Electrophysiologic Testing, including His Bundle and Other Intracardiac Electrograms

The Cleveland Clinic Cardiology Board Review, 2ed.

Edwin T. Zishiri and Mina K. Chung

This chapter aims to summarize the components of a comprehensive electrophysiology (EP) study. However, the components of a diagnostic EP study are usually selected based upon the indications for the study. Readers who are primarily aiming for a board certification exam should primarily direct their attention to components listed in the Summary to this chapter and to the Review questions.

INDICATIONS FOR ELECTROPHYSIOLOGIC TESTING

Indications for performance of an EP study have evolved somewhat in recent years with the indications for implantable cardioverter–defibrillators (ICDs) expanding to defined populations without the need for a “positive” EP study. Thus, the use of EP studies for risk stratification of patients at possible high risk for sudden cardiac death has become more limited. Based on recent multicenter trials, ICDs are being indicated for primary prevention of sudden cardiac death in patients with:

Prior myocardial infarction (MI), at least 40 days before and left ventricular ejection fraction (LVEF) ≤35% with New York Heart Association (NYHA) functional class II or III; or LVEF <30% with NYHA functional class I

Nonischemic cardiomyopathy, LVEF ≤35%, and NYHA functional class II or III

These patients do not require EP studies to qualify for ICD implantation. However, ICD implantation is also indicated in patients who have LVEF <40%, prior MI, nonsustained ventricular tachycardia (NSVT), and inducible sustained ventricular tachycardia (VT) or ventricular fibrillation (VF) at EP study. Thus, EP studies can be indicated for risk stratification in patients who do not yet have indications for an ICD. These patients include patients with coronary artery disease (CAD), prior MI, LVEF ≤40%, and NSVT. Clinical guidelines regarding the use of EP studies in the risk stratification of patients prior to device implantation may be obtained from the American College of Cardiology/American Heart Association/Heart Rhythm Society (ACC/AHA/HRS) 2008 guidelines for device implantation.¹

An EP study is also helpful in the diagnosis of patients presenting with syncope of undetermined etiology and in the diagnosis of wide complex tachycardia. EP studies may also be used to assess for bradyarrhythmias, including sinus node or atrioventricular (AV) conduction system disease, particularly in patients with possible infra-Hisian conduction system disease.

The most common application for EP studies, however, is for the diagnosis and mapping of tachyarrhythmias as part of a catheter mapping and ablation procedure. The diagnosis of supraventricular tachycardia (SVT) type and localization of ablatable supraventricular and ventricular substrates are integral parts of ablation procedures (see ACC/AHA/ESC guidelines for management of patients with supraventricular arrhythmias²).

Clinical competency guidelines are reported in the ACC/AHA clinical competence statement on invasive EP studies, catheter ablation, and cardioversion.³

THE BASICS OF ELECTROPHYSIOLOGY STUDIES

During an EP study, multipolar catheters are positioned, typically in the right ventricular apex (RVA) and/or right ventricular outflow tract, the His bundle, the coronary sinus (CS), and/or the right atrium (RA) (Fig. 26.1). Programmed electrical stimulation (PES) is performed via bipolar electrodes by pacing at various rates and by introduction of premature extrastimuli. Typical baseline recordings include the surface electrocardiograms (ECGs), particularly leads I, AVF, V₁, and V₆, as well as intracardiac electrograms (EGMs) from the high right atrium (HRA), His bundle (His, or HBE), RVA, and CS. The electrodes are by convention numbered consecutively with the most distal electrode being number 1.

FIGURE 26.1 Typical catheter positions and recordings during EP studies. RA, right atrium; LA, left atrium; LV, left ventricle, RV, right ventricle.

Intracardiac Electrograms

When approaching the interpretation of intracardiac EGMs, it is useful to understand the differences between the surface ECG and intracardiac EGMs. The surface ECG is recorded on the body surface and reflects the electrical activity of the whole heart. The intracardiac EGM is recorded within the heart and is usually filtered differently from surface ECGs to remove high-frequency noise and low-frequency interference (e.g., from respiration). The intracardiac EGM reflects local electrical activity in the heart near the recording electrodes. The display or paper speed is generally faster than the conventional 25 mm/s surface 12-lead ECG speed. Time markers are generally present at the top or bottom of EGM tracings.

When interpreting intracardiac EGMs, the reader should orient himself/herself to the tracings, using the labels, which are usually displayed along the left margin. The atrial and ventricular activity can be identified by correlation with the surface ECG recordings. EGMs reflect local depolarization. EGMs from atrial or ventricular catheters show local atrial or ventricular depolarization, respectively. EGMs recorded at either the mitral or tricuspid annulus show both atrial and ventricular depolarization. Thus, EGMs from the CS show both atrial and ventricular EGMs. In the CS, the atrial EGMs are typically large in amplitude and the ventricular EGMs smaller, unless the catheter is advanced into a ventricular branch. His bundle EGMs are recorded at the tricuspid annulus and will typically display atrial, His, and ventricular EGMs with the size of the atrial or ventricular component dependent on whether the recording electrodes are situated more proximally in the atrium or distally in the ventricle.

