter enters the PV, the tip is seen outside the heart shadow on fluoroscopy, the impedance values significantly increase (over 4 Ohms above the left atrial impedance), and the atrial electrograms disappear. Once the PVs are displayed, a detailed sequential reconstruction of the left atrium is performed, including the rear and front walls, the LAA, the roof, the septum and the mitral annulus with its isthmus. The septum and the channel between LAA and the LSPV often require the acquisition of many more points than in other areas. LAA, which is identified with the presence of unfractionated and large amplitude atrial electrograms and large ventricular electrograms with an electrical activity organized in AF, is one of the last areas that is mapped. The channel between LAA and LSPV shows potentials that are typically smaller than those of LAA but higher and more fractionated than in the rest of the left atrium. If the canal is not accurately rebuilt, the left side of the circumferential lesion can be positioned too close to the LAA or within the PV ostium, which can result in poor efficacy and major complications, such as perforation of the LAA stenosis of the PV. Although roof reconstruction is easier by requiring fewer points to acquire, incorrect interpolation of the roofs should be avoided when using the CARTO system.
Ablation of desired targets
Once the left atrium and the main pulmonary veins have been adequately reconstructed, radio frequency energy is supplied, which in our laboratory is the most frequently used type of energy, for the endocardial ablation of the aforementioned electrophysiological and anatomical targets. Over the past three years, we have used an irrigated 4 mm catheter instead of the irrigated 8 mm, which has been shown to have some limitations, including the propensity for clot formation and insufficient energy delivery in areas with low blood flow. The irrigated catheter allows to adequately distribute the energy and to obtain larger lesions, minimizing the embolic risk. In our approach, the effectiveness of radio frequency delivery is and remains important, but we try to moderate the power in risk areas for greater safety. We usually use a lower power setting (30-50 W) and an irrigation flow of 2 ml/min (during mapping) and up to 50 ml/min during ablation (based on the site of delivery of the radio frequencies). For circumferential lesions, radiofrequencies are delivered at a distance of about 1 cm from the ostia (instead of 5 mm), thus reducing the risk of stenosis of the pulmonary veins. If an increase in impedance occurs (> 10 Ohms) or the patient experiences burning pain, the radio frequencies are stopped immediately. When the ablation starts, the irrigation flow increases from 2 to 17 ml/min, while the impedance and temperature values at the tip of the catheter are constantly monitored. The output energy is limited to 50 W with a maximum temperature of 48 degrees C throughout the procedure, but lower values are used in the posterior wall and in the coronary sinus to reduce the risk of injury to adjacent structures. Usually the circumferential lesion lines are practiced starting from the lateral portion of the tricuspid annulus and moving posteriorly, then anteriorly to the left of the pulmonary veins, passing the ridge between the LSPV and the atrium and going close to the lesion on the posterior wall of the atrium. The right pulmonary veins are isolated in a similar way, and two further lines connecting the two circumferential lines are made posteriorly. The circumferential lines are adapted according to the individual anatomy of the junction between the pulmonary vein and the atrium. A single circumferential line surrounds the two ipsilateral VPs in the presence of ostia less than 20 mm apart, in the presence of a common ostium or an early branch division. If anatomically possible, we also practice a line of injury between the two ostia to further reduce the anatomical and electrophysiological substrate. Characteristically, in patients with permanent AF and dilated atria, while performing the disconnection of the coronary sinus and before restoring the sinus rhythm, there is a regularization of the cycle with a transformation in CT and a uniform morphology of the P wave. With our approach, there is a restoration of the sinus rhythm (SR) in almost all patients with permanent AF. The restoration to SR occurs immediately or after transformation into AT. The procedure is successful when all endpoints are reached.
Ablation of critical areas
Obtaining all endpoints is crucial but can be difficult in specific areas. Repeated applications of short duration radio frequency, high intensity and higher irrigation flow are usually needed around the VPSS, where atrial potential is difficult to eliminate. The complete removal of atrial potentials in the ridge between the VPSS and the auricular requires longer RF applications with higher power. If the ridge is too narrow, the ablation line is made by passing to the base of the auricle. The VPDs and the mitral isthmus are two other difficult sites for both mapping and ablation and require constant adjustments in the RF setting. Incomplete lesion lines, especially in the vicinity of the mitral isthmus, can remain in gaps that support an incessant post-ablation atrial tachycardia. In patients with mechanical valve prostheses, mapping and ablation near the mitral area can be difficult; however, no experience of catheter entrapment has occurred in our experience. The mitral isthmus line requires validation of the disconnection with pacing maneuvers and in a minority of patients also applications within the coronary sinus. The ablation of the connection sites between the SC and the atrial musculature requires a lot of attention and requires lower settings in the energy and irrigation flow to avoid perforation and cardiac tamponade. Usually we practice two low energy radio frequency applications (between 15 and 30 W) from the distal to the proximal, instead of a single application, to keep the temperature low and avoid potential complications. The posterior wall also represents an area potentially at risk of complications, such as atro-esophageal fistula and cardiac tamponade. It is well known that the posterior wall is not only the thinnest wall of the left atrium, but is in close correlation with the esophagus. When we apply radio frequencies in this area, we use a lower setting in terms of energy and irrigation flow.
Management post-procedure and of complications
At the end of the procedure, we usually use protamine sulphate to allow the removal of the introducers. Subsequently, management includes anticoagulant therapy, while in the past embrication with heparin was used. Currently with DOAC drugs, this is no longer necessary and only oral anticoagulant is continued. The possibility of optimizing the parameters according to the most critical areas allows for a lower incidence rate of major complications. Cardiac tamponade should be excluded in all patients who have post-procedure hypotension. In our experience, however, this complication is very rare if you pay attention to the settings used. Only a few patients required pericardiocentesis following pericardial effusion, and we reported only one case of atrioesophageal fistula. The late onset (6-10 days after ablation) of a febrile state with or without neurological symptoms should always lead to suspicion of esophageal atrium fistula, which should be excluded by means of a spiral CT with contrast. In our extensive experience covering over 15,000 cases of CPVA, there have been no perioperative deaths, or major complications, such as VP stenosis, phrenic nerve injury or coronary artery occlusion. Minor complications are infrequent, while a non-hemodynamically significant pericardial effusion affects about 4% of patients. Pericarditic pain may be present in the early days of the post-procedure and is usually responsive to salicylates.
Post PTCA rhythm control
The absence of symptoms may not correspond to a stable restoration of the sinus rhythm, and the accuracy of the evaluation of post-ablation recurrences most of the time depends on the duration of the ECG recordings. To assess what the burden of asymptomatic recurrences of arrhythmia is, usually after ablation, patients undergo a loop recorder implant (generally within 45 days of ablation), followed by remote monitoring. Alternatively, patients can undergo Holter ECG recordings after 1, 3, 6 and 12 months and a transtelephonic ECG (cardiotelephone) monitoring.
Effectiveness
In the first two months after the procedure, atrial fibrillation recurrences may occur, however in half of the cases they constitute a transient phenomenon and do not require a second procedure. The long-term efficacy of CPVA is > 90% in patients with paroxysmal atrial fibrillation, and approximately 85% in patients with permanent atrial fibrillation, when it was not possible to induce AF or AT at the end of the procedure. The long-term success rate is higher in patients with paroxysmal atrial fibrillation and local vagal denervation. If there is a recurrence of persistent atrial fibrillation or frequent episodes of symptomatic atrial fibrillation or the presence of a symptomatic right or left atrial flutter, a second procedure is proposed at least six months after the first. The procedure is repeatable for a maximum of three times.
