Transcatheter Ablation page Archivi - AF-ABLATION

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What is Atrial Flutter?

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). 

 Atrial Flutter

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

AFL substrate

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). 

Ablazione transcatere del Flutter Atriale

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.

Ablazione transcatere del Flutter Atriale

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.

Ablazione transcatere del Flutter Atriale

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.

Ablazione transcatere del Flutter Atriale

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.

Ablazione transcatere del Flutter Atriale

At the end of the procedure, the achievement of the bidirectional conduction block is highlighted.

Ablazione transcatere del Flutter Atriale

Ablazione transcatere del Flutter Atriale

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.




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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.

Wolff-Parkinson-White syndrome ablation

For more information on the clinical presentation of WPW syndrome and on the location of accessory pathways on the surface ECG trace, click here.

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).

Wolff-Parkinson-White syndrome ablation

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.

Wolff-Parkinson-White syndrome ablation
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.

Wolff-Parkinson-White syndrome ablation
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. 

Wolff-Parkinson-White syndrome ablation

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).

Wolff-Parkinson-White syndrome ablation
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

Wolff-Parkinson-White syndrome ablation

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.

Wolff-Parkinson-White syndrome ablation

The figure above shows how in basal conditions the signs of ventricular pre-excitation are not very evident

Wolff-Parkinson-White syndrome ablation

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. 

Wolff-Parkinson-White syndrome ablation

Here, radiofrequency is delivered with the disappearance of the ventricular pre-excitation. 

Wolff-Parkinson-White syndrome ablation

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. 

Wolff-Parkinson-White syndrome ablation

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. 

Wolff-Parkinson-White syndrome ablation

Some atrial or ventricular pacing maneuvers can be helpful if the accessory pathway is not immediately identifiable. 

Wolff-Parkinson-White syndrome ablation

The figure above shows how in basal conditions the signs of ventricular pre-excitation are not very evident.

Wolff-Parkinson-White syndrome ablation

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. 

Wolff-Parkinson-White syndrome ablation

Here, radiofrequency is delivered with the disappearance of the ventricular pre-excitation. 

Wolff-Parkinson-White syndrome ablation

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. 

Wolff-Parkinson-White syndrome ablation

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.

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When to ablate atrial tachycardias?

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.

For further information, please see… Atrial tachycardias

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.

Ablation of Atrial Tachycardia

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).

Ablation of Atrial Tachycardia

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.

Ablation of Atrial Tachycardia

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.


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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:

  1. Idiopathic ventricular tachycardias, i.e. not associated with recognizable cardiac structural changes;
  2. 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:

  1. 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.
  2. 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:

  1. The anterior and posterior fascicles of the left branch (fascicular tachycardias)
  2. The outflow tract of the right and left ventricle
  3. The aortic valve cusps
  4. Mitro-aortic continuity
  5. The papillary muscles
  6. 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:

  1. Ablation in the presence of a macroscopic arrhythmogenic substrate (typically in postinfarction heart disease and manifest forms of arrhythmogenic dysplasia)
  2. 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:

    1. 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.
    2. Induction of tachycardia by programmed electrical stimulation of the heart. 
    3. 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.
    4. Ablation of the circuit responsible for tachycardia
    5. 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:

  1. 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”).
  2. 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.
  3. 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.




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Brugada syndrome

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).

For more details on the disease click here. 

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.

If you need information about click here

References

  1. Pappone C, Brugada J, Vicedomini G, Ciconte G, Manguso F, Saviano M, Vitale R, Cuko A, Giannelli L, Calovic Z, Conti M, Pozzi P, Natalizia A, Crisà S, Borrelli V, Brugada R, Sarquella-Brugada G, Guazzi M, Frigiola A, Menicanti L, Santinelli V. Electrical Substrate Elimination in 135 Consecutive Patients With Brugada Syndrome. Circ Arrhythm Electrophysiol. 2017 May;10(5):e005053. doi: 10.1161/CIRCEP.117.005053. PubMed PMID: 28500178.
  1. Brugada J, Pappone C, Berruezo A, Vicedomini G, Manguso F, Ciconte G, Giannelli L, Santinelli V. Brugada Syndrome Phenotype Elimination by Epicardial Substrate Ablation. Circ Arrhythm Electrophysiol. 2015 Dec;8(6):1373-81. doi: 10.1161/CIRCEP.115.003220. Epub 2015 Aug 19. PubMed PMID: 26291334.
  1. Pappone C, Ciconte G, Manguso F, Vicedomini G, Mecarocci V, Conti M, Giannelli L, Pozzi P, Borrelli V, Menicanti L, Calovic Z, Della Ratta G, Brugada J, Santinelli V. Assessing the Malignant Ventricular Arrhythmic Substrate in Patients With Brugada Syndrome. J Am Coll Cardiol. 2018 Apr 17;71(15):1631-1646. doi: 10.1016/j.jacc.2018.02.022. PubMed PMID: 29650119.
  1. Pappone C, Santinelli V. Brugada Syndrome: Progress in Diagnosis and Management. Arrhythm Electrophysiol Rev. 2019 Mar;8(1):13-18. doi: 10.15420/aer.2018.73.2. PMCID: PMC6434501.
  1. Pappone C, Brugada J. Ventricular Arrhythmias Ablation in Brugada Syndrome. Current and Future Directions. Rev Esp Cardiol (Engl Ed). 2017 Dec;70(12):1046-1049. doi: 10.1016/j.rec.2017.06.018. PubMed PMID: 28734879.
  1. Pappone C, Santinelli V. Implantable cardioverter defibrillator and catheter ablation in Brugada syndrome. J Cardiovasc Med (Hagerstown). 2017 Jan;18 Suppl 1:e35-e39. doi: 10.2459/JCM.0000000000000449. PubMed PMID: 27801684.



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