In the present era, EPS for tachyarrhythmias is generally performed with ablation or device therapy as the goal. The mechanism of all tachyarrythmias is either macro-reentry or focal. Macro-reentrant arrhythmias are most common. Focal arrhythmias may be caused by automaticity, micro-reentry, or triggered activity.24 Reentry requires (1) two functionally or anatomically separate pathways, (2) unidirectional block in one pathway, and (3) recovery of excitability in blocked pathway to initiate or maintain reentry.25 In the present era, EPS for tachyarrhythmia is generally performed with ablation or device therapy as the goal.
For the purposes of EPS, all tachyarrhythmias can be classified as either narrow-complex or wide-complex tachycardias. The mode of tachycardia initiation and termination as well as tachycardia characteristics can provide clues for diagnosis of the mechanism of arrhythmia. Additionally, pacing maneuvers (such as entrainment) and activation mapping together with three-dimensional (3D) electroanatomic mapping can be utilized to confirm the diagnosis and subsequently be used to guide catheter ablation (see Chap. 88).
A detailed discussion of entrainment is beyond the scope of this chapter.26,27 However, briefly, entrainment mapping involves overdrive pacing the tachycardia from a catheter. The tachycardia is paced at slightly faster than the tachycardia cycle length (TCL). If tachycardia is accelerated, then certain findings such as progressive fusion during overdrive pacing suggests entrainment and a reentrant mechanism. If pacing were performed from within the reentry circuit, then the interval between the last paced beat and the subsequent sensed electrogram (postpacing interval, or PPI) would be equal to TCL. The farther the catheter is from the circuit, the longer the PPI (Fig. 82–7).
Entrainment of typical counterclockwise atrial flutter. A. Left anterior oblique fluoroscopic view is shown with catheters positioned at the His, in the right ventricle (RV), and coronary sinus (CS). The circle represents the atrial flutter circuit, and the arrows show the direction of the circuit in the right atrium. The time to travel around the circumference of the circle represents the tachycardia cycle length (TCL), which in this case is 270 ms. Overdrive pacing from CS 7,8 (proximal CS, site X) is performed. The postpacing interval (PPI) is equal to the time to reach the circuit from the pacing site (left-pointing dashed arrow) + TCL + time to return to pacing site (right-pointing dashed arrow). B. In this case, the PPI is 275 ms. C. Overdrive pacing is repeated from CS 1,2 (distal CS, site X). D. Overdrive pacing from this second site would be expected to yield a longer PPI as it is more remote from the tachycardia circuit than the proximal CS. This was indeed observed (320 ms). Overdrive pacing from a site within the circuit would yield a PPI that is equal to TCL, and the further away the overdrive pacing is performed, the longer the PPI.
Activation mapping is performed in a chamber using a roving catheter and timing the local electrogram relative to a reference electrogram. A focal arrhythmia would reveal a small area of earliest activation in the chamber from which the activation spreads centrifugally (Fig. 82–8). A macro-reentrant tachycardia would not have a focal area of early activation, but would demonstrate early meets late activation, where the areas of earliest activation are adjacent to those with the latest activation times (Fig. 82–9). Electroanatomic mapping systems are utilized to record local electrical information (local activation time or voltage) in a 3D chamber reconstruction during mapping so that ablation can be targeted at the appropriate sites.
A three-dimensional activation map (left anterior oblique projection) of the left atrium is shown in a patient with focal atrial tachycardia. The red area represents the site of earliest activation, which is in the left superior pulmonary vein (LSPV). The blue areas represent the sites of late activation. A circular mapping catheter was used for mapping and is seen positioned in the distal LSPV. LAA, left atrial appendage; LIPV, left inferior pulmonary vein; RIPV, right inferior pulmonary vein; RSPV, right superior pulmonary vein.