Atrial remodeling
The assessment of the potential consequences of ablation on the contractility of the atrium is important for the correlation of this with the thromboembolic risk. After ablation, we carefully evaluate the contractile function of the left atrium, both in the immediate post-procedure and during long-term follow-up. In our experience, after ablation, the diameters of the left atrium are reduced and the contractile function improves, but the significance of these improvements depends strictly on the atrial dimensions before ablation. In patients without relapses and with good atrial function, we stop anticoagulant therapy.
Post-ablation atrial tachycardia
If all objectives have been achieved during the procedure, post ablation atrial tachycardia develops in less than 5% of cases, and it is usually macro / micro re-entry tachycardia, rather than focal atrial tachycardia. In our experience, these tachycardias should initially be treated conservatively through drug therapy or cardioversion. Only in symptomatic patients is the procedure repeated in order to optimize ablative therapy, and in many cases therapeutic success is achieved. Ablation should be performed not through empirical lesions but after recognition of the underlying mechanism. The morphology of the P wave, its axis, and the continuous activation of the atrium leads to a macro-reorientation mechanism, while the observation of an isoelectric line between the P waves leads to a focal tachycardia. We routinely perform both a voltage and activation map; combining them together with pacing maneuvers for a better result of ablative therapy. Usually the activation map shows the earlier and later activation with a chromatic scale that refers to a time window equal to the tachycardia cycle. The most common post-ablation atrial tachycardia is due to one originating from the mitral annulus. Entering with post-pacing intervals equal to the tachycardia cycle measured at more than three sites around the upper and lower mitral annulus, with an activation time around the tricuspid annulus equal to the tachycardia cycle, strongly suggest a diagnosis of atrial tachycardia originating from the mitral annulus. As in the case of the isthmus-dependent right atrial flutter, the narrowest area of the circuit is located between the VPIS and the annulus. Consequently, the best place to look for the residual gaps and to repeat the ablation is the mitral isthmus. For micro reentrant atrial tachycardias (cycle length less than 80%) originating from the reconnection of the VP ostia, the ablation of the sites with earlier activation that have an occult entrainment proves to be very effective. Frequently the voltage maps show areas of voltage preserved at the early activation sites, suggesting the presence of areas not previously ablated or insufficiently ablated. The re-entry around the right or left pulmonary veins can be demonstrated by pacing from the distal and proximal coronary sinus, from the septum and from the roof of the atrium. Their management requires the use of 3-D activation maps to outline the course of tachycardia and to identify a lesion line that connects the anatomical barriers in order to interrupt the atrial tachycardia circuits. RFs are delivered after having clearly identified the critical isthmuses with a detailed electroanatomical map. Usually only a few RF applications are needed to eliminate tachycardia circuits and their inducibility.
Anticoagulation
Stroke is a possible and feared complication of AF ablation, in particular if one considers the possibility that there may be asymptomatic ischemic episodes. To prevent stroke or other embolic thrombus events in patients who are not chronically taking anticoagulant therapy, a trans-esophageal echocardiogram is performed after short-term anticoagulant therapy, instead of after three weeks. Pre-ablation anticoagulation patients with permanent atrial fibrillation, the patients at risk (patients with persistent atrial fibrillation or with paroxysmal atrial fibrillation associated with other risk factors), require oral anticoagulation therapy for at least three weeks documented by a careful monitoring of the value of INR. We also recommend performing a TEE before the procedure in all patients who have AF or who have a high risk of thrombotic events.
Anticoagulant therapy during the ablation procedure
Anticoagulation should be performed after performing the transseptal puncture and it is often necessary to maintain an ACT value > 300 sec to reduce the risk of thrombosis of the introducer. What is the best protocol for anticoagulation in the post-procedure has not yet been established. Due to the embolic risk in the post-procedure, the patient is suggested to observe oral anticoagulant therapy in the first 3-4 months. In selected patients who have no evidence of arrhythmic episodes 4-6 months after ablation, we stop coumadin and set up aspirin therapy (75-325 mg/day). In any case, patients with high embolic risk should continue warfarin therapy even if there is no evidence of arrhythmic recurrences.
Remote mapping and ablation with Stereotaxis
Currently most of the transcatheter ablation procedures are performed manually in a traditional way, and this requires qualified and experienced personnel in the handling of the catheters and in the ablation. In a modern electrophysiology laboratory, the presence of magnetic navigation systems means that the differences due to the human factor are limited, and the results are more reproducible. The feasibility of a remote system that is not an employee operator, could represent an interesting and attractive alternative for laboratories, which could thus obtain a high success rate while minimizing risks. The recent possibility of having a magnetic catheter with an irrigated tip will increase the benefits of the remote system by being able to perform deeper procedures regardless of the operator’s experience. We have shown that remote navigation could facilitate both mapping and aeration regardless of the dexterity of the electrophysiologist. The magnetic navigation system uses soft catheters equipped with three small magnets on the tip for optimal orientation in the magnetic field created by two large magnets positioned on both sides of the operating table. This system consists of two independent components that communicate with each other: the Niobe Stereotaxis MNS and the electro-anatomical mapping system CARTO-RMT. The Niobe includes a computer interface that is controlled by a keyboard and a joystick that changes the orientation of the two magnets by changing the orientation of the magnetic field and therefore the location and orientation of the tip of the catheter. The operator is in a separate room, away from fluoroscopy and the patient’s body. This system is combined with the CARTO mapping system which has been modified to support magnetic navigation. A 4-8 mm magnetic tip catheter (Navistar-RMT, Biosense Webster, Inc.) can be connected to the CARTO-RMT, and irrigated tip catheters are also available in Europe. The three magnets present in the distal portion of the catheter allow the catheter to have wide orientation possibilities, while the movement is guaranteed by a mechanical device (Cardiodrive Stereotaxis). The magnetic field vectors used for each navigation and ablation target can be stored and reused for automated ablation. An accurate electroanatomical map can be created simply by using the automatic function present in the Navigant software, which has been specifically designed for the mapping of the left atrium. There is also the possibility of taking additional points in areas of particular interest. The sequential acquisition of different points all around the left atrium with a stable wall contact of the lead allows to accurately recreate the cardiac geometries of even the most complex areas with a surprising degree of accuracy and effectiveness. In our experience, remote mapping and ablation was possible in all patients who underwent atrial fibrillation ablation. Initially, the procedure times were a little longer than manual procedures, and this was due to the learning curve, which, in the early stages, requires frequent adjustments in the orientation of the catheter tip. The ablation times to complete the lesion lines around critical areas, such as the right VP, are shorter remotely than with manual ablation, suggesting that, with magnetic navigation, there are no sites difficult to ablate, thus avoiding unnecessary RF applications and consequently major complications.
Advantages of the remote system
The orientation of the lead is entirely guided by the magnetic field vectors, and also the RMT catheter is much softer than traditional catheters near the distal segment. If the catheter does not reach the predetermined location, the operator must simply move the catheter from the anatomical obstacle and advance to the desired location by manipulating the magnetic field. This leads to a lower traumatization of the endocardium and a lower risk of cardiac perforation. Also in our experience, no cases of cardiac perforation have been reported during the mapping of the areas of the left atrium with thin muscle walls. The “soft touch” catheters used in magnetic navigation lead to a lower deformation of the heart chambers compared to traditional catheters, and this to the advantage of a more accurate anatomical reconstruction and less use of fluoroscopy.
