Tachycardias Associated with Accessory Pathways: Mechanisms and Catheter Ablation

Abstract

Accessory pathways (AP) of abnormal conduction are pathways between the ventricular and atrial myocardium that exist apart from the conduction system structures. Patients with AP of abnormal atrioventricular conduction may have ventricular tachycardia known as atrioventricular (AV) reciprocating tachycardia (AVRT). Orthodromic AVRT often occurs in the presence of AP. The pathological impulse passes antegrade via the normal AV conduction system, whereas retrograde conduction to the atria via AP. Rarely, conduction occurs in the opposite direction, resulting in antidromic AVRT. APs occur at all points of the AV ring and usually as isolated anomalies, although in some patients, congenital anomalies are observed. Most APs have non-decremental conduction properties and are conducted more rapidly than normal tissue with AV conduction. In many patients with AP, baseline ECG reveals clear preexcitation signs and special algorithms can be used to presume their localization. Electrophysiologic study in these patients is often performed with in the purpose of diagnosing, localizing, and determining AP’s functional characteristics. Drug therapy for AVRT prevention is useful for temporary control while waiting for drastic actions and, in some cases, for long-term treatment. Over the last few decades, a radical treatment option as catheter ablation has emerged in patient’s treatment with WPW syndrome.

1. Introduction

Accessory pathways are tracts formed by modified myocardiocytes or cells of the cardiac conduction system, connecting the myocardium of the atria and ventricles or various parts of the cardiac conduction system. Being morphologically similar to the tracts of the conduction system, APs have higher conductivity. As a result of their functioning, pre-excitation of the ventricles is formed, and tachyarrhythmias occur, which often have hemodynamic significance. APs are the morphological substrate of Wolff–Parkinson–White (WPW) syndrome. WPW syndrome is the most common congenital heart disease, and supraventricular tachycardias (SVT) that occur with this syndrome are rarely associated with life-threatening conditions. Still, despite this, they are the most common reason for seeking emergency medical care. Drug therapy for this pathology cannot radically help such patients; resistance to antiarrhythmic drugs develops in 56–70% of patients within 1–5 years. Timely diagnosis and treatment of AVRT in WPW syndrome is an urgent problem in clinical cardiology since it develops at working age in most cases. The radiofrequency ablation (RFA) of the APs has become widespread due to its safety and high efficiency in treating patients with AVRT. Today, it is generally accepted that radiofrequency catheter ablation of the additional atrioventricular junction is a highly effective method of treating WPW syndrome, characterized by a low risk of complications and thereby ensuring the return of patients to normal, full-fledged life activities.

2. Accessory pathways of cardiac conduction system

F. Wood et al. first described accessory pathways (APs) of the cardiac conduction system during histologic examination of a deceased patient’s heart with WPW syndrome. Shortly after, its most accurate description was given by R. Ohnell, who found that the accessory pathways are “thin threads” of atrial myocardium. According to the data obtained by A. Becker et al. in 1978, the APs are thicker at their origin in the atrium. Spreading in the ventricular myocardium, they branch like tree roots [1, 2, 3]. Histologically, they are fibers, typically consisting of working atrial myocardium, located at various depths in the fatty tissue of the atrial-ventricular sulcus and connect the atrial and ventricular myocardium. The thickness of these bundles ranges from 0.1 to 7 mm (1.3 mm on average). In accordance with the anatomical classification of APs, “connection” refers to abnormal conductive pathways penetrating the contractile ventricular myocardium, and “tract” refers to abnormal pathways terminating in specialized conductive tissue [4, 5, 6].

The main ones are the following:

1. Atrioventricular (AV) pathways (“Kent bundles”).

2. Nodoventricular tract between the AV pathway and the right side of the interventricular septum (Mahaim fibers).

3. Nodofascicular tract between AV pathway and the branching of the right branch of the His bundle (Mahaim fibers).

4. Fasciculoventricular junction between the common His bundle and the myocardium of the right ventricle (Mahaim fibers). Generally, it functions in rare cases.

5. Atriofascicular tract connecting the right atrium to the common His bundle (Breschenmacher tract). It tends to be rare.

6. Atrionodal tract between the SA node and the inferior part of the AV pathway (posterior inter-nodal James tract). This tract is present in all humans but is usually non-functional (Figure 1).

Figure 1.

The figure illustrates possible types of existing AP. A description is given in the text (above).