A three-dimensional activation map (anteroposterior projection) of the left atrium is shown in a patient with a macro-reentrant atypical atrial flutter. The red area represents the site of earliest activation and the blue area represents the site of latest activation. The activation pattern is consistent with a macro-reentrant circuit around the mitral annulus with appearance of early meets late activation. LSPV, left superior pulmonary vein; MV, mitral valve; RIPV, right inferior pulmonary vein; RSPV, right superior pulmonary vein.
Atrial fibrillation, atrial tachycardia or flutter, and supraventricular tachycardia (SVT), in the absence of aberrant ventricular conduction, are all narrow-complex tachycardias where the QRS duration is < 120 ms (see Chap. 84).
Atrial fibrillation is easily diagnosed on surface ECG. Pulmonary vein isolation continues to be the ablation strategy for both persistent and paroxysmal atrial fibrillation.28 Hence, detailed EPS is generally not performed before atrial fibrillation ablation.
Atrial tachycardia is a focal or micro-reentry arrhythmia, whereas atrial flutter is macro-reentrant (see Figs. 82–8 and 82–9). As described earlier, entrainment and activation mapping along with 3D electroanatomic mapping can be used to differentiate these arrhythmias. Atrial tachycardia or flutter is easily identified on intracardiac electrograms when there are more atrial than ventricular electrograms (Fig. 82–10). However, when a narrow-complex tachycardia has a 1:1 atrial to ventricular electrogram ratio, EPS can help differentiate between atrioventricular nodal reentrant tachycardia (AVNRT), atrioventricular reentrant tachycardia (AVRT), and atrial tachycardia.
Atrial tachycardia is seen in this tracing of a patient undergoing electrophysiology studies (EPS) for supraventricular tachycardia. The intracardiac electrograms demonstrate that there are more atrial electrograms than ventricular electrograms, which is consistent with a diagnosis of atrial tachycardia. The atrial electrograms are seen in the high right atrium (HRA D) and coronary sinus (CS) catheters. Ventricular electrograms are best appreciated in the right ventricular catheter (RV D).
Atrial flutter can be classified as cavotricuspid isthmus dependent (typical) and nonisthmus dependent (atypical). Typical atrial flutter commonly occurs in patients that have no atrial scar and is often associated with atrial fibrillation. On the other hand, atypical atrial flutter is usually seen in patients with atrial scar resulting from prior ablation, cardiac surgery, and so on. EPS can differentiate between these two types and is typically performed with catheter ablation as the goal.29
Atrioventricular Nodal Reentrant Tachycardia
AVNRT is a reentry arrhythmia involving the two pathways of the AV node. In typical AVNRT, antegrade conduction is via the slow pathway and retrograde conduction via the fast pathway. In contrast, atypical AVNRT has antegrade conduction through the fast pathway and retrograde conduction through the slow pathway. In those with multiple slow pathways, atypical AVNRT may also be the result of antegrade and retrograde conduction over different slow pathways.
During EPS, atrial pacing demonstrates evidence of dual AV node pathways as described above and isoproterenol is often required to induce tachycardia. In typical AVNRT, the AV node excites the ventricle and atrium in parallel; hence the ventriculoatrial (VA) relationship is 1:1 and often simultaneous (VA time ≤ 60 ms).30 As atrial activation is retrograde from the AV node, the atrial activation sequence is concentric and demonstrates earliest activation on the septum and later activity in the distal coronary sinus and high right atrium (Fig. 82–11). Rarely, AVNRT may demonstrate 2:1 AV block resulting from functional infranodal block.31
Typical atrioventricular nodal reentrant tachycardia (AVNRT) is associated with near simultaneous activation of the atrium and ventricle as demonstrated on intracardiac electrograms. Atrial electograms are evident on the high right atrium (HRA D) and coronary sinus (CS) catheters. Ventricular electrograms are seen on the His (HIS) and right ventricular (RV D) catheters. The tachycardia cycle length is 356 ms, and retrograde atrial activation is concentric with earliest activity on the septum (CS 9-10) and later activity in the distal coronary sinus (CS 1-2) and high right atrium (HRA D).
In atypical AVNRT, retrograde VA conduction is via the slow pathway. Therefore, the VA relationship is not simultaneous (VA time > 60 ms) although retrograde atrial activation remains concentric. A similar finding is seen with orthodromic AVRT utilizing a posteroseptal accessory pathway. Pacing maneuvers are required to differentiate between the two.32
Atrioventricular Reentrant Tachcyardia
In AVRT or orthodromic reciprocating tachycardia, the reentry circuit is formed by antegrade conduction down the AV node and retrograde conduction over an accessory pathway that can be located anywhere along the tricuspid annulus, mitral annulus, and aortic cusps region. The accessory pathway may demonstrate antegrade conduction that is visible on the ECG as ventricular preexcitation, ie, WPW pattern, or may demonstrate only retrograde conduction properties that is not appreciated on the ECG, ie, concealed accessory pathway.
In AVRT, the approach to the tachycardia remains similar to in AVNRT. The tachycardia is induced either by burst pacing or program electrical stimulation in atrium and ventricle with or without isoproterenol. Tachycardia activation sequence is observed and entrainment maneuvers are performed. The VA relationship is 1:1 with a long VA time (VA > 70 ms). Pacing maneuvers are required to differentiate AVRT from atypical AVNRT and atrial tachycardia. For accessory pathways that are not located near the septum, retrograde atrial activation during tachycardia may be eccentric, ie, earliest atrial activation may be in the distal coronary sinus or lateral mitral annulus for a left lateral accessory pathway (Fig. 82–12). If tachycardia cannot be initiated, the finding of nondecremental or eccentric retrograde VA conduction during ventricular pacing also suggests the presence of an accessory pathway. In contrast, retrograde AV node conduction is decremental and concentric.
Orthodromic atrioventricular reentrant tachycardia (AVRT) using a left lateral accessory pathway. The surface electrocardiogram leads and intracardiac tracings demonstrate a narrow-complex tachycardia. Retrograde atrial activation is eccentric demonstrating earliest activation in the distal coronary sinus (CS 1,2), which is located at the lateral mitral annulus. The ventriculoatrial (VA) time during tachycardia is > 60 ms. HRA, high right atrium; HIS, His electrodes (P, proximal; M, mid; D, distal); RV, right ventricular.
Rarely, a narrow QRS ventricular tachycardia originating from the upper septal fascicular region can be observed. The HV interval during tachycardia is shorter than HV interval during sinus rhythm.33 The mechanism described for this tachycardia is reentry. The antegrade limb is part of the left posterior fascicle and retrograde limb is septal Purkinje fibers. The simultaneous activation of left anterior fascicle and right bundle branch during antegrade conduction leads to narrow QRS.34,35
SVT with aberrant conduction, antidromic reciprocating tachycardia, and ventricular tachycardia all represent wide QRS complex tachycardias.
Supraventricular Tachycardia with Aberrancy
Atrial fibrillation, atrial tachycardia or flutter, AVNRT, and AVRT could all present with aberrant conduction including left bundle branch or right bundle branch block aberrancy. It can be challenging to differentiate it from ventricular tachycardia using a surface ECG alone. Various criteria have been developed to differentiate ventricular tachcardia from SVT with aberrancy.36,37
EPS can differentiate ventricular tachycardia from SVT with aberrancy. If the intracardiac electrograms reveal VA dissociation with more ventricular electrograms than atrial electrograms, then a diagnosis of ventricular tachycardia is suggested. However, if VA association is seen, then ventricular tachycardia cannot be ruled out, as retrograde conduction from the ventricle to atrium through the AV node may occur in a 1:1 manner. Additionally, aberrancy during SVT would demonstrate antegrade conduction through the His-Purkinje system. Therefore, intracardiac electrograms would demonstrate a His electrogram prior to every ventricular electrogram (Fig. 82–13), which is not seen during ventricular tachycardia with the exception of bundle branch reentry ventricular tachycardia. Even in the presence of abberancy, the mechanism of the SVT can be further defined.38,39
Orthodromic atrioventricular reentrant tachycardia (AVRT) with left bundle branch aberrancy. The 12-lead electrocardiogram demonstrates a left bundle branch block. The diagnosis of supraventricular tachycardia with aberrancy is confirmed by the presence of His electrograms (encircled, HIS catheter) prior to the QRS and ventricular electrogram seen on the right ventricular catheter (RVAd). HRA, high right atrium.
Antidromic tachycardia is characterized by reentry utilizing a bypass tract for antegrade conduction and AV node for retrograde conduction in antidromic AVRT. Antidromic tachycardia would show maximum preexcitation as complete antegrade ventricular conduction is through the bypass tract. An ECG during sinus rhythm can demonstrate a similar pattern of preexcitation as seen during tachycardia. Intracardiac electrograms would reveal retrograde ventricle to His activation followed by atrial activation. On rare occasions, bypass tracts may demonstrate decremental AV conduction properties, and may be either atriofascicular or atrioventricular connections and are referred to as Mahaim fibers.40 These are right-sided accessory pathways, and the associated tachycardias have left bundle branch block morphology.
Sustained ventricular tachycardia is defined as a tachycardia originating from the ventricle that lasts ≥ 30 seconds or that causes hemodynamic instability. The majority of ventricular tachycardias are scar-related in patients with structural heart disease. Idiopathic ventricular tachycardia is seen in patients without structural heart disease. Reentry is the mechanism in scar-related ventricular tachycardia and idiopathic ventricular tachycardias are commonly caused by triggered activity.
EPS for induction of ventricular arrhythmias is indicated (1) for syncope in those with structural heart disease and suspected ventricular arrhythmias; (2) for risk-stratification in asymptomatic patients with coronary artery disease, depressed left ventricular function (ejection fraction ≤ 40%), and nonsustained ventricular tachycardia (41); (3) to define the mechanism of wide-complex tachycardia; (4) to guide catheter ablation (see Chap. 88); and (5) for risk-stratification in Brugada syndrome.
EPS for induction of ventricular arrhythmias consists of burst pacing and programmed electrical stimulation (PES) with delivery of up to three ventricular extrastimuli during two paced cycle lengths and from two ventricular locations. Induction of sustained monomorphic ventricular tachycardia anytime during the study or induction of ventricular fibrillation or polymorphic ventricular tachycardia with up to two premature stimuli is considered positive (Fig. 82–14). A positive study would warrant implantable cardioverter-defibrillator (ICD) implantation in those who do not have one, and potentially catheter ablation in those with an ICD.
Programmed ventricular stimulation utilizing triple ventricular extra stimuli from the right ventricle was performed in a patient for risk stratification of sudden cardiac death. Sustained monomorphic ventricular tachycardia was induced that required defibrillation for termination. This patient subsequently underwent implantation of an implantable cardioverter-defibrillator.
The role of EPS in Brugada syndrome remains a controversial topic (see Chap. 80). In asymptomatic patients with Brugada syndrome, whether the induction of ventricular tachycardia/fibrillation during EPS predicts future risk of sudden death is ambiguous, with studies both supporting and refuting this.42,43 However, a history of syncope and spontaneous type 1 Brugada ECG pattern have been shown to be predictors of future SCD.44 As ECG findings in Brugada syndrome may be transient, in addition to recording the right precordial leads (V1 and V2) from higher intercostal (second or third) positions, sodium channel blockers (procainamide, flecainide, and ajmaline) can be administered to unmask a type 1 pattern in those with type 2 or 3 patterns (Fig. 82–15).45,46,47
A. The baseline 12-lead electrocardiogram of a patient who presented with syncope is shown. A type 2 Brugada pattern is seen in lead V2. B. Following administration of procainamide, a type 1 pattern is elicited.