Limitations of the remote system
There are some limitations of the system that can be resolved as technological progress advances. The size and position of the magnets can interfere with the fluoroscopic vision of the heart during the procedure. However, this drawback can be overcome by the presence of a more accurate electroanatomical map.
Typical or common atrial flutter (AFL type 1), is a relatively frequent form of atrial arrhythmia that often occurs in association with atrial fibrillation and may be the cause of major adverse events, such as cardioembolic stroke, myocardial ischemia, and sometimes tachycardia-induced cardiomyopathy, due to rapid atrioventricular conduction.
The AFL is typically a regular atrial rhythm due to a re-entry circuit that involves most of the right atrium (right atrial macrorientro). The atria depolarize at a frequency of 250-350 beats / min. Since the atrioventricular node is not able to conduct at this speed, the impulses are conducted to the ventricles according to a conduction ratio that can be fixed, giving a regular ventricular rhythm (for example in case of conduction 2: 1, with FC 150 bpm) or variable from moment to moment, according to variable conduction ratios (3: 1, 4: 1, or 5: 1), giving a regular ventricular rhythm and sometimes irregular.
AFL symptoms include palpitations, exercise intolerance, dyspnea and presyncope. As in atrial fibrillation, atrial thrombi can form, which can then embolize. The AFL diagnosis is based on the ECG, which highlights the atrial activation with the typical saw-tooth pattern (called F waves), evident in the lower derivations (D2, D3, avF).
The treatment of AFL includes the control of frequency with drugs, the prevention of thromboembolism with anticoagulant therapy and, often, the conversion to sinus rhythm with drugs, cardioversion, or transcateter ablation of the substrate (right atrial macrorientro).
What is the electrophysiological substrate of atrial flutter?
The AFL substrate is complex and includes conduction slowing in the vicinity of the cable-tricuspidal isthmus (CTI) and / or the functional conduction block along the crista terminalis and Eustachian crest. This electrophysiological background determines an ideal condition for the formation of a macrorientro circuit at the level of the right atrium. The triggers of atrial flutter may be various, and include atrial extrasystole or atrial fibrillation itself.
Schematic representation of the activation pattern in typical flutter and in typical reverse flutter. (visualization through the tricuspid valve looking from the ventricle towards the atrium). In typical flutter (A) the falling front wave rotates in the right atrium counterclockwise, while in the flutter, reverse clockwise. The terminal ridge and the Eustachian ridge represent anatomical blocks. The area of the cavotricuspidal isthmus is a slowing conduction area. SVC: superior vena cava; CT: terminal ridge; IVC: inferior vena cava; ER: eustachian crest; CS: coronary sinus; TV: three-way valve
What are the techniques for the transcatheter ablation of Atrial Flutter?
In consideration of its well-defined anatomical and electrophysiological substrate and its resistance to drug therapy, the catheter ablation of AFL has established itself as the therapy of choice.
TCRF ablation techniques are multiple and can sometimes employ the latest 3D electroanatomical mapping systems. To date, however, the most widely diffused is the fluoroscopic technique focused on the ablation of the tricuspid histology.
Following local anesthesia and mild sedation, puncture of the right femoral vein and left subclavian vein is performed using the Seldinger technique. They are positioned under fluoroscopic guidance of diagnostic leads at the apex of the right ventricle (tetra-polar) and right atrium (duodecapular HALO) via the femoral vein, and of the coronary sinus via the subclavian vein (tetra-polar).
If the procedure is carried out in the course of atrial flutter, the typical counter-clockwise propagation of the flutter is observed, which proceeds from the atrial septum to the lateral region of the isthmus.
An ablator lead is then introduced and a lesion line is made at the level of the hollow-tricuspid isthmus by means of radiofrequency deliveries with consequent interruption of the atrial flutter.
Alternatively, if it is not possible to induce the clinical arrhythmia during the procedure, it is possible to perform the ablation of the hollow-tricuspid isthmus even in sinus rhythm during fixed pacing by the coronary sinus.
Stimulating the atrium from the coronary sinus, it is possible to notice how the impulse can travel in two directions, meeting at the level of the lateral wall of the right atrium. By creating a lesion line at the level of the CT isthmus, the impulse can propagate in only one direction.
At the end of the procedure, the achievement of the bidirectional conduction block is highlighted.
How does the Transcatheter Ablation (TCA) procedure of atrial flutter occur?
The AFL TCA procedure takes place in a hospital. The procedure is performed with the patient conscious, after local anesthesia in the venous access area (right femoral). The duration of the procedure may vary depending on the difficulty of identifying and interrupting the return circuit (on average 1-2 hours). In the absence of complications, discharge takes place 1-2 days after the procedure.
What are the risks of atrial flutter ablation?
The procedure is generally well tolerated; the only discomforts for the patient may be the finding of vascular access and, in some cases, the at the time of ablation when a burning sensation can occur in the chest. During the procedure, it is possible that the patient also feels tachycardia, which the operator tries to trigger in order to be able to adequately map it and find its source circuit.
The complications of atrial flutter ablation are very rare. The AFL TCA procedure takes place in a suitable environment and by personnel trained to deal with any rare complications.
How does the follow up of the Atrial Flutter ablation take place?
Subsequent AFL follow-up checks for TCA include clinical evaluations and periodic execution of Holter ECG monitoring in order to detect possible recurrences. In our center, generally after ablation, the insertion of an implantable loop recorder is scheduled, which allows the monitoring of the cardiac rhythm for about 3 years, even through remote monitoring.
The Atrio-Ventricular Abnormalities (Wolff-Parkinson-White syndrome WPW) Ablation consists of administering thermal energy (radio frequency) near the accessory pathway in order to create irreversible cell damage and therefore make it electrically inert.
What is Wolff-Parkinson-White syndrome (WPW)?
Wolff-Parkinson-White syndrome (WPW) is characterized by the association of symptoms due to tachyarrhythmias with the presence of pre-excitation on the surface ECG tracing (WPW pattern). In WPW syndrome, tachyarrhythmias are due to a phenomenon of atrio-ventricular macro-re-entry, which recognizes two anatomically defined conduction pathways: The hisian node system and the atrio-ventricular accessory pathway itself. It is sufficient that between these two ways there is a difference in the refractory period or in the conduction speed for a return circuit to be created. Atrio-ventricular re-entry tachycardias (AVRT) are commonly distinguished in orthodromic and antidromic depending on whether the anterograde conduction occurs through the node-hisian system or through the accessory pathway.
What is the role of the electrophysiological study in patients with WPW?
The electrophysiological study in patients with WPW is useful to confirm the diagnosis, study the mode of initiation of tachycardias, locate the accessory pathways, demonstrate that the accessory pathway participates in tachycardias, evaluate the refractory nature of the accessory pathway and its implications for the risk of dangerous arrhythmias, stop tachycardias in drug therapies, and stimulate or ablate arrhythmias associated with WPW syndrome.
The episodes of recurrent supraventricular tachycardia (SVT) can start from early childhood, but their onset is more frequent during adolescence or adulthood. Paroxysmal atrial fibrillation, on the other hand, appears almost exclusively in adults. It is not uncommon to see signs of pre-excitation ECG at birth, which disappear after some time, as the accessory pathway degenerates and becomes fibrotic, becoming unable to conduct; however the disappearance of the pre-excitation signs of the ECG does not necessarily mean that there is a complete elimination of the conduction on the Kent beam, since both the latent and hidden pre-excitation do not associate with the typical ECG scheme (delta wave, short interval PR, etc.) but both are capable of inducing arrhythmias (3).