The Breschenmacher tract and the posterior inter-nodal James tract are also called the AV nodal bypasses since they allow sinus or atrial impulses to reach the common His bundle without delay at the AV junction. The same category includes so-called short pathways in the AV node, along with “small” and “underdeveloped” AV nodes. The above classification does not reflect concealed retrograde “Kent bundles” and multiple APs [7, 8]. Accessory atrioventricular pathways can be located at any point of the atrial-ventricular sulcus except for the area between the aorta and the mitral valve ring. They are commonly divided into parietal and septal. The first one attaches to the free walls of the left and right ventricles, and the others connect the interatrial septum with the interventricular septum, terminating anteriorly or posteriorly in its membranous part, in the right triangle of the central fibrous body, generally under the endocardium near the typical structures of the conduction system. W. Untereker et al. (1980) summarized the anatomical data available in the literature on the hearts of 35 deceased patients whose ECG registered signs of WPW syndrome during life. Short (1 to 10 mm) and narrow (average diameter - 1.3 mm) muscle bundles starting in the lower atrial regions and penetrating into the ventricular muscle were found in 30 cases. In most cases, left-sided APs were located outside the compact, well-formed fibrous mitral annulus and crossed the fatty layer of the epicardial sulcus close to it. Right-sided APs pass to the ventricular myocardium through congenital disabilities “gaps” of the tricuspid fibrous ring, whose backbone is “weaker”. There are also superficial APs lying distant from the fibrous rings in the fatty tissue of the venous sulcus. In 1986, G. Guiraudon et al. showed that posterior-septal APs can connect the left ventricle’s posterior part with the right atrium’s adjacent part [9, 10, 11]. In 1988, W. Jackman, based on the analysis of delta wave morphology in 12 standard leads of the surface ECG and fluoroscopy localization, proposed to distinguish the following APs in WPW syndrome:

1. Septal APs: - right anterior or anterior-septal; − right medial-septal; − right posterior-septal; − left posterior-septal; − subepicardial.

2. Right APs: - right; − anterolateral; − lateral.

3. Left-sided APs: - anterolateral; − lateral; − posterior. Considering the anatomical location of the heart in the thorax, in 1999, F.G. Cosio proposed an anatomical classification of localization of accessory atrioventricular pathways in WPW syndrome. This classification divides all WPWs into right-sided, left-sided, and paraseptal (Figure 2)

Figure 2.

Generally accepted classification of AP localization.

Accessory pathways also can be divided in accordance with their location, direction, arrhythmia mechanism, and conduction characteristics.

Further, according to the anatomical properties they are subdivided into septal, left-sided, and right-sided conduction pathways. Posterior septal, medial septal, and anteroseptal can be combined into septal pathways, and left-/right-sided pathways can be subdivided into posterior, posterolateral, lateral, anterolateral, and anterior.

Several accessory pathways may be located in unusual anatomical spots, such as the epicardial connections between the left ventricle and the coronary sinus, the left ventricle and the noncoronary cusp of the aortic valve, the right ventricle and the right atrial appendage, or the left ventricle and the left atrial appendage. In addition, a few accessory pathways may be connected to a specialized conducting system straightaway, such as fasciculoventricular, nodofascicular, and atriofascicular pathways.

Accessory pathways also can be characterized in accordance with their conduction direction (e.g., retrograde, anterograde, or bidirectional - see above), or according to their conductive features. Regarding the latter, most accessory pathways have fast, non-decremental conduction, but some paraseptal pathways might have slow or decremental conduction, the same as the AV node.

3. Mechanisms of arrhythmias involving accessory pathways

The first classification of arrhythmia mechanisms was presented in 1964: (1) impulse formation disturbance, (2) impulse conduction disorders, and (3) their combinations. These works were based on studies on the transmembrane potential of cardiomyocytes.

As a rule, most myocardium and conduction system cells have negative resting potential (−80 mV). Exceptions are cells of the sinus node (SN), atrioventricular node (AVN), and atrioventricular valve area, where resting potential is higher (−70 mV). A negative potential on the membrane surface is due to a potassium gradient associated with the potassium-sodium pump’s function. The depolarization phase of the cell is due to the exit of sodium ions from the cell, and the “plateau” phase is due to the slow exit of calcium and potassium entry. Automatism or spontaneous generation of impulses is caused by phase 4 of depolarization, which can be suppressed by overdrive pacing, as the potassium-sodium pump, in this case, leads to the cell hyperpolarization [12, 13].

Impulse conduction disorders are caused by the presence of cells with pathological resting potential and slowly increasing action potential (induced by calcium ion current) or by disruption in intercellular contacts (desmosomes). These factors create conditions for conduction delay and macroreentry formation. The formation of an unidirectional blockade in a system of multiple myocardial fibres may also lead to the development of excitation re-entry or macroreentry. In 1983, the possibility of re-entry formation in a small area of the atrial border ridge was demonstrated, even in the presence of anisotropy [4, 12].

Excitation re-entry wave underlies most tachyarrhythmias. The rhythm of heartbeats arising from this conduction disturbance is caused by electric current circulation in the myocardial area, leading to periodic depolarization of the cardiomyocyte membrane.

Under normal conditions, impulses from the sinus node propagate through the myocardium in a strictly ordered manner, after which they decay. Each section of the conducting system and each region of the myocardium is depolarized under the action of a single excitation impulse only once (due to the refractoriness of cells preventing tissue reactivation immediately after the impulse passage) [13]. The mechanism of the excitation re-entry wave is shown in Figure 3.

Figure 3.

The primary mechanism of arrhythmia with the participation of the AP is re-entry.

This circle can exist indefinitely, with each impulse passage activating distal parts of the conducting system, after which the excitation wave propagates throughout the myocardium, causing tachyarrhythmias. Theoretically, retrograde conduction slowing is not a prerequisite for the existence of the re-entry mechanism. The excitation wave re-entry is possible only if the propagating impulse reaches cells whose membrane can be depolarized. Consequently, the pulse travel time through the re-entry circuit must be longer than the refractory period of the excitable tissue. If the re-entry circuit transit time is less than this period, the impulse will fade after reaching the refractory tissue [14]. As a rule, the pulse conduction velocity is about 50 cm/s, and the duration of the refractory period is −200 ms. Obviously, for the realization of the re-entry mechanism, the circuit length should be at least 10 cm. However, in practice, the circulation of excitation impulses is observed in much smaller areas of the myocardium, so retrograde impulse conduction slowing down is still necessary in most cases to develop the re-entry mechanism and persistent heart rhythm disruption.

Thus, two conditions are necessary to develop a mechanism of the excitation wave re-entry: (1) unilateral conduction blockade and (2) slowing of impulse conduction along the re-entry circuit. Compliance with these conditions is possible if neighboring cells differ in the rate of impulse conduction and the refractory period duration [15].

A classic example of an arrhythmia re-entry is orthodromic or antidromic atrial-ventricular tachycardia involving an accessory conduction pathway. Due to its abnormal location, this bundle links the atrial myocardium to the ventricular myocardium (Figure 4). The accessory pathway conducts the impulse rapidly, and the typical delay of the excitation wave in the AV node does not occur. Consequently, the ventricles are excited earlier than usual, accompanied by a shortening of the P-R interval on the ECG (usually less than 0.12 sec). Moreover, in such individuals, ventricular depolarization is caused by impulses from both the AV node and the accessory conduction pathway. As a result, vast QRS complexes with earlier than regular rise in the initial complex part are observed on ECG. There are many variations in the severity of the delta wave (ventricular preexcitation) (depending on the electrophysiologic properties of WPW and AV node), up to its complete absence in patients with intermittent, latent, or latent WPW syndrome. Also, in these patients, there are signs of repolarization disruption in the form of various changes in the T waveform (due to atopic ventricular depolarization, the repolarization process is also atopic), which is often mistakenly interpreted as an ischemia manifestation [16].

Figure 4.

Scheme of premature impulse conduction through the AP and the ventricle’s preexcitation.

The accessory conduction pathway is the anatomical basis of the long re-ventricular chain. The components of this circuit are, on the one hand, the accessory pathway and, on the other hand, the AV node. The conduction velocity and refractory period duration of the accessory and regular pathways usually differ, so appropriate frequency impulses can lead to tachyarrhythmias by the re-entry mechanism.

Under regular sinus rhythm, conduction can be antegrade down the AP or via the AV node, resulting in an obvious preexcitation on the ECG. Frequently, this might not be obvious in the case of the ventricle depolarization via the AV node before conduction via the accessory pathway is complete, as in a slow-conducting left lateral accessory pathway. This phenomenon is known as latent preexcitation because the 12-lead ECG during typical sinus rhythm might appear normal. In case accessory pathways conduct uniquely retrogradely during regular sinus rhythm, the ECG will also appear normal, and this is so-called concealed accessory conduction pathway. Concealed accessory conduction pathways are commonly regarded as less dangerous in terms of sudden death risk because they cannot conduct fast AF. Most accessory pathways have antegrade and retrograde properties [17].

If the antegrade accessory pathway is refractory and conduction takes place antegradely (via the AV node, which leads to the activation of His and the ventricle), and retrogradely (via the accessory pathway) Orthodromic AVRT takes place, which is illustrated in Figure 5. Typically, this occurs when the required VA time is greater than 70 ms. In spite of, insignificant changes in antegrade conduction via the AV node, the VA time, which indicates the time required for conduction via the accessory pathway, is usually steady and unchanged. In antidromic AVRT, conduction happens once the AV node is refractory, which favours antegrade conduction via the accessory pathway and retrograde atrial activation via the AV node and His, which is usually interconnected with QRS preexcitation because ventricular activation occurs only via the accessory pathway. Whereas conduction occurs via the AV node, the HA conduction time is typically more than 70 ms. This is more frequent in left lateral accessory pathways, as longer conduction times are required for the AV node to recover.

Figure 5.

Schemes of the orthodromic and antidromic tachycardia development with the AP participation. AVN- AV node, AP-accessory pathway.

4. Electrophysiologic study of supraventricular tachycardias associated with accessory pathway of cardiac conduction system

Objectives of electrophysiologic study (EPS) in patients with supraventricular tachycardia (SVT) associated with accessory pathway of cardiac conduction system:

• verification of SVT-AVRT;

• management of its induction and determination modes;

• differential diagnosis with AVNRT, atrial and intra-atrial tachycardia, atrial fibrillation, and atrial flutter. In cases with antidromic tachycardia or AVRT with aberrant conduction along the His bundle branches, the differential diagnosis is carried out with ventricular tachycardia as well;

• obtaining information on the AP electrophysiological properties and determining its localization;

• determination of further treatment tactics;

• endocardial mapping of AP and RFCA.

Indications for EPS in patients with WPW syndrome are described in detail in the recommendations as 2019 ESC Guidelines for the management of patients with supraventricular tachycardia [18].

The study is performed in the X-ray operating room after withdrawal of all antiarrhythmic drugs for at least 6 half-lives.

Under local anesthesia, the left subclavian vein, right common femoral vein, and right femoral artery are punctured according to the Seldinger technique (in the case of left-sided localization of AP). 6–7 Fr diameter 2–3 introducers are inserted into the right common femoral vein. A 6 Fr diameter introducer is placed in the left subclavian vein and a 7 Fr in the right femoral artery (in left-sided localization of atrioventricular appendages).

Under X-ray control, diagnostic electrodes are placed in the coronary sinus (CS), His bundle region (HIS), and right ventricular apex (RVA) (Figure 6).

Figure 6.

Diagnostic electrode location during EP study and catheter ablation procedures, and recording electrograms.

The protocol for EPS in patients with WPW syndrome includes evaluation of sinus node function recovery time, corrected sinus node function recovery time, anterograde and retrograde values of AP ERP and AV node, Wenckebach points, and verification of clinical AVRT (Figure 7). As a rule, APs are characterized by a nondecremental conduction.

Figure 7.

Orthodromic tachycardia induction involving the AP left lateral localization during EP study.