Cycle Lengths versus Rates

During an EP study, intervals are more commonly measured than rates. The “cycle length” of pacing drives or rhythms is measured. The conversion between cycle length and rates are as follows: Cycle length (milliseconds) = 60,000 per rate (bpm). Conversely, rate (bpm) = 60,000 per cycle length (milliseconds). Thus, a rate of 60 bpm corresponds to a cycle length of 1,000 milliseconds, 100 bpm corresponds to 600 milliseconds, 120 bpm corresponds to 500 milliseconds, 150 bpm to 400 milliseconds, and 200 bpm to 300 milliseconds.

Baseline Intervals

Typical baseline intervals reported in EP studies include the sinus cycle length (SCL), defined as the interval between sinus atrial EGMs (A-A interval or P-P interval), the surface PR, QRS, and QT intervals. The AH and HV intervals are the most commonly measured intervals (Fig. 26.2). The AH interval is measured on the His bundle catheter (HBE) as the time interval from the first major deflection at its baseline crossing to the onset of the His bundle EGM. The AH interval estimates conduction time across the AV node (AVN). The AH interval is highly variable and dependent upon vagal tone, medications, and preceding atrial rates, but typically ranges from 50 to 130 milliseconds. The HV interval is also measured on the HBE. The HV interval is the interval from the onset of the His deflection to the earliestonset of ventricular activation on any surface lead or intracardiac EGM. The normal HV interval ranges from 35 to 55 milliseconds. Other baseline intervals are less commonly measured unless markedly abnormal. These include the PA interval, defined as the earliest onset of surface P wave to the earliest intra-cardiac atrial EGM (normal 20 to 60 milliseconds). The His width from the beginning to end of the His deflection generally ranges from 10 to 25 milliseconds. The RB-V interval measures the interval from the onset of the right bundle potential to the earliest ventricular activation on any surface lead or intracardiac EGM.

FIGURE 26.2 AH and HV intervals.

Normal Activation Sequences

Anterograde Atrial and Ventricular Activation Sequence. Normal atrial activation during sinus rhythm is from the HRA to low RA and then concentrically from proximally to distally along the CS. Normal ventricular activation is from the RV apex and concentrically from proximal to distal along the CS (Fig. 26.3 left panel).

FIGURE 26.3 Normal activation patterns: anterograde and retrograde activation.

Retrograde Atrial Activation Sequence. The sequence of atrial activation during ventricular pacing is from the septum proximally to distally along the CS and from low RA in the midline to high RA (Fig. 26.3right panel).

PES. During an EP study, pacing at various cycle lengths (or rates) or various intracardiac sites is performed. The length of this pacing train can be programmed. Common paced cycle lengths (PCLs) are at 600 milliseconds (100 bpm), 500 milliseconds (120 bpm), and 400 milliseconds (150 bpm). The stimuli during the fixed drive train are termed S₁. Premature extrastimuli may be introduced in intrinsic rhythm or after a fixed paced drive train (Fig. 26.4). The first extrastimulus is termed S₂. The second extrastimulus, when introducing double extrastimuli, is termed S₃. The third extrastimulus, when introducing triple extrastimuli, is termed S₄, and so on. The common terminology of the paced stimuli, their subsequent intracardiac EGMs and intervals, is summarized below:

FIGURE 26.4 Programmed ventricular stimulation.

Pacing Drive Trains and Extrastimuli

S₁ = drive train pacing stimulus

Continuous overdrive burst, or

During programmed extrastimuli, typically eight pacing stimuli at a fixed PCL

PCL = paced cycle length (e.g., PCL 600 milliseconds = S₁S₁ interval, pacing rate 100 bpm)

S₂ = first extrastimulus (S₁-S₂ = coupling interval between S₂ and S₁)

S₃ = second extrastimulus (S₂-S₃ = coupling interval between S₂ and S₃)

S₄ = third extrastimulus (S₃-S₄ = coupling interval between S₃ and S₄)

A₁ = atrial EGM associated with S₁ drive or spontaneous atrial rhythm

A₂ = atrial EGM associated with S₂ or the first spontaneous atrial EGM after A₁

A₃ = atrial EGM associated with S₃ or the second spontaneous atrial EGM after A₁

H₁ = His bundle EGM associated with S₁ drive or spontaneous rhythm

H₂ = His bundle EGM associated with S₂ or after second spontaneous depolarization

V₁ = ventricular EGM associated with S₁ drive or spontaneous ventricular rhythm

V₂ = ventricular EGM associated with S₂ or the first spontaneous ventricular EGM after A₁