An extremely low percentage of patients with WPW suddenly die from ventricular fibrillation. The mechanism is almost certainly an atrial fibrillation with a high ventricular response, which degenerates into a ventricular fibrillation due to the high ventricular rate. This is a dramatic event that can also occur in asymptomatic subjects, with an incidence of 1:1000 people per year. It was observed that all patients with pre-excitation who were revived from cardiac arrest had a short antegrade refractory period (< 250 ms) of the accessory pathway. On the basis of these data it has been proposed to consider patients “at risk” with this electrophysiological result (4). However, the positive predictive value of this parameter is very low, since about 20% of the subjects subjected to an EP study have these characteristics and should therefore be considered at risk, while the actual incidence of sudden death is considerably lower.
What is the role of endocardial mapping in WPW?
The ECG can help locate the accessory pathways (AP), while the electrophysiological study and intracavity mapping provide precise data on its position and on the electrophysiological properties of the accessory pathways. In order to define the exact position of the Kent beam, the AV annulus is mapped in order to find the point with the shortest AV interval during the antegrade conduction on the Kent beam or the shortest AV interval during the ventricular pacing or orthodromic tachycardia. This type of mapping can be performed using bipolar or unipolar recordings and is based on the principle that the activation of the first chamber (ventricular during antegrade, atrial conduction during retrograde conduction) allows to locate the insertion of the accessory pathway in the chamber. Therefore, the scaler catheter must be positioned on the right or left AV ring, in contact with the endocardium, and then moved until the shortest conduction interval is found. The position of the catheter is confirmed by fluoroscopy and the recorded potential, which is composed of two deflections, the atrial and ventricular ones. If the catheter is on the Kent beam, it is easy to record almost fused A and V waves, indicating an extremely short conduction time. Sometimes it is even possible to record the potential of the Kent beam, seen as a rapid short-term deflection, between A and V, expressing the depolarization of the accessory pathway: the waves A and V and the Kent potential are continuous, and the different components are difficult to separate. The identification of this continuous electrical activity strongly indicates the presence of an accessory route.
Antegrade mapping
The first ventricular activation site during manifest pre-excitation (pre-excited sinus rhythm, antidromic AVRT) identifies the site of ventricular insertion of the accessory pathway. Target site criteria for ablation during antegrade mapping include: 1) AP potential (Kent potential), 2) first local ventricular activation related to the onset of the delta wave (pre-delta) and 3) fusion of atrial and ventricular electrograms. The potentials of the accessory path reflect a rapid local activation of the accessory pathway and are acute and high frequency deflections between the atrial and ventricular electrograms that precede the onset of the delta wave. The more the local ventricular electrogram on the ablation catheter precedes the onset of the delta wave, the greater the probability of success.
Retrograde mapping
The first atrial activation site during retrograde conduction on the accessory pathway (ventricular pacing, orthodromic AVRT) identifies its atrial insertion site. A limitation of the mapping during ventricular pacing is that retrograde conduction on the AV node may interfere with the identification of the first atrial activation site on the accessory pathway (in particular, septal accessory pathways). Potential solutions include stimulation at a higher speed (to cause decrease or blockage in the AV node), administration of drugs that slow AV nodal conduction or mapping during orthodromic AVRT (where retrograde conduction occurs only on the accessory pathways). The criteria for defining the site for ablation include: 1) potentials on the accessory pathways, 2) the first atrial activation site and 3) fusion of electrograms A and V.
Based on the recommendations of the ACC / AHA / ESC guidelines of 2019, in the case of asymptomatic pre-excitation, the execution of the EP test is recommended in the young person, in the athlete and in subjects in which the non-invasive tests suggest a non-low risk situation. In subjects with asymptomatic WPW, where the EP test with the use of isoprenaline shows high risk properties, such as SPERRI < 250 ms, AP ERP < 250 ms, multiple accessory pathways and tachycardia mediated by inducible accessory route, there is a class I indication for RF.
What are the features of atrioventricular accessory pathway-mediated tachycardias (AVRT)?
The most common tachycardias associated with WPW syndrome are circuit tachycardias, 95% of which are orthodromic; that is, they lead downwards with respect to the normal A-V conduction system and retrograde on the bypass section. The conduction and refractory relationship of the normal A-V conduction system and the bypass section, as well as the stimulation site, determine both the ability to start the tachyarrhythmia circuit, and, theoretically, the type of tachycardia. The conduction and refractory nature of the accessory pathways in most cases behave like contractile muscle tissue; therefore, the accessory pathways demonstrate rapid conduction and present refractory periods, which tend to shorten with the reduction of the lengths of the stimulation cycle (PCL).
WPW syndrome allows to verify the presence of all the requisites for a re-entering rhythm: (a) two anatomical pathways determining from the functional point of view; (b) one-way block in one of the paths (in this case, in the accessory path or in the nodal A-V path); (c) a sufficient slowdown in a part of the circuit to overcome the refractoriness before the circulating impulse; and (d) the impulse conduction time must exceed the longest effective refractory period of any component in the circuit. Both the antegrade and retrograde refractory periods of the accessory pathway are the main determinants of: (a) ability to initiate and sustain circular movement, and (b) ventricular response to atrial tachyarrhythmias (e.g. atrial fibrillation, atrial flutter, and atrial tachycardia).
AVRT is a re-entrant arrhythmia and is classified into orthodromic and antidromic variants. During orthodromic tachycardia, the antegrade pathway is the AV-His-Purkinje node system and the retrograde pathway is the accessory pathway. On the contrary, during antidromic tachycardia, the antegrade pathway is the accessory pathway and the retrograde pathway is the normal conduction system. Orthodromic AVRT constitutes about 95% of spontaneous and laboratory-induced AVRT. For the onset of tachycardia, a premature atrial complex (APC), spontaneous or induced by stimulation, hangs on the accessory pathway and travels along the AV-His-Purkinje node. The impulse conducted reaches the ventricle and returns to the atrium on the accessory route, which has now recovered its excitability. The impulse then returns to the AV-His-Purkinje system, perpetuating tachycardia. Orthodromic tachycardia can also be initiated by a premature ventricular complex (PVC). In this case, PVC blocks the His-Purkinje system but travels on the accessory route to the atrium. If the node’s AV-His-Purkinje system has recovered excitability, the impulse then travels along the node and returns to the ventricle, and orthodromic tachycardia is initiated.
Induction of orthodromic AVRT by the atrial premature complex (a) or the ventricular premature complex (b).
What are the goals in the treatment of WPW syndrome?
Pre-excitement therapy has four different objectives: 1. To cure symptoms; 2. Prevent the risk of sudden death; 3. Prevent or cure, in case of chronic tachycardia, the worsening of the ventricular function; 4. Allow subjects with pre-excitement to carry out all activities that are otherwise prohibited by law when there is pre-excitement on the ECG, for example in competitive sportsmen or in workers of professions at risk.
In other cases, therapy is not indicated: in particular in asymptomatic subjects, who present with only pre-excitation on the ECG, no treatment is necessary, once the absence of risk parameters in the electrophysological properties of the accessory pathways has been verified, given except that in rare cases, the risk of developing dangerous arrhythmias is very limited.
There are four different types of therapeutic approaches: antiarrhythmic drugs, transcatheter ablation of accessory pathways, surgical ablation of accessory pathways, and electrical therapy (cardioversion, stimulation).
What are the pharmacological treatments of AVRT in WPW?
In orthodromic AVRT, the AV node is the weak link, and drugs that prolong AV nodal refractoriness or depress its conduction can lead to a blockage in the node with consequent interruption of tachycardia. Vagal maneuvers end tachycardia, causing blockage in the node. First-line drugs that are effective in the acute termination of orthodromic AVRT include the administration of adenosine, verapamil, diltiazem, or beta-blockers via IV route. Digoxin is less effective due to the delayed start of the action. Among class 1a antiarrhythmic drugs, procainamide is a valid alternative, since it depresses conduction, prolongs refractoriness in most cardiac tissues (i.e. atrium, ventricle and His-Purkinje system) and also blocks conduction in the accessory pathway. Ic class antiarrhythmic drugs are more effective than class Ia drugs in blocking AP conduction; however, they should be avoided in patients with structural heart disease. Amiodarone has various electrophysiological effects but is no more effective than class IC drugs used alone or in combination with beta-blockers. In general, amiodarone should be reserved for those who are candidates refractory to drugs, elderly, or unfit for ablative therapy. Sotalol can be effective in preventing tachycardia, although it is associated with a 4% risk of torsades de pointes, especially in those with significant structural heart disease and congestive heart failure. Oral digoxin is not effective as a monotherapy for orthodromic AVRT and, due to its direct effects on the accessory pathway, this drug can actually accelerate conduction on the accessory pathway during atrial fibrillation. Therefore, digoxin should never be used to treat patients with pre-excitation.
In antidromic AVRT, retrograde AV nodal conduction can be the weak link in the re-entry circuit. Calcium channel blockers, beta blockers and adenosine can be used for the acute cessation of tachycardia. Procainamide IV is the drug of choice in the acute treatment of antithromic AVRT. Also this drug does not stop tachycardia: it can slow down the rate of tachycardia. In the absence of contraindications, class 1c drugs are the drugs of choice for the long-term oral treatment of antidromic tachycardia.
How is radiofrequency catheter ablation performed in WPW?
Radiofrequency ablation (RF) is the procedure of choice for patients with symptomatic WPW syndrome and for those who respond poorly to medical therapy. In the more experienced centers, the success rate is between 95% and 97% with a recurrence rate of 6%. The success of the ablation depends critically on the accurate location of the accessory route. The location of the preliminary route can be obtained from the delta wave and QRS morphologies (see location of accessory pathways from the surface ECG).
In general, the endocavity electrophysiological study precedes the ablation of the accessory pathway, locating its exact location. The ablation procedure is performed under local anesthesia and a mild pharmacological sedation. Multiple venous accesses (usually right femoral and left subclavian) are obtained by the Seldinger technique. If the accessory pathway has a left localization, an arterial access (right femoral artery) is also positioned in order to allow ablation by transaortic approach. Alternatively, the left heart chambers can be reached by transseptal puncture.
The quadripolar diagnostic leads are positioned at the level of the upper right atrium, the bundle of His, at the apex of the right ventricle and in the coronary sinus (cardiac vein that surrounds the left ventricular atrium sulcus and allows to record the electrical activity in the left part of the heart).
The ablation consists of administering thermal energy (radio frequency) near the accessory pathway in order to create irreversible cell damage and therefore make it electrically inert.
HRA: high right atrium; His: bundle of His; CS: coronary sinus; RV: right ventricle; ABL: scaler catheter
If the ventricular excitation occurs during the electrophysiological study, the valve rings are mapped, and it is identified where the earliest ventricular activation or the characteristic Kent potential is present.
Some atrial or ventricular pacing maneuvers can be helpful if the accessory pathway is not immediately identifiable.
When pre-excitation is not maximum, rapid atrial stimulation or adenosine I.V. can be used to obtain complete pre-excitation in order to improve the accuracy of the location. This is particularly useful in the left lateral accessory pathways where pre-excitation can be improved with left atrial stimulation (from the coronary sinus, CS, catheter). The criteria of the intracardiac electrogram (8) used to identify the appropriate target sites for the ablation of the manifested pathways include the presence of a long potential at the accessory avia (Fig. 5), the early onset of local ventricular activation with respect to onset of the delta wave, the stability of the electrogram, and the continuous anterograde electrical activity (fused atrial and ventricular electrodes).
Fig. 5 From top to bottom are the conductors DI, DIII, V1 and the electrograms from the proximal area of the bundle (HBE p), from the coronary sinus proximal to the distal one (from CS 7-8 to CS 1-2) , the proximal and distal scaler (ABLp and ABLd) and right ventricular apex (RV Ap): the distal scaler records a rapid potential (potential Kent, K) between atrial (A) and ventricular (V) electrograms.
What are the criteria for choosing the approach for ATCRF of abnormal pathways?
The criteria used to identify the appropriate target sites for the ablation of the hidden pathway include the presence of retrograde potential along the accessory pathway, continuous retrograde electrical activity with ventricular stimulation or during tachycardia and electrogram stability. Ablation can be guided by the catheter in the coronary sinus used to fix the position of the path. The anomalous route can be ablated through a trans-septal or trans-aortic retrograde approach, depending on the experience and preferences of the operator. In the absence of a PFO, the trans-septal approach involves puncture through the oval fossa. With the trans-aortic approach, the tip of the ablation catheter is curved to avoid damaging the coronary arteries, advancing retrograde through the aortic valve in the left ventricle and positioned along the mitral ring.
Catheter ablation is associated with a very high success rate. The correct ablation of the paths of the free walls on the right requires a detailed mapping of the lateral tricuspid annulus. The overall success rate for ablation of the free wall of the right ventricle is the lowest of all accessory pathways, with an average of 90% and a recurrence rate of 14%. The reasons for the reduction of the success rate include the instability of the catheter and the lack of a coronary sinus-like structure on the right side, parallel to the tricuspid ring, to facilitate mapping.
Ablation of the antero-septal and median pathways can be difficult due to the proximity to the A-V node and His bundle, however it is associated with an overall success rate of 95% to 98% and a risk of 1% to 3% of permanent A-V blockade. Ablation of the posterior-septal pathways can be challenging due to the complex anatomy of the posterior-septal area. Most postero-septal pathways can be ablated from the right side, although in 20% of cases a left side approach is needed (Fig. 6).
ECG and electrophysiological aspects that suggest the need for a left-sided approach include a positive delta wave or a positive QRS complex in V1, the first retrograde atrial activation at the coronary sinus ostium (CS) and an increase in the VA interval with the presence of BBSX during orthodromic tachycardia.
A small percentage of the accessory pathways have an epicardial site. Between 5% and 17% of postero-septal and posterior APs are located at the epicardial level and ablation by CS is necessary. The presence of epicardial accessory pathways could be suggested by the discovery of small or absent potentials during endocardial mapping and larger potentials during CS level mapping. The epicardial accessory pathways on the left side can be successfully ablated within the CS in the case of routes with high potential. However, the ablation of accessory pathways in other epicardial sites may require a percutaneous epicardial approach, as an alternative to cardiac surgery.
Overall, AP ablation is associated with a complication rate of 1% to 4% and a procedure-related mortality rate of approximately 0.2%. Complication of complete A-V block occurs in about 1% of patients and is most frequently found in patients undergoing septal pathway ablation. Autonomic dysfunction and inappropriate sinus tachycardia are rare complications of radiofrequency ablation of the atrium-ventricular accessory pathways and are less frequent than those observed in AVNRT ablation. Today, advances in lead design, energy delivery systems, mapping systems, and remote robotic navigation systems have made transcatheter ablation the therapy of choice for most macro-tachycardias (ARVT and AVNRT).
Presence of multiple accessory routes.