The study includes the determination of the induction mode and clinical AVRT management (Figure 8). Frequently, in patients with WPW syndrome the VA interval exceeds 120 ms on the AVRT background. On intracardiac electrograms, the geometry of atrial myocardium retrograde activation will depend on the site of AP entry into the atrial myocardium. If the pulse propagates retrogradely along the left lateral AP, the earliest atrial activation will be observed in the distal regions of the CS from the electrode pairs of the catheter located in the coronary sinus, in this case, CS1-2 (see Figure 9). On the orthodromic AVRT background in cases of functioning posterior or mid-septal APs, there is a “central type” of retrograde atrial activation, which complicates the differential diagnosis with atypical forms of AVNRT. In this case, to exclude AVNRT during the tachycardia paroxysm, the synchronized technique within 50 ms with the His bundle, ahead of the release of ventricular extrastimulus from the right ventricle apex is used. In typical or atypical AVNRT, synchronized extrastimulus (S2) does not alter the retrograde atrial activation geometry. The intervals during tachycardia (A-A, H-H) and after extrastimulus administration (A-ASt, H-HSt) remain identical because the extrastimulus cannot capture the atria as a result of the His bundle activation by the anterograde front and retrograde conduction is not possible. The H-H interval during tachycardia and after extrastimulus does not change, indicating the absence of extrastimulus conduction through the His-Purkinje system. In case of retrograde conduction along the AP during a tachycardia paroxysm, the ventricular extrastimulus synchronized with the His bundle activation captures the atria. In this case, the electrogram reveals advancement of retrograde atrial activation (change of A-ASt intervals during tachycardia and after the administered extrastimulus). The earliest atrial activation is seen at the atrial output site of the AP. Premature ventricular extrastimulus can interrupt the paroxysm of AVRT. If there are difficulties in the differential diagnosis between AVNRT and AVRT, we recommend para-Hisian pacing to exclude concealed septal APs. The para-Hisian pacing stimulation technique is conducted in asynchronous pacing of ventricles with a cycle length of 500–600 ms from an area anatomically located close to the His bundle area (para-Hisian area). The electrophysiological properties of ventricular myocardium in this region differ significantly from those of the His bundle itself. At high values of current strength in the para-Hisian area, simultaneous capture of the His bundle or the proximal part of the His bundle right branch and adjacent contractile myocardium of the right ventricle occurs. On the baseline ECG, this is manifested by relatively narrow stimulation QRS complexes. Once the current is reduced or the patient breathes on the stimulating electrode, there might be a loss of the His bundle or right bundle branch capture, however, the capture of the contractile myocardium of the right ventricle is preserved (wide ventricular stimulation complexes are recorded on the ECG). In this case, the ventricular conduction system is activated retrogradely: first the ventricular myocardium and only then the Purkinje fibres - the His bundle legs - the His bundle. If the series of retrograde atrial activation does not change and the time intervals reflecting retrograde atrial activation remain unchanged in the case of trapping and non-trapping His-Purkinje complexes, then retrograde conduction via the concealed septal AP is assumed.

Figure 8.

Tachycardia induction with frequent pacing during EP study.

Figure 9.

The early point of atrial activation during retrograde pacing indicates the left anterior location of the AP.

If there is no AP, retrograde conduction to the atria will depend on the direction of direct involvement of the His-Purkinje system elements in the retrograde activation circuit. In addition to the widening of the QRS complex, the absence of the His bundle “capture” will be accompanied by a prolongation of the interval illustrating retrograde activation of the atria. Thus, analysis of the retrograde atrial activation features on the para-Hisian stimulation in patients with SVT, first of all, allows differential diagnosis between atypical forms of AVNRT and orthodromic AVRT with the participation of retrogradely functioning septal APs. Occasionally, AV block of the second degree of Mobitz II may appear on the SVT background, which excludes AVRT as a cause of tachycardia. This phenomenon indicates that the maintenance of tachycardia does not require the involvement of underlying structures of the conducting system not involved in the loop of re-entry, such as the His bundle, the His bundle branch, and ventricular myocardium. In some cases, tachy-dependent blockade of impulse conduction along the His bundle branch is noted during an AVRT attack. As a rule, in this case, blockade of the His bundle branch on the side of the bundle location (ipsilateral blockade) prolongs the tachycardia cycle length and correspondingly decreases the ventricular activation rate, whereas in AVNRT the value of tachycardia cycle length before and after the onset of blockade does not change [19]. The differential diagnosis of AVNRT with “wide” QRS complexes during endocardial EPS is carried out primarily with ventricular tachycardias. Registration of endocardial electrograms from atria and ventricles greatly facilitates verification of ventricular-atrial dissociation during tachycardia based on different values of V-V and A-A intervals and makes the diagnosis of VT undoubted.

Differential diagnosis is also performed with SVT with wide QRS complexes. As a rule, this is not difficult in patients with antidromic AVRT and signs of preexcitation on the sinus rhythm (delta wave) background. During tachycardia the degree of their severity increases, because in this case, anterograde excitation of ventricles occurs only by AP, and retrograde - by the His-Purkinje system. In this case, the direction of the initial vector of ventricular depolarization in 12 leads of ECG will be the same both on the sinus rhythm background and during tachycardia. Difficulties may arise in the differential diagnosis of antidromic AVRT in a patient with no evidence of delta waves during sinus rhythm, which is sometimes observed in antidromic AVRT with anterograde conduction along the nodofascicular and nodoventricular tracts (Mahaim fibres). In such cases retrograde conduction is carried out by His-Purkinje system and analysis of atrial activation geometry will not clarify the situation completely. The sign characteristic for antidromic AVRT with anterograde conduction by Mahaim fibres is the change in the degree of pre-excitation depending on the cycle length of atrial pacing (the greater the frequency of atrial stimulation, the more pronounced the degree of ventricular pre-excitation) [20].

As a rule, the differential diagnosis of AVRT and atrial tachycardia is not difficult. The signs characterizing more atrial tachycardia than AVRT include the increase of PR interval during tachycardia, occurring at the shortening of tachycardia cycle length, appearance of AV blockade due to AAT administration or reflex techniques. If the tachycardia mechanism is abnormal automatism, in addition to the above, these tachycardias are characterized by the fact that they are not induced or interrupted by asynchronous or programmed atrial stimulation, and spontaneous induction does not require a delay in intraatrial or nodal conduction [21, 22, 23]. Atrial tachycardias based on abnormal automaticity are often characterized by the so-called “warm-up” phenomenon (gradual shortening of the tachycardia cycle length with each successive complex).

The characteristic features of atrial tachycardias based on a trigger mechanism are an increase in the cycle length of the tachycardia followed by its cessation; the initial cycle length of the tachycardia is equal to the cycle length of the asynchronous stimulation or the value of the coupling interval of the programmed extrastimulus; asynchronous or programmed atrial stimulation may induce (interrupt) or have no effect on the tachycardia.

The peculiarities of intra-atrial tachycardias that distinguish them from AVRT are that the start of intra-atrial tachycardia occurs after conduction delay in the atria, whereas in AVRT, conduction delay occurs after conduction delay in the His-Purkinje system [24]. Intra-atrial tachycardias, unlike AVRT, are generally not provoked by ventricular stimulation. Moreover, the very existence of an intra-atrial tachycardia whose loop of re-entry involves ventricular structures is improbable.

5. Catheter ablation of accessory pathways in WPW syndrome

Nowadays, due to relative safety and high efficiency, the technique of radiofrequency catheter ablation (RFCA) of APs in the treatment of patients with WPW syndrome, even with minimal disease symptoms, has become widespread. The indications for RFCA in patients with WPW developed by the 2019 ESC Guidelines for the Management of Patients with supraventricular tachycardia” are used in everyday clinical practice [18]. In fact, RFCA is a method of choice in patients with WPW.

5.1 Mapping technique for AP topic initialization

Determination of the area of interest for the effective RF application is based on the data of activation mapping, which verifies the area where the elimination of APs conduction is most likely to occur during RF application. APs mapping is performed on the sinus rhythm (possible only in manifest WPW syndrome), asynchronous ventricular and/or atrial stimulation, as well as on AVRT background [25, 26, 27]. The key point for determining the point of effective radiofrequency application is the simultaneous registration of bipolar and unipolar signals from the ablation electrode.

5.2 Using of 3D cardiac mapping system for accessory pathway ablation

Advanced 3D cardiac mapping systems are commonly used to detect and ablate regular APs located in AV rings. Modern 3D mapping systems like Carto, NAVX, and Rhythmia have several advantages in treating complex arrhythmias. These are activation mapping with a 3D mapping system that allows accurate catheter location and facilitates the identification of the ablated target. In addition, the 3D mapping system can reconstruct detailed 3D surface anatomy of structures and catheter markings in real-time virtual space.

Previous studies have shown that the 3D cardiac mapping approach significantly reduces fluoroscopic exposure time but does not increase the probability of acute success of supraventricular tachycardia ablation [28, 29]. However, some recent studies have found that the 3D mapping technique had a significantly higher acute success rate and lower recurrence rate than the standard technique in patients with posterior septal APs associated with CS diverticulum. In addition, fluoroscopy time and procedure time were also significantly reduced while using the 3D mapping system method. These results are consistent with previous studies that demonstrated the efficacy and 3D mapping system method safety in the ablation of various APs types [30, 31]. Therefore, the 3D mapping method had more benefits for these patients with posterior septal APs associated with CS diverticulum, as no recurrence and no complications were observed in patients under 3D mapping method control at follow-up.

5.3 RFCA performing

Both conventional and irrigated electrodes can be used to perform RFCA of APs. The following parameters of RFCA are applied: average power –40 ± 10 W, average heating temperature – 51 ± 9°C, during conventional ablation electrode. Occasionally, if the actions mentioned above do not lead to effective RFCA of APs, it is reasonable to use irrigated electrodes. Their application is especially relevant for the ablation of septal and right APs, localized in the free wall. As a rule, we use average power parameters of 35 ± 5 W and average temperature parameters of 45 ± 5°C at an irrigation rate of 17 ml/min [15].

Both transaortic (retrograde) and transseptal access can be used for RFCA of left-sided APs.

5.4 In transaortic positioning

Under X-ray control, the ablation catheter is retrogradely inserted into the left heart and positioned in the area of the APs location - the zone of its optimal mapping on the sinus rhythm (in case of manifest APs), asynchronous or programmed ventricular stimulation (in case of concealed APs) or AVRT background (if the patient can tolerate tachycardia well) (Figure 10).

Figure 10.

Transaortic (retrograde) placement of an ablation catheter into the left ventricle where the AP is located.

Transseptal access is performed after the transseptal puncture, which is performed under X-ray and transesophageal or intracardiac ultrasound control. After the atrial septal puncture under X-ray control, an ablation electrode is positioned into the area of interest in the left atrium via a long introducer.

Figure 11 illustrates the position of the ablation electrode inserted into the left atrium using a transseptal approach for the left anterior localization of AP.

Figure 11.

Transseptal catheter access into the left atrium for ablation of left side located AP.

When the optimal positioning and stabilization of the ablation catheter in the point of interest is achieved during RF exposure on the sinus rhythm background, conduction elimination along the APs is noted (Figure 12).

Figure 12.

Ablation effect during the procedure: The AP is closed; the impulse passes through the AV conduction (indicated by the arrow). P-R was 116 ms, after ablation prolonged to 179 ms.

Upon successful RF treatment of the concealed left lateral APs during ventricular stimulation, a change in the type of retrograde atrial activation from eccentric to central type is observed (Figure 13).

Figure 13.

One of the criteria for the effectiveness of ablation with retrograde stimulation is that the conduction along the AP is stopped, and retrograde atrial activation changes from eccentric to central type.

In certain cases, V-A dissociation, detected during asynchronous ventricular stimulation, is a sign of effective APs elimination.

5.5 Evaluation of RFСA efficacy

A repeated EP studies protocol is performed to assess efficacy, confirming persistent conduction elimination by APs (absence of AVRT induction, presence or absence of VA -conduction - VA dissociation, change in geometry to a central type of atrial retrograde activation (Figures 12 and 13).

The operation is considered successful after intravenous administration of 1 ml of 0.1% atropine sulphate solution during the control protocol of EP studies and a waiting period approaching 30 minutes [32].

5.6 Cryotherapy in the ablation of tachycardias associated with APs

Catheter-based cryotherapy has been introduced for the treatment of various arrhythmia types. The main advantage of using cryoenergy is to avoid the formation of useless and undesirable lesions by cryomapping [33]. Cryomapping allows an accurate map of a needed region in advance. This aspect of cryoenergetics may help to reduce the risk of AV node damage. In addition, catheter adhesion (“cryoadhesion”) to cardiac tissue prevents the catheter tip displacement or sliding motion during lesion formation seen with radiofrequency energy application [34].

Recent studies have demonstrated the safety of the cryoablation system in terms of preventing damage to the compact AV node. It should be pointed out that the tip size of the cryoablation catheter varied in different studies. Khairy et al. reported that a cryocatheter with a more extended electrode tip could cause larger lesions of equal depth according to a comparative study using a cryocatheter with a tip of 4, 6, and 8 mm [35]. The 8 mm tip cryocatheter may provide a higher success rate, but it may increase the incidence of adverse events by creating larger lesions that may reach the compact AV node.

5.7 Complications associated with RFCA of APs

Currently, complications during endocardial EP studies and RFCA of APs can be divided into three groups:

• complications associated with a puncture and catheterization of vessels (haematoma, deep vein thrombosis, marginal damage of the femoral artery wall, arteriovenous fistula, and pneumothorax);

• complications during catheter manipulations (heart valve damage, microembolism, perforation of myocardial wall or coronary sinus, dissection of coronary sinus, and its thrombosis);

• complications caused by RF exposure (AV blockade of various degrees, myocardial perforation, spasm or occlusion of coronary arteries, transient cerebral circulatory disturbance, and other cerebrovascular complications).