V₃ = ventricular EGM associated with S₃ or the second spontaneous ventricular EGM after A

Refractory Periods

The effective refractory period (ERP) is defined as the longest interval after onset of depolarization that fails to propagate. The ERP is usually determined during PES with the delivery of single extrastimuli after paced drive trains. With each successive drive train, the coupling interval is progressively shortened, until the extrastimulus fails to capture the stimulated tissue. This coupling interval identifies the ERP (Fig. 26.5). This interval represents the longest coupling interval that fails to capture the conduction system or myocardium distal to the stimulus (e.g., in the ventricle, S₁-S₂ interval that produces a V₁ but no V₂) The relative refractory period (RRP) is the longest S₁-S₂ interval resulting in conduction delay distal to the stimulus, for example, when the output interval (V₁-V₂) is longer than the S₁-S₂ interval (e.g., when “latency” of ventricular activation is observed). The functional refractory period (FRP) is the minimum interval between two consecutively conducted impulses, that is, the shortest output possible (e.g., the shortest V₁-V₂ interval). A summary and the normal ranges of ERPs are as follows:

FIGURE 26.5 VERP. A: PCL 400 milliseconds, CI 280 milliseconds. B: PCL 400 milliseconds, CI 260 milliseconds (VERP).

ERP—longest interval (e.g., S₁-S₂ interval) that fails to propagate.

S₁-S₂ = V₁—no V₂ (input measurement)

RRP—Longest S₁-S₂ interval resulting in conduction delay

S₁-S₂ ≠ V₁-V₂ (input ≠ output)

FRP—minimum interval between two consecutively conducted impulses. Shortest V₁-V₂ (shortest output possible)

Normal Effective Refractory Periods

Atrial ERP	170–300 ms
AVN ERP	230–430 ms
His ERP	330–450 ms
Ventricular ERP	170–290 ms

BRADYARRHYTHMIA EVALUATION BY EPS

EP study to assess bradyarrhythmias is not indicated if symptomatic bradycardia has already been documented or if patients already have a clear indication for a permanent pacemaker. However, EP study may be helpful in patients with sinus node or AV conduction disease and symptoms but for whom noninvasive monitoring has failed to document correlation of the bradyarrhythmia with symptoms; patients in whom symptoms might also be due to another arrhythmia (e.g., atrial, supraventricular, VT); or patients with a permanent pacemaker who continue to have symptoms.

SINUS NODE FUNCTION

The sinus cycle length (SCL) is defined as the A-A interval during sinus rhythm. Assessment of sinus node function may include assessment of the sinus node recovery times (SNRTs) and/or the sinoatrial conduction time (SACT).

SNRT. Atrial overdrive pacing is performed at a rate faster than the sinus rate for approximately 30 seconds, usually at multiple PCLs (e.g., PCL 700, 600, 500, 400 milliseconds). The SNRT is the interval from the last paced atrial EGM to the return sinus atrial EGM (Fig. 26.6). SNRT usually lengthens as PCL shortens until retrograde sinus node entrance block occurs at which point the sinus node is no longer being overdriven as quickly. Then, as PCL shortens further, SNRT typically shortens. Maximal SNRT is the longest SNRT measured after pacing at different PCLs and is reported with the PCL that produces the longest SNRT.

FIGURE 26.6 Determination of SNRT.

Corrected Sinus Node Recovery Time (CSNRT). The CSNRT is the difference between the maximal SNRT and the SCL. Normal CSNRT is <550 milliseconds. The CSNRT corrects for the variation of SNRT with baseline SCL.

Total Sinus Node Recovery Time. After overdrive atrial pacing, the time from the last paced atrial EGM until the SCL returns to prepaced rate represents the total SNRT. Normal is <5 seconds.

Secondary Pauses. The presence of secondary pauses should be noted after testing for SNRT. A secondary pause represents an interval longer than the initial SNRT interval occurring after the initial sinus recovery beat after overdrive atrial pacing.

SACT. The SACT is a measure of conduction time from sinus activation to local atrial activation in the region surrounding the sinus node. SACT can be estimated by pacing and recording close to the sinus node and measuring the time to the first spontaneous atrial beat after a single premature beat or slow overdrive train of atrial pacing. (Normal 50 to 125 milliseconds.)

Indirect SACT—Narula Method (Fig. 26.7).From a catheter placed in the HRA in the region of the sinus node, a drive train (commonly eight beats) of atrial overdrive pacing is delivered at a PCL approximately 50 milliseconds (50 to 150 milliseconds) faster than the sinus rate. This rate is assumed to be fast enough such that the last beat will capture the sinus node but slow enough to avoid significant prolongation of SNRT. The interval from the last paced stimulus to the first return sinus activation recorded by the atrial EGM on the pacing catheter is measured. The estimated SACT = (Escape interval – SCL)/2. This assumes that the conduction times into and out of the sinus node are equal.