In about 10-15% of subjects with pre-excitation, there are multiple accessory pathways. Histopathological data show a higher frequency of multiple accessory pathways than those observed clinically. The presence of multiple accessory pathways increases the incidence of symptoms and is associated with a higher risk of sudden death due to atrial fibrillation that degenerates into ventricular fibrillation. Patients with pre-excitation resurrected from sudden death had a higher incidence of multiple accessory pathways than the control group that had not had cardiac arrest (5). Diagnosis of multiple accessory pathways on the ECG is possible, although not in all cases.
EXAMPLES OF ABLATION PROCEDURES IN SPECIFIC SITUATIONS ARE SHOWN BELOW
Ablation of a manifest left postero-septal AP using a retrograde trans-aortic approach (LAO projection). The ablation catheter is positioned along the postero-septal mitral annulus where it records potential on the accessory pathways between the atrial and ventricular electrograms. The application of RF energy on this site caused the loss of pre-excitation within seconds. The CS catheter provides a useful reference to the mitral ring.
The figure above shows how in basal conditions the signs of ventricular pre-excitation are not very evident
Proceeding with an asynchronous stimulation from the coronary sinus increases the degree of ventricular pre-excitation with the shortest AV interval detectable near the distal coronary sinus.
In the above case, for example, the scaler catheter is positioned trans-aortically in the left lateral position and the typical Kent potential is recorded on the distal dipole.
Here, radiofrequency is delivered with the disappearance of the ventricular pre-excitation.
Note how the atrial and ventricular signals appear more spaced on the dipole in the coronary sinus.
At the end of the ablation procedure, the electrocardiogram no longer shows the stigmata of the pre-excitation and therefore a complete normalization of the same is obtained.
Sometimes accessory pathways can complicate other arrhythmic diseases, such as nodal re-entry tachycardia or atrial fibrillation. Just the latter when associated with ventricular pre-excitation can constitute a real clinical emergency due to the lack of “filter” of the AV node and the high ventricular response conferred by the low refractory period of the accessory pathway.
Some atrial or ventricular pacing maneuvers can be helpful if the accessory pathway is not immediately identifiable.
The figure above shows how in basal conditions the signs of ventricular pre-excitation are not very evident.
Proceeding with an asynchronous stimulation from the coronary sinus increases the degree of ventricular pre-excitation with the shortest AV interval detectable near the distal coronary sinus.
In the above case, for example, the scaler catheter is positioned trans-aortically in the left lateral position and the typical Kent potential is recorded on the distal dipole.
Here, radiofrequency is delivered with the disappearance of the ventricular pre-excitation.
Note how the atrial and ventricular signals appear more spaced on the dipole in the coronary sinus.
At the end of the ablation procedure, the electrocardiogram no longer shows the stigmata of the pre-excitation and therefore a complete normalization of the same is obtained.
When is transcatheter ablation recommended in asymptomatic subjects with WPW?
Currently, the importance of electrophysiological study (EP) and transcatheter ablation of accessory pathways are well established in symptomatic patients with WPW syndrome. Based on the recommendations of the 2019 ACC / AHA / ESC guidelines, in the case of symptomatic pre-excitation, transcatheter ablation has a class I indication.
The approach to asymptomatic patients is less clear. The increased safety of the EP study and catheter-based ablation techniques provide an impetus to prophylactic ablation of the pathway. To support this, randomized studies have shown that prophylactic ablation in asymptomatic patients who are at high risk of arrhythmias, performed in experienced centers, reduces the risk of life-threatening arrhythmias.
What is the role of surgical ablation in WPW?
Elective surgical treatment of WPW has been largely abandoned. Until the 1980s, several patients underwent surgery to stop conduction on the AP, but since catheter ablation became available, it has been universally accepted that the risk / benefit ratio of this surgery was unacceptable, since better results were obtained using simpler and less traumatic methods.
What is the role of electric therapy in WPW?
Electrical pre-excitation therapy is based on cardioversion, which is used in case of pre-excited atrial fibrillation and rarely for AVRT, and on atrial or ventricular stimulation in case of re-entering tachycardia. Atrial stimulation can be performed through the endocavitary or transesophageal pathway, while ventricular stimulation can only be performed through the endocavitary pathway. This type of approach is recommended in subjects where drug administration is not possible or an AVRT does not stop after vagal maneuvers and the arrhythmia is not well tolerated.
What are the risk parameters of dangerous arrhythmias in WPW?
Unlike the AV node, the accessory pathways do not demonstrate a frequency-dependent decremental conduction that slows down with faster atrial rates. The following characteristics identify low risk accessory pathways: 1) intermittent pre-excitation, 2) exercise induced blockage of the accessory pathway, 3) shorter pre-excited RR interval during AF > 250 ms and 4) loss of pre-excitation with procainamide, ajmaline or disopyramide (7). Intermittent pre-excitation demonstrates that the accessory pathway is unable to sustain 1:1 conduction during sinus rhythm, and therefore cannot conduct rapidly during AF.
Similarly, the sudden loss of pre-excitation during exercise shows that the accessory pathway is unable to sustain 1:1 conduction during exercise-induced sinus tachycardia. During exercise, the sudden loss of pre-excitation (blockage of the accessory pathway dependent on frequency) must be differentiated from the gradual loss of pre-excitation (pseudonormalization) due to a better AV nodal conduction. During pseudonormalization, the accessory pathway continues to lead anterograde, but the delta wave slowly disappears as the contribution to the ventricular activation by the AV-His-Purkinje system increases. Since the antegrade effective refractory period (ERP) is related to the shortest expected RR interval during AF, an antegrade ERP along the accessory pathway or a duration of the atrial pacing cycle maintaining a 1:1 conduction shorter than 250 ms is a reasonable, but not ideal substitute for the minimum RR interval, in cases where AF is absent.
Nodal re-entry tachycardia (NRT or AVNRT, AV-nodal reentrant tachycardia) is the most common of the paroxysmal supraventricular tachycardias (PSVT) due to a re-entry mechanism. NRT is more frequent in women. Generally, it is not associated with organic heart disease. The first clinical manifestation occurs in the third or fourth decade of life, while it is rare in childhood and adolescence. The main symptom is palpitation with sudden onset and term, which can be associated with angina, anxiety, syncope, or cardiovascular failure. The severity of the clinical manifestations depends on the patient’s age, the duration of the arrhythmia, the frequency of tachycardia, and the presence or absence of associated heart disease.
What is the atrioventricular node?
The atrioventricular node (NAV) is formed by coalescence of two bundles of atrial fibers. These two beams not only have different electrophysiological properties but appear to be two distinct anatomical structures; the front section corresponds to the rapid route, while the rear section corresponds to the slow route. To better visualize these two ways, it is very important to know the anatomy of the Koch triangle. The three sides of the triangle are delimited by the tricuspid annulus (the portion of the annulus adjacent to the septal cusp), Todaro’s tendon and the coronary sinus ostium. The His bundle is located at the apex of the triangle. It is important to know that the apex of the Koch triangle (where the AV node and His bundle is located) is an anterior structure, while the coronary sinus is posterior and defines the posterior portion of the atrial septum.
How is transcatheter ablation of nodal re-entry tachycardia (NRT) performed?
In patients with nodal re-entry tachycardia (NRT), the slow pathway and the rapid pathway can be imagined as two bundles of atrial fibers: the rapid pathway is anterior and superior and is located along the Todaro tendon; the slow path is posterior and inferior and is located along the tricuspid annulus near the ostium of the coronary sinus (CS).
Since these two pathways are clearly identifiable, they can be subjected to the radiofrequency transcatheter ablation procedure. Initially the target of ablation was the rapid route, but being an anterior structure and very close to the AVN and the His bundle, the intervention was complicated in about 20% of cases with a complete AV block. The target then moved to the slow path, which, being rear and further away from sensitive structures, possesses a greater safety margin, since complete AV block in this case is described in less than 1% of cases.
Fig.3Fluoroscopic images of leads placed during ablation of nodal re-entry tachycardia
Two different types of approach are possible for slow path ablation: through electrophysiological or anatomical mapping. In both cases, the anatomical limits of the Koch triangle are first identified by placing one catheter on the His and one in the Coronary Sinus. The ablator catheter is then advanced through the femoral vein to the tricuspid annulus near the osteon of the coronary sinus (CS).
If you want to map the slow path, the scaler catheter is carefully moved along the tricuspid annulus in search of the slow path potential that represents its depolarization. In the endocavitary ECG, the slow path potential is located between atrial deflection and ventricular deflection. When the slow path potential is identified, radio frequencies (RF) are delivered near this site. In the case of an anatomical approach, only the fluoroscopic landmarks are used.
Generally, the portion of the tricuspid annulus between the ostium of the coronary sinus and the bundle of His is divided into three segments: posterior (near the ostium of the coronary sinus), medium, and anterior (near the bundle of His). The catheter is placed along the tricuspid valve and slid until the atrial and ventricular potential are recorded with the largest atrial deflection of the ventricular deflection. At this point RF is delivered, and generally if the position of the catheter is correct, it is possible to observe junctional beats or a junctional tachycardia. If after 10-15 seconds of RF, no junctional beats appear, it is good to stop the delivery and change the position of the scaler catheter. If, on the contrary, the junctional beats appear, it is good to supply RF for another 30-60 sec.
What is the goal of ablation in the NRT?
The ablation is considered successful if arrhythmia induction is impossible during the follow up electrophysiological study.
The main objective of the RF is the modulation of conduction along the slow path, blocking the nodal re-entry mechanism. The procedural objectives are summarized in the following table:
What are the risks of ablation in NRT?
Currently, given that the ablation target is now the slow path, positioned more posteriorly and therefore further away from the AVN and the His bundle, potentially sensitive structures, the intervention has a greater safety margin, with complete AV block (AVB) occurring in less than 1% of cases.
This risk is very reduced compared to the past, when the target of ablation was the rapid route, with a complete AVB risk of about 20%.
In the rare cases where a complete AVB is created today, even with the ablation of the slow path, pacemaker implantation may be necessary.
Atrial tachycardias constitute a heterogeneous group of atrial arrhythmias which differ in their location and pathophysiological mechanism and which, however, represent an uncommon cause of supraventricular arrhythmias.
It is estimated that 5% of supraventricular arrhythmias in adulthood and 15% of pediatric arrhythmias are attributable to this group of arrhythmias.
If drug therapies are not sufficient to control arrhythmic manifestations, it is possible to resort to transcatheter ablation with the goal to eliminate by thermal energy (radio frequency or cryablation) those cells that are responsible for the genesis of the arrhythmia. TCRF ablation is always preceded by an electrophysiological study that enables the identification of the targets and which is often integrated with the new electro-anatomical mapping systems.
What is the role of the electrophysiological study in patients with atrial tachycardia?
The electrophysiological study is the first step for ablation. It enables the identification of the specific location and the pathophysiological mechanism of the arrhythmic phenomenon. The surface electrocardiogram is not sufficient in most cases to specify these aspects.
Typically, 3 or 4 femoral venous accesses (from the groin) and one subclavian (from the acellar cavity) are obtained. Through these accesses, quadripolar leads are positioned in the right atrium at the level of the sinus node, then at the bundle of His and the right ventricle. An additional diagnostic lead is placed in the coronary sinus, a vein that runs into the left ventricular atrium sulcus and therefore shows us the electrical signals that come from the left side of the heart.
At this point it is possible to start stimulation maneuvers through which the arrhythmia is triggered. Sometimes it is necessary, especially in automatic forms, to resort to the use of drugs such as isoproterenol, capable of mimicking an adrenergic stimulation (similar to that which occurs when doing physical activity).
Studying the activation sequence of the atrial signal and mapping the greater advance of the atrial signal with the ablator catheter makes it possible to identify the origin site and therefore proceed to ablation, which is a burning of those cells that are involved in the genesis of the arrhythmia.
The electrophysiological study is also essential to make a differential diagnosis with other arrhythmias that may “resemble” atrial tachycardia.
What are the mapping systems used in the ablation of atrial tachycardia?
Non-fluroscopic three-dimensional mapping systems represent a considerable technological advancement in electrophysiology laboratories. These are software that allow you to “reconstruct the heart chambers” by adding the electrical substrate of each cardiac region to the anatomy. The three-dimensional mapping systems give information on the voltage of the fabric allowing us to obtain an indirect measure of the quality of the fabric itself (an electrically inert fabric or without measurable electrical signals is a “dead” fabric, or a scar, called “scar”), and to obtain information on the propagation of the signal of the electrical signal in real-time (activation map) and on the presence of anomalous electrical signals such as fragmented potentials.
The mapping systems are therefore a valuable aid for identifying the location and pathophysiological mechanism of atrial tachycardia.
Also of primary importance is the possibility of minimizing exposure to ionizing radiation from the scopia, making the procedure safer also from this point of view for both the patient and the operator.
What are the risks of ablation of atrial tachycardias?
The risks related to the ablation of atrial tachycardia are minimal and generally related to venous access. In fact, vascular damage could occur in the femoral puncture, which could remain in the formation of a hematoma, an arteriovenous fistula or a pseudoaneurysm. In most cases these complications require only a conservative attitude or compressive dressings. Other times it is necessary to resort to more invasive procedures, such as percutaneous embolization or surgical approach for the exclusion of the fistula or pseudoaneurysm.
Subclavian access in less than 1% of cases is complicated by the formation of a pneumothorax (presence of air inside the pleural cavity) or even more rarely by an hemothorax (presence of blood in the pleural cavity). These occurrences may require the placement of a drain that allows air or blood to escape.
Among the risks of the procedure, even if present in the literature, cardiac perforation with consequent cardiac tamponade is very rare. Even these complications, although serious, can be safely managed in the operating room and rarely require a surgical approach.
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.
How are ventricular tachycardias classified?
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:
Idiopathic ventricular tachycardias, i.e. not associated with recognizable cardiac structural changes;
Tachycardias associated with structural heart disease, i.e. associated with diseases of the structure and cardiac function, such as post-infarct ischemic heart disease, idiopathic dilated heart disease, hypertrophic heart disease, arrhythmogenic dysplasia of the right or biventricular ventricle, cardiac sarcoidosis, post-myocardial heart disease.
This diagnostic element has an important meaning in pathophysiological and prognostic terms, in fact:
Idiopathic ventricular tachycardias usually have a single and isolated origin, a typically endocardial origin (the inner part of the heart) and a usually favorable prognosis.
Ventricular tachycardias associated with structural heart disease can have multiple origins, an origin not only endocardial (the inner surface of the heart) but also epicardial (the outer part of the heart) or transmural (in the thickness of the heart muscle) and are associated with a more challenging prognosis. They occur in patients with a sick heart and suffering from developmental pathologies and can lead to cardiac arrest. Often patients with these tachycardias are already carriers of implantable defibrillators (ICDs), and ICD implantation is typically required when such arrhythmias occur.
What does ablation of ventricular tachycardias consist of?
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.
Ablation of idiopathic ventricular tachycardias
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 anterior and posterior fascicles of the left branch (fascicular tachycardias)
The outflow tract of the right and left ventricle
The aortic valve cusps
Mitro-aortic continuity
The papillary muscles
The epicardial region of the top of the ventricule
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.
Ablation of ventricular tachycardias associated with structural heart disease
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:
Ablation in the presence of a macroscopic arrhythmogenic substrate (typically in postinfarction heart disease and manifest forms of arrhythmogenic dysplasia)
Ablation in the presence of a diffuse and infiltrative arrhythmogenic substrate (typical of idiopathic dilated heart disease and in some forms of ventricular dysplasia).
What are the stages of ablation of ventricular tachycardias?
The ventricular tachycardia ablation procedure involves a series of different and successive stages:
Electroanatomical mapping of the ventricular cavity as alleged origin of tachycardia. This phase involves the complete reconstruction of the anatomy of the cardiac chamber concerned together with a high density evaluation of electrical potentials (electroanatomical mapping). This mapping enables the identification of areas of less amplitude of the electrical signal, indicative of the presence of scar tissue. The characteristics of the electrical signals in this location (fragmented potentials, slow electrical conduction areas, conduction block areas) are of fundamental importance to guide ablative therapy.
Induction of tachycardia by programmed electrical stimulation of the heart.
Electroanatomical mapping of tachycardia. This phase is only possible if the tachycardia is haemodynamically tolerated, i.e. if, during the tachycardia, the heart is able to pump enough blood to maintain an adequate circulatory function.
Ablation of the circuit responsible for tachycardia
Validation of the ablation result with programmed cardiac stimulation.
What are the problems and critical issues of ablation of ventricular tachycardias?
Particular problems of ablation of ventricular tachycardias include:
Induced ventricular tachycardia is not haemodynamically tolerated. In this case, it is necessary to support the circulation with assistance through particular forms of extracorporeal circulation (ECMO, “extracorporeal membrane oxygenation”).
Clinical ventricular tachycardia (that with which the patient spontaneously presented and for which ablation is performed) is not inducible. In this case, an attempt is made to identify the arrhythmogenic substrate of spontaneous tachycardia (areas of low electrical voltage, fragmentation of electric potentials, slow conduction areas) by electro-anatomical mapping, and extensive ablation is carried out in this location until the disappearance of the slow and fragmented potentials. This approach is limited to those forms of tachycardia associated with macroscopic scar areas.
Multiple forms of tachycardia are induced. In this case, if possible, we try to map and ablate all the inducible forms of tachycardia. The final objective of the procedure is to obtain an elimination of the arrhythmias (non-inducibility during electrophysiological study).
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.
Brugada syndrome (BrS) is a genetic disease that mainly affects men in the third and fourth decades of life, and, in the absence of obvious structural heart disease, leads to an increased risk of sudden death due to malignant ventricular arrhythmias (ventricular tachycardia or ventricular fibrillation).
Therapeutic options and the rationale for ablative therapy
The main problem in the treatment of this disease is linked to the fact that the cardiac arrest itself can suddenly arise in the absence of warning signs. For this reason, patients discovered to be at the greatest risk for developing fatal arrhythmias can use an implanted defibrillator, which is able to stop a potentially fatal arrhythmia through an electric shock and prevent cardiac arrest.
Although this strategy is extremely effective, it must be admitted that use of these devices comes with the burden of potential side effects, with a significant impact on the quality of life of younger patients.
Furthermore, the defibrillator is a palliative and non-curative therapy of the syndrome, because, although it is extremely effective in interrupting potentially deadly arrhythmias, it is not able to prevent their onset.
Hence, there is the need to identify the mechanisms of the disease itself in order to be able to offer a therapeutic strategy aimed at distorting the natural progression of BrS, to prevent sudden death more effectively.
The discovery of the arrhythmic substrate in BrS
In 2015, for the first time, the group directed by Prof. Pappone demonstrated and identified a group of cells, which express abnormal electrical potentials, on the external surface (epicardial) of the heart at the level of the right ventricle.
These cells are grouped together and form a confluent area, which is found in all patients with BrS.
The characteristics of this abnormal electrical substrate are the basis of the electrical and clinical manifestations of the syndrome itself, explaining the presence of the typical BrS electrocardiogram. In particular, the arrhythmic substrate is associated with the clinical presentation of the disease and the risk of suffering from a more aggressive form of BrS with a more unstable electrical substrate prone to the development of malignant ventricular arrhythmias.
The ablation of the arrhythmic substrate
As previously explained, the BrS arrhythmic substrate is located on the epicardial surface of the right ventricular outflow tract.
To reach this site, it is necessary to perform a subxiphoid puncture (figure 1) and therefore this procedure is performed under general anesthesia.
Figure 1. Epicardial access (video).
Once the pericardial space is reached, a catheter equipped with electrodes with a mapping function that is able to record the electrical activity of the heart is inserted.
Through the use of dedicated software that is associated with mapping systems, it is possible to reconstruct the three-dimensional geometry of the heart and to identify with precision the areas of myocardium affected by the disease (figure 2).
Figure 2. Mapping of the abnormal epicardial area
To achieve this goal, it is necessary to administer ajmaline during this mapping phase. This drug is able to unmask the cardiac electrical anomalies to the maximal degree, enabling the visualization and pronounced definition of the area of anomalous substrate to be treated.
Once the anomalous electrical substrate has been identified, it is possible to perform the ablation of this area. Radiofrequency disbursements are rapid and precise, in order to limit ablation to only the outer surface of the heart, enabling the elimination of only surface cells (figure 3).
Figure 3. Ablation of the arrhythmic substrate.
The purpose of the ablation is to eliminate all the anomalous electric potentials located on the epicardium (figure 4), resulting in a complete normalization of the electrocardiogram which no longer shows, after ablation, the classical electrical anomalies of BrS (figure 5). These elements are also associated with the disappearance of malignant ventricular arrhythmias in post-ablation follow-up.
Figure 4. Disappearance of abnormal electrical potentials after ablation.
Figure 5. Normalization of the post-ablation electrocardiogram.
The discovery of the arrhythmic substrate in BrS establishes the first step towards a better knowledge of the disease and towards the development of increasingly effective treatment strategies available to the patient.
What is the ablation procedure for modulating the atrio-ventricular node?
The catheter-based radiofrequency ablation procedure of the atrio-ventricular node is aimed at patients suffering from persistent atrial fibrillation, in which drug therapies for rhythm and heart rate control are not effective. This procedure is always preceded by the installation of an electrostimulation device, generally with resynchronization function (CRT-D; CRT-P). This approach to treating atrial fibrillation is known as “ablate-and-pace”.
How is the ablation procedure performed for the atrio-ventricular node modulation?
After local anesthesia in the femoral site, the Seldinger technique is followed by cannulation of the right femoral vein. Through this venous access, a scaler catheter is advanced near the atrium ventricular node (compact part). By delivering radiofrequency, electrical communication between the atria and ventricles is interrupted, thus allowing the implanted device to stimulate the heart at the desired frequency.
After modulation of the atrioventricular node in general, an intrinsic escapement rhythm at the junctional level can remain, the frequency of which is generally between 30 and 50 bpm.
What are the effects of the ablation procedure for modulating the atrio-ventricular node?
The “ablate-and-pace” approach is the approach of choice in patients with atrial fibrillation, in which a high ventricular response reduces the effectiveness of cardiac resynchronization. Therefore, this procedure is an important therapeutic measure, especially in patients in whom atrial fibrillation appears to be associated with heart failure, and is very effective in controlling relapses and symptoms of heart failure.
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