Percutaneous interventional electrophysiology

Before the 1980s, cardiac electrophysiology was primarily used to confirm mechanisms of arrhythmia, with management mainly by pharmacological means. However, recognised shortcomings in antiarrhythmic drugs spurred the development of non-pharmacological treatments, particularly radiofrequency ablation and implantable defibrillators.

Figure 1.

Mechanism of a re-entry circuit. An excitation wave is propagated at a normal rate down path A, but slowly down path B. An excitation wave from an extrasystole now encounters the slow pathway (B), which is still refractory, creating unidirectional block. There is now retrograde conduction from path A, which coincides with the end of the refractory period in path B. This gives rise to a persistent circus movement

The two major mechanisms by which arrhythmias occur are automaticity and re-entrant excitation. Most arrhythmias are of the re-entrant type and require two or more pathways that are anatomically or functionally distinct but in electrical contact. The conduction in one pathway must also be slowed to a sufficient degree to allow recovery of the other so that an electrical impulse may then re-enter the area of slowed conduction.

Figure 2.

Classification of arrhythmias

Intracardiac electrophysiological studies

Intracardiac electrophysiological studies give valuable information about normal and abnormal electrophysiology of intracardiac structures. They are used to confirm the mechanism of an arrhythmia, to delineate its anatomical substrate, and to ablate it. The electrical stability of the ventricles can also be assessed, as can the effects of an antiarrhythmic regimen.

Table 1.

Indications for electrophysiological studies

Investigation of symptoms

• History of persistent palpitations

• Recurrent syncope

• Presyncope with impaired left ventricular function

Interventions

• Radiofrequency ablation—Accessory pathways, junctional tachycardias, atrial flutter, atrial fibrillation

• Investigation of arrhythmias (narrow and broad complex) with or without radiofrequency ablation

• Assessment or ablation of ventricular arrhythmias

Contraindications

• Severe aortic stenosis, unstable coronary disease, left main stem stenosis, substantial electrolyte disturbance

Atrioventricular conduction

Electrodes positioned at various sites in the heart can give only limited data about intracardiac conduction during sinus rhythm at rest. “Stressing” the system allows more information to be generated, particularly concerning atrioventricular nodal conduction and the presence of accessory pathways.

Figure 3.

Diagrams showing position of pacing or recording electrodes in the heart in the right anterior oblique and left anterior oblique views (views from the right and left sides of the chest respectively). HRA=high right atrial electrode, usually on the lateral wall or appendage; HBE=His bundle electrode, on the medial aspect of the tricuspid valve; RVA=right ventricular apex; CSE=coronary sinus electrode, which records electrical deflections from the left side of the heart between the atrium and ventricle

By convention, the atria are paced at 100 beats/min for eight beats. The ninth beat is premature (extrastimulus), and the AH interval (the time between the atrial signal (A) and the His signal (H), which represents atrioventricular node conduction time) is measured. This sequence is repeated with the ninth beat made increasingly premature. In normal atrioventricular nodal conduction, the AH interval gradually increases as the extrastimulus becomes more premature and is graphically represented as the atrioventricular nodal curve. The gradual prolongation of the AH interval (decremental conduction) is a feature that rarely occurs in accessory pathway conduction.

Figure 4.

A normal atrioventricular nodal “hockey stick” curve during antegrade conduction of atrial extrastimuli. As the atrial extrastimulus (A₁-A₂) becomes more premature, the AH interval (H₁-H₂) shortens until the atrioventricular node becomes functionally refractory

Retrograde ventriculoatrial conduction

Retrograde conduction through the atrioventricular node is assessed by pacing the ventricle and observing conduction back into the atria. The coronary sinus electrode is critically important for this. It lies between the left ventricle and atrium and provides information about signals passing over the left side of the heart. The sequence of signals that pass from the ventricle to the atria is called the retrograde activation sequence.

Figure 5.

Coronary sinus electrode signals, with poles CS9-10 placed proximally near the origin of the coronary sinus and poles 1-2 placed distally reflecting changes in the left ventricular-left atrial free wall. Top: normal retrograde activation sequence with depolarisation passing from the ventricle back through the atrioventricular node to the right atrium and simultaneously across the coronary sinus to the left atrium. Bottom: retrograde activation sequence in the presence of an accessory pathway in the free wall of the left ventricle showing a shorter ventriculoatrial (VA) time than would be expected in the distal coronary sinus electrodes (CS1-2). Such a pathway would not be discernible from a surface electrocardiogram

If an accessory pathway is present, this sequence changes: with left sided pathways, there is an apparent “short circuit” in the coronary sinus with a shorter ventriculoatrial conduction time. This is termed a concealed pathway, as its effect cannot be seen on a surface electrocardiogram. It conducts retrogradely only, unlike in Wolff-Parkinson-White syndrome, where the pathway is bidirectional. Often intracardiac electrophysiological studies are the only way to diagnose concealed accessory pathways, which form the basis for many tachycardias with narrow QRS complexes.

Supraventricular tachycardia

Supraventricular tachycardias have narrow QRS complexes with rates between 150-250 beats/min. The two common mechanisms involve re-entry due to either an accessory pathway (overt as in Wolff-Parkinson-White syndrome or concealed) or junctional re-entry tachycardia.

Figure 6.

Mechanisms for orthodromic (left) and antedromic (right) atrioventricular re-entrant tachycardia

Accessory pathways

These lie between the atria and ventricles in the atrioventricular ring, and most are left sided. Arrhythmias are usually initiated by an extrasystole or, during intracardiac electrophysiological studies, by an extrastimulus, either atrial or ventricular. The extrasystole produces delay within the atrioventricular node, allowing the signal, which has passed to the ventricle, to re-enter the atria via the accessory pathway. This may reach the atrioventricular node before the next sinus beat arrives but when the atrioventricular node is no longer refractory, thus allowing the impulse to pass down the His bundle and back up to the atrium through the pathway. As ventricular depolarisation is normal, QRS complexes are narrow. This circuit accounts for over 90% of supraventricular tachycardias in Wolff-Parkinson-White syndrome. Rarely, the circuit is reversed, and the QRS complexes are broad as the ventricles are fully pre-excited. This rhythm is often misdiagnosed as ventricular in origin.

Treatment—Pathway ablation effects a complete cure by destroying the arrhythmia substrate. Steerable ablation catheters allow most areas within the heart to be reached. The left atrium can be accessed either retrogradely via the aortic valve, by flexing the catheter tip through the mitral valve, or transeptally across the atrial septum. Radiofrequency energy is delivered to the atrial insertion of a pathway and usually results in either a rapid disappearance of pre-excitation on the surface electrocardiogram or, in the case of concealed pathways, normalisation of the retrograde activation sequence. Accessory pathway ablation is 95% successful. Failure occurs from an inability to accurately map pathways or difficulty in delivering enough energy, usually because of positional instability of the catheter. Complications are rare (< 0.5%) and are related to vascular access—femoral artery aneurysms or, with left sided pathways, embolic cerebrovascular accidents.

Figure 7.

Surface electrocardiogram leads V1 and V5 and signals from the distal coronary sinus electrodes (CS dist), proximal electrodes (CS prox), and the tip of the ablation catheter (ABL CATH) during pathway ablation to treat Wolff-Parkinson-White syndrome. The onset of radiofrequency energy (thin arrow) produces loss of pre-excitation after two beats with a narrow complex QRS seen at the fourth beat (broad arrow). Prolongation of the AV signal in the coronary sinus occurs when pre-excitation is lost

Junctional re-entry tachycardia

This is the commonest cause of paroxysmal supraventricular tachycardia. The atrioventricular nodal curve shows a sudden unexpected prolongation of the AH interval known as a “jump” in the interval. The tachycardia is initiated at or shortly after the jump. The jump occurs because of the presence of two pathways—one slowly conducting but with relatively rapid recovery (the slow pathway), the other rapidly conducting but with relatively slow recovery (the fast pathway)—called duality of atrioventricular nodal conduction. This disparity between conduction speed and recovery allows re-entrance to occur. On a surface electrocardiogram the QRS complexes are narrow, and the P waves are often absent or distort the terminal portion of the QRS complex. These arrhythmias can often be terminated by critically timed atrial or ventricular extrastimuli.

Figure 8.

Atrioventricular nodal curves. In a patient with slow-fast junctional re-entrant tachycardia (left) there is a “jump” in atrioventricular nodal conduction when conduction changes from the fast to the slow pathway. In a patient with accessory pathways conducting antegradely (such as Wolff-Parkinson-White syndrome) there is no slowing of conduction as seen in the normal atrioventricular node, and the curve reflects conduction exclusively over the pathway (right)

In the common type of junctional re-entry tachycardia (type A) the circuit comprises antegrade depolarisation of the slow pathway and retrograde depolarisation of the fast pathway. Rarely (< 5% of junctional re-entry tachycardias) the circuit is reversed (type B). The slow and fast pathways are anatomically separate, with both inputting to an area called the compact atrioventricular node. The arrhythmia can be cured by mapping and ablating either the slow or fast pathway, and overall success occurs in 98% of cases. Irreversible complete heart block requiring a permanent pacemaker occurs in 1-2% of cases, with the risk being higher for fast pathway ablation. Therefore, slow pathway ablation is the more usual approach.

Figure 9.

Mechanism of slow-fast junctional re-entrant tachycardia. A premature atrial impulse finds the fast pathway refractory, allowing retrograde conduction back up to the atria

Atrial flutter and atrial fibrillation

Atrial flutter is a macro re-entrant circuit within the right atrium. The critical area of slow conduction lies at the base of the right atrium in the region of the slow atrioventricular nodal pathway. Producing a discrete line of ablation between the tricuspid annulus and the inferior vena cava gives a line of electrical block and is associated with a high success rate in terminating flutter. Flutter responds poorly to standard antiarrhythmic drugs, and ablation carries a sufficiently impressive success rate to make it a standard treatment.

Atrial fibrillation is caused by micro re-entrant wavelets circulating around the great venous structures, or it may be related to a focus of atrial ectopy arising within the pulmonary veins at their junction with the left atrium. The first indication that atrial fibrillation was electrically treatable came from the Maze operation (1990). Electrical dissociation of the atria from the great veins was carried out by surgical excision of the veins from their insertion sites and then suturing them back. The scarred areas acted as insulation, preventing atrial wave-fronts from circulating within the atria. Similar lines of block can be achieved by catheter ablation within the right and left atria. The results look promising, although this is a difficult, prolonged procedure with a high relapse rate. Of more interest is a sub-group of patients with runs of atrial ectopy, which degenerate to paroxysms of atrial fibrillation. These extrasystoles usually originate from the pulmonary veins, and their ablation substantially reduces the frequency of symptomatic atrial fibrillation. With better understanding of the underlying mechanisms and improved techniques, atrial fibrillation may soon become a completely ablatable arrhythmia.

Figure 10.

Diagram of basket-shaped mapping catheter with several recording electrodes (red dots). The basket retracts into a catheter for placement in either the atria or ventricles. Once it is in position, retraction of the catheter allows the basket to expand

Ventricular tachycardia

Ventricular tachycardia carries a serious adverse prognosis, particularly in the presence of coronary artery disease and impaired ventricular function. Treatment options include drugs, occasional surgical intervention (bypass or arrhythmia surgery), and implantable defibrillators, either alone or in combination. Ventricular tachycardia can be broadly divided into two groups, ischaemic and non-ischaemic. The latter includes arrhythmias arising from the right ventricular outflow tract and those associated with cardiomyopathies.

Since the radiofrequency energy of an ablation catheter is destructive only at the site of the catheter tip, this approach lends itself more to arrhythmias where a discrete abnormality can be described, such as non-ischaemic ventricular tachycardia. In ischaemic ventricular tachycardia, where the abnormal substrate often occurs over a wide area, the success rate is lower.

Ideally, the arrhythmia should be haemodynamically stable, reliably initiated with ventricular pacing, and mapped to a localised area within the ventricle. In many cases, however, this is not possible. The arrhythmia may be unstable after initiation and therefore cannot be mapped accurately. The circuit may also lie deep within the ventricular wall and cannot be fully ablated. However, detailed intracardiac maps can be made with multipolar catheters. A newer approach is the use of a non-contact mapping catheter, which floats freely within the ventricles but senses myocardial electrical circuits.

Although the overall, long term, success rate for radiofrequency ablation of ischaemic ventricular tachycardia is only about 65%, this may increase.

Conclusion

The electrophysiological approach to treating arrhythmias has been revolutionised by radiofrequency ablation. Better computerised mapping, improved catheters, and more efficient energy delivery has enabled many arrhythmias to be treated and cured. The ability to ablate some forms of atrial fibrillation and improvement in ablation of ventricular tachycardia is heralding a new age of electrophysiology. Ten years ago it could have been said that electrophysiologists were a relatively benign breed of cardiologists who did little harm but little good either. That has emphatically changed, and it can now be attested that electrophysiologists exact the only true cure in cardiology.