FIGURE 26.7 Estimation of SACT, Narula method.

Indirect SACT—Strauss Method (Fig. 26.8). During sinus rhythm (A₁), single premature atrial beats (A₂) are delivered, starting with a long coupling interval and decrementing by 10 milliseconds. The atrial EGM of the sinus return beat (A₃) is recorded. The sinus return intervals after the premature beats (A₂-A₃) are plotted against A₁-A₂ intervals (Fig. 26. 8E). Four zones can be described:

FIGURE 26.8 Estimation of SACT, Strauss method. A: Zone 1,zone of collision. B: Zone 2, zone of reset. C: Zone 3, zone of interpolation. D: Zone 4, zone of re-entry. E: A₁–A₂ versus A₂–A₃.

Zone of Collision or Nonreset (Zone 1, Fig. 26. 8A). Very late-coupled premature atrial beats (A₂) collide with the preceding sinus node outgoing activation (A_t) and do not penetrate into the sinus node. Thus, the sinus node is unaffected, and the next sinus activation (A₃) occurs on time (i.e., the sinus node timing is not reset). In this A₁-A₂ zone of collision, as A₁-A₂ coupling interval shortens, A₂-A₃ prolongs by the same amount. Thus, (A₁-A₂) + (A₂-A₃) = 2 × (A₁-A₁).

Zone of Reset (Zone 2, Fig. 26. 8B): In this zone, the premature atrial extrastimuli (A₂) penetrate the sinus node and reset the timing of the sinus node, resulting in an advancement in the time of the next sinus activation (A₃). During this zone, A₂-A₃ interval stays relatively constant, representing a plateau in the A₁-A₂ versus A₂-A₃ plot. This A₂-A₃ interval consists of the escape interval of the sinus node and the two-way SACT (A₂-A₃ = A₁-A₁ + 2-way SACT). The two-way SACT is estimated as the difference between the plateau A₂-A₃ and the SCL (A₁-A₁). Thus, two-way SACT = A₂A₃-A₁-A₁

Zone of Interpolation (Zone 3, Fig. 26. 8C): As the premature atrial extrastimulus (A₂) coupling interval (A₁-A₂) shortens further, entrance block may occur in the tissue surrounding the sinus node. In this zone, the premature atrial impulse may not penetrate the sinus node. The escape or return sinus interval (A₂-A₃) shortens, because A₂ does not reset the node. The A₁-A₃ interval may be the same as the A₁-A₁ interval (SCL). In other words, (A₁-A₂) + (A₂-S₃) = (A₁-A₁). However, if A₂ conducts to the perinodal tissue, causing the return or escape sinus beat to conduct slower on its way out of the sinus node, A₂-A₃ may be slightly prolonged, so the sum of (A₁-A₂) + (A₂-S₃) may be slightly longer than A₁-A₁ during some parts of this zone.

Zone of Reentry (Zone 4, Fig. 26. 8D): In some patients, a reentrant beat is induced by a short-coupled atrial extrastimulus. In this zone, A₁-A₃ is shorter than the SCL A₁-A₁.

The SACT by Strauss method may be estimated in a shorter protocol by introducing atrial premature beats (A₂) at approximately 40% to 60% of the SCL and measuring A₂-A₃ at several A₁-A₂ coupling intervals. If the A₂-A₃intervals are relatively constant (variation <50 milliseconds), then it is assumed these have been delivered during the plateau phase (Zone 2) and the SACT can be calculated. However, if a stable A₂-A₃ is not achieved, then the Strauss SACT should not be reported.

Sinus Node Effective Refractory Period (SNERP): Sinus node depolarization may be recorded directly, but is technically difficult. Recording may not be successful even with use of high gains and filtering to allow low-frequency signals. SNERP may be indirectly estimated as the A-A₂ interval at which Zone 3 interpolation begins in the Strauss SACT method. At this A-A₂ interval, neither sinus node reset nor activation occurs.

Intrinsic Heart Rate (IHR): The intrinsic sinus rate is inferred as the sinus rate after application of autonomic blockade, using both atropine and propranolol to block vagal and sympathetic inputs, respectively IHR varies with age and can be estimated by the formula: IHR = 118.1 – 0.57 (age)

The sensitivity for sinus node dysfunction causing symptoms is approximately 54% for CSNRT, approximately 51% for SACT, approximately 64% for combined CSNRT + SACT with specificity approximately 88%. The low sensitivity and specificity of EP study for detection of sinus node dysfunction limits its value in prediction of future events in asymptomatic patients.

Response to Carotid Sinus Massage: Right and left carotid sinus massage may be performed in patients with syncope of undetermined etiology and no evidence of carotid vascular disease. A sinus pause or AV block >3 seconds with reproduction of clinical symptoms is considered a positive response to carotid sinus massage. A cardioinhibitory response occurs in >70% of patients with a positive response, a vasodepressor response (BP drop <50 mm Hg) in approximately 15%, and both in others.

ASSESSMENT OF AV CONDUCTION

The AVN and His-Purkinje system (HPS) function are tested using atrial pacing, atrial extrastimuli, and pharmacologic challenge techniques. The AH interval estimates conduction time through the AVN. The HV interval assesses infra-Hisian conduction and estimates conduction time from the His bundle to the first onset of ventricular activation. Retrograde conduction is tested by ventricular pacing and ventricular extrastimuli.

Baseline AV Conduction

AH Interval. The AH interval (Fig. 26.2), an estimation of the conduction time through the AVN, is measured on the HBE from the first major deflection as it crosses baseline to the onset of the His bundle EGM. Normal range is greatly variable based on autonomic tone and medications. The input to the AVN is estimated by the atrial EGM and the output of the AVN by the His deflection on the HBE tracing.

HV Interval. The HV interval (Fig. 26.2) is measured on the HBE from the onset of the His deflection to the earliest onset of ventricular activation seen on any surface lead or intracardiac EGM. The normal range for HV intervals is 35 to 55 milliseconds. A short HV interval may be seen in ventricular preexcitation syndromes, where HV may be negative when ventricular activation is preexcited by anterograde conduction through an accessory pathway that beats out ventricular activation by the AVN to HPS. A short HV may also be measured if a premature ventricular depolarization occurs prior to ventricular activation, and also if the HBE is placed distally and is recording a distal His or right bundle potential. A long HV interval suggests HPS conduction disease.

RB-V Interval. This interval measures the onset of the right bundle potential to the earliest ventricular activation on any surface lead or intracardiac EGM.

Incremental Atrial Pacing

Anterograde AV conduction can be studied during incremental atrial pacing, which refers to atrial pacing at shorter and shorter PCLs. The presence of decremental AV conduction, typical of AVN conduction, and the pattern of ventricular activation are determined to help distinguish whether anterograde conduction occurs via the AVN or via an accessory pathway.

AH Decrement. The AH interval normally prolongs as atrial pacing rate increases (as PCL is shortened). This is termed “decremental conduction,” which is a property of AV nodal tissue. Failure to decrement AV conduction (AH may decrement but AV interval may stay constant with shortening of the HV interval) suggests the presence of an accessory pathway. Conduction through a typical accessory pathway is usually nondecremental.

Pattern of Ventricular Activation. Conduction through the AVN and HPS inscribes a narrow QRS in the absence of aberrancy, or block in a component of the HPS. Conduction through a typical accessory pathway usually does not decrement. However, as atrial PCL shortens (at faster paced rates), conduction through the AVN will decrement. In the presence of an accessory pathway, slower conduction through the AVN may allow a larger contribution of ventricular activation to occur via the accessory pathway. This may be manifest as a wider QRS with more and more preexcitation becoming evident at faster PCLs.

PCL of AV Block. The longest atrial PCL associated with a failure of AV conduction is considered the PCL of AV block. This PCL is sometimes termed the “Wenckebach PCL” when conduction block occurs in a second-degree AV block Mobitz I pattern, which is the normal response of the AVN to atrial pacing at shorter PCLs. A typical accessory pathway generally blocks in a 2:1 fashion rather than in a Wenckebach pattern.

PCL of HV Block. This interval is the longest atrial PCL at which block occurs below the His bundle (His deflection without following ventricular activation). This represents an abnormal finding if infra-Hisian block or HV prolongation occurs at atrial PCLs longer than 400 milliseconds.

AV BLOCK: AV NODE VERSUS INFRA-HISIAN BLOCK

EP studies can be useful in determining the level of AV block. Block in the AVN is usually associated with a narrow QRS. On intracardiac EGMs recorded at the HBE, an atrial EGM that blocks with no His deflection indicates block occurred in the AVN (Fig. 26.9 left panel). Infra-Hisian block is usually associated with a wider QRS. At the HBE, an atrial EGM and His deflection is inscribed, but with no succeeding ventricular activation. Thus, activation proceeded from the atrium, through the AVN, to the His bundle, with subsequent block occurring below the His bundle (Fig. 26.9 right panel).

FIGURE 26.9 Level of AV block.

AV block occurs when the atrial impulse either is not conducted to the ventricle or is conducted with delay at a time when the AV junction is not refractory. It is classified on the basis of severity into three types.

First-Degree AV Block. In first-degree AV block, conduction is prolonged (PR interval >200 milliseconds), but all impulses are conducted. The conduction delay may be due to conduction slowing in the AVN, the HPS, or both. If the QRS complex is narrow and normal, the AV delay usually occurs in the AVN. This may be determined on baseline His bundle recordings, where AH or HV interval prolongation indicates the level of delayed conduction (Fig. 26.10).

FIGURE 26.10 First-degree AV block. In this example, the PR interval is 255 milliseconds. The AH interval is 90 milliseconds and the HV interval is 65 milliseconds. At least part of the prolonged conduction is due to delay in the HPS.

Second-Degree AV Block. In second-degree AV block, intermittent block in conduction occurs. In Mobitz type I (Wencksebach) second-degree AV block, progressive prolongation of the PR interval occurs before the block in conduction. In the usual Wenckebach periodicity (Fig. 26.11), the PR interval gradually increases, but with a decreasing increment, thus leading to a gradual shortening of the RR intervals. The longest PR interval usually precedes the block, and the shortest PR interval usually occurs after the block, thereby resulting in the long RR interval of the blocked impulse being shorter than twice the basic PP interval.

FIGURE 26.11 Second-degree AV block, Mobitz type I (Wenckebach) periodicity. A: Ladder diagram of Wenckebach periodicity. The AV interval gradually prolongs prior to the blocked beat. B: Intracardiac EGMs of second-degree AV block with Wenckebach block. The AH gradually prolongs prior to the blocked atrial impulse. The block occurs in the AVN.

Variants of this pattern are not uncommon. In Mobitz type II second-degree AV block, PR intervals before the block are constant, and there are sudden blocks in P-wave conduction. Advanced or high-degree AV block refers to a block of two or more consecutive impulses. In Mobitz type I block, the level of the block is almost always at the AVN, particularly with a narrow QRS complex. Rarely, type I Wenckebach periodicity in the HPS may be seen in patients with a wide QRS or bundle branch block. In contrast, Mobitz type II block is almost always at the level of the HPS and has a higher risk of progressing to complete AV block. In 2:1 AV block, conduction block may occur in either the AVN or HPS. Again, a narrow QRS suggests the level of block is at the AVN and a wide QRS suggests block is infra-Hisian; however, there are exceptions, as can be confirmed by His bundle recordings (Figs. 26.12 and 26.13). It should also be noted that block can occur in both the AVN and infra-Hisian levels.

FIGURE 26.12 2:1 AV block in the AVN during atrial pacing.

FIGURE 26.13 2:1 AV block due to infra-Hisian block during atrial pacing.

Third-Degree AV Block. In third-degree (complete) AV block, no impulses are conducted from the atria to the ventricles. The level of the block can occur at the AVN (usually congenital), His bundle, or in the HPS (usually acquired). Escape beats that are junctional (often with narrow QRS) at rates of 40 to 60 bpm generally occur with congenital complete AV block. Escape beats that are ventricular in origin (with wide QRS) often are slow, ranging from 30 to 40 bpm. The level of block can again be confirmed by His bundle recordings.

Atrioventricular Dissociation. It should be noted that AV dissociation, which refers to independent depolarization of the atria and ventricles, is not always due to complete AV block. It may be caused by:

1. Physiologic interference resulting from slowing of the dominant pacemaker (e.g., sinus node) and escape of a subsidiary or latent pacemaker (e.g., junctional or ventricular escape),

2. Physiologic interference resulting from acceleration of a latent pacemaker that usurps control of the ventricle (e.g., accelerated junctional tachycardia or VT), and

3. AV block preventing propagation of the atrial impulse from reaching the ventricles, thus allowing a subsidiary pacemaker (e.g., junctional or ventricular escape) to control the ventricles.

Patients with complete AV block have AV dissociation and, generally, a ventricular rate that is slower than the atrial rate. Patients with AV dissociation, however, may have complete AV block or dissociation resulting from physiologic interference, with the latter typically having a ventricular rate that is faster than the atrial rate.

ASSESSMENT OF AV NODE PHYSIOLOGY

Besides incremental atrial pacing to assess the AVN conduction, including the point at which block occurs (Wenckebach cycle length), AVN physiology can be more carefully dissected and studied using atrial extrastimulus testing.

Atrial Extrastimulus Testing. AV nodal physiology assessment is generally performed at several atrial PCLs (e.g., PCL 600, 500, 400 milliseconds) with eight-beat trains of atrial overdrive pacing (A₁), followed by delivery of a premature atrial extrastimulus (A₂). The coupling interval of the extrastimulus (A₁-A₂) is shortened by 10 to 20 milliseconds with each succeeding drive train.

Dual AVN Pathway Physiology. AV nodal conduction curves (Fig. 26.14) can be plotted (A₁-A₂ vs. A₂H₂ or A₁-A₂ vs. H₁H₂). A discontinuous AV nodal conduction curve (AH interval jump of >50 milliseconds after a decrease in A₁-A₂ coupling interval of 10 milliseconds) suggests the presence of two conduction pathways (typically a fast-conducting AV nodal pathway with a longer refractory period than a slow-conducting AV nodal pathway which has a shorter refractory period) (Fig. 26.15). Dual AVN physiology is confirmed by the occurrence of an AV nodal echo beat, in which antero-grade conduction down the slow AVN pathway is followed by retrograde conduction to the atria via the slow pathway (Fig. 26.15). This typical echo beat occurs with atrial activation occurring within 70 milliseconds of the onset of ventricular activation; on intracardiac EGMs, atrial and ventricular activation occurs near simultaneously.

FIGURE 26.14 Normal AVN conduction curve.

FIGURE 26.15 AH jump and AVN echo beat. A: Single atrial premature extrastimuli are delivered after eight-beat paced drive cycles. The AH interval is 140 milliseconds with a coupling interval of 290 milliseconds. After a coupling interval of 280 milliseconds, the AH interval “jumps” to 470 milliseconds, indicating the presence of dual AVN pathway physiology. The atrial EGMs evident in the CS leads (arrows) indicate the AVN echo beat with retrograde conduction to the atria. B: AVN conduction curve demonstrating an AH jump at the fast pathway ERP of 420 milliseconds and induction of echo beats and AVNRT.

AV Nodal Refractory Periods. The AV Nodal Effective Refractory Period (AVN ERP) is the longest A₁-A₂ interval that fails to conduct through the AVN (Fig. 26.16). Prolongation may occur with high vagal tone or concomitant medications. Other refractory periods that can be measured include the AV Nodal Relative Refractory Period (AVN RRP), which represents the longest A₁-A₂ which results in an H₁H₂ > A₁-A₂ during atrial extrastimulus testing. The AV Nodal Functional Refractory Period (AVN FRP) is the shortest H₁H₂ interval (AVN output) observed during extrastimulus testing.

FIGURE 26.16 AV node effective refractory period (AVN ERP).

Incremental Ventricular Pacing

While not a component of EP testing that directly assesses anterograde AV conduction, incremental ventricular pacing (pacing in the ventricle at faster and faster cycle lengths) can help determine whether retrograde conduction occurs via the AVN (Fig. 26.17) or an accessory pathway (Fig. 26.18). Atrial activation occurring with a midline activation pattern that decrements with more rapid pacing rates or a shorter premature extrastimulus coupling interval suggests conduction via the His-Purkinje–AVN system. In this pattern, concentric activation is seen in the CS leads with earliest atrial activation occurring at the AVN, septal region, and later activation occurring at more lateral atrial sites (Fig. 26.17).

FIGURE 26.17 Normal anterograde and retrograde activation.

FIGURE 26.18 Abnormal anterograde and retrograde activation: left-sided accessory pathway.

In contrast, retrograde conduction via a left lateral free wall accessory pathway (Fig. 26.18) would cause an eccentric activation pattern with earliest ventricular activation occurring near the accessory pathway in the lateral CS leads and earliest retrograde atrial activation in the distal CS as well.

PCL of VA Block. The longest ventricular PCL associated with failure of retrograde VA conduction is determined by decremental ventricular pacing. Pacing is performed at shorter and shorter cycle lengths. During retrograde AV nodal conduction, VA intervals gradually increase as pacing cycle length shortens. PCL is shortened until VA block occurs (e.g., retrograde Wenckebach or 2:1 VA block). In the presence of a typical accessory pathway, a constant VA interval is usually observed, and VA block occurs when the accessory pathway refractory period is reached. This usually occurs with a 2:1 VA block pattern, rather than in a retrograde Wenckebach pattern.

Ventricular Extrastimulus Testing. Analogous to atrial extrastimulus testing, single premature ventricular extrastimuli (V₂) are delivered after eight-beat trains of ventricular pacing (V₁) at several ventricular PCLs (e.g., PCL 600, 500, 400 milliseconds). The coupling interval of the extrastimulus (V₁V₂) is shortened by 10 to 20 milliseconds with each succeeding drive train. In this manner, retrograde VA conduction can be assessed. Decremental retrograde conduction suggests conduction is occurring via the His-Purknje – AVN system. Retrograde conduction via a typical accessory pathway is generally nondecremental, unless the accessory pathway is an atypical, decremental pathway. In addition, retrograde atrial activation patterns are examined to determine if atrial activation occurs with a typical AV nodal midline activation pattern (Fig. 26.17).

TACHYARRHYTHMIA EVALUATION BY EPS

Ventricular Tachycardia

Most patients undergoing EP study for assessment of ventricular arrhythmias have coronary artery disease or dilated cardiomyopathy, and reduced left ventricular function.

In selected patients, EP study may be useful for assessment of risk and need for ICD implantation, drug testing, assessment of device/antitachycardia pacing function, or mapping for ablation. EP testing has limited sensitivity and specificity in the prediction of arrhythmic events in nonischemic disease. EP studies have been more useful in risk stratification of patients with CAD after MI. Based on data from Multicenter Unsustained Tachycardia Trial (MUSTT)⁴ and Multicenter Automatic Defibrillator Implantation Trial (MADIT),⁵ survival is improved with ICD implantation in patients with CAD, prior MI, nonsustained VT, and LVEF ≤40%, and inducible sustained VT or reproducibly inducible VF with double ventricular extrastimuli that is not suppressible with an antiarrhythmic drug (MADIT).⁵ These studies provide a rationale for performing EP studies for risk stratification in these patient groups. MADIT II⁶ demonstrated the value of prophylactic ICD implantation without EP testing in patients with CAD and LVEF ≤30%. DEFINITE⁷ and SCDHeFT⁸ studied the value of prophylactic ICD implantation and included patients with nonischemic cardiomyopathy. SCD-HeFT demonstrated survival benefits for ICD implantation in ischemic or nonischemic cardiomyopathy patients with heart failure and LVEF ≤35% without the need for EP testing. EP testing is generally not necessary in patients who have criteria that already meet approved ICD indications.

Patients with normal LV function and VT usually have special types of ventricular arrhythmias that may be studied by EP testing, particularly in conjunction with mapping and ablation.

Ventricular Programmed Stimulation Protocols

Several stimulation protocols have been of utility in stratifying risk for sustained ventricular arrhythmias. Some of the most common are summarized below:

Short-long-short protocol:

Ventricular overdrive burst pacing.

Ventricular Effective Refractory Period (VERP). Single ventricular premature extrastimuli are delivered with shortening coupling intervals until the stimulus fails to capture the ventricle (Fig. 26.19). The VERP is the longest ventricular extrastimulus V₁V₂ that fails to capture the ventricle during ventricular extrastimulus testing. It is measured from pacing stimulus to pacing stimulus and is recorded at different sites (e.g., right ventricular apical [RVA], right ventricular outflow tract [RVOT]) and PCLs (e.g., 600, 400 until S₂ is refractory).

FIGURE 26.19 Determination of VERP by ventricular extrastimulus delivery. Single ventricular premature extrastimuli are introduced with shortening coupling intervals until the stimulus fails to capture the ventricle. In this example, at PCL 400 milliseconds, a ventricular premature extrastimulus captures the ventricle at a coupling interval of 280 milliseconds, but fails to capture the ventricle at 260 milliseconds. The VERP is 260 milliseconds at PCL 400 milliseconds.

Ventricular Functional Refractory Period (VFRP). The VFRP is the shortest ventricular coupling interval produced with premature ventricular stimulation. The VFRP is measured from EGM to EGM and recorded at different sites (e.g., RVA, RVOT) and PCLs (e.g., 600, 400 until S₂ is refractory).

Induced Arrhythmias. Definitions of ventricular arrhythmias that can be induced with programmed ventricular stimulation include the following:

Repetitive ventricular responses—1 to 3 PVCs

NSVT—three or more ventricular complexes lasting <30 seconds

Sustained VT—VT lasting >30 seconds or requiring earlier termination due to hemodynamic compromise

Sustained monomorphic VT—sustained VT of uniform morphology

Sustained polymorphic VT—sustained VT of multiform morphology

Pleiomorphic VT—multiple morphologies of monomorphic VT

Ventricular flutter—rapid VT<220 or 240 milliseconds CL with no isoelectric baseline and a sine wave appearance

VF—disorganized chaotic ventricular complexes with loss of organized ventricular contraction.

Morphology. Morphology of VT can be described by bundle branch block morphology and axis using surface ECG leads I, aVF, and V₁:

VA Relationship During VT. VA dissociation can be readily recognized using intracardiac atrial and ventricular EGMs (Fig. 26.20), helping to confirm the diagnosis of VT.

FIGURE 26.20 Ventricular stimulation and induction of sustained monomorphic VT with VA dissociation, LB/LSA morphology. VA dissociation is evident during the induction pacing sequence as well as during VT. A, atrial activation.

Supraventricular Tachycardia

During EP studies performed for the diagnosis and mapping of SVT, multipolar catheters are generally placed in the HRA or CS, at the His bundle (HBE), and in the right ventricle (RVA or RVOT). SVT mechanisms include atrial arrhythmias (including ectopic atrial tachycardia, macroreentrant atrial tachycardia, atrial flutter, and atrial fibrillation), AV node reentrant tachycardia (AVNRT), and atrioventricular reciprocating tachycardia (AVRT) mediated by an accessory pathway.

Stimulation Protocols. Programmed atrial and ventricular stimulation protocols are used in the determination of SVT mechanism and are summarized as follows:

Ventricular Pacing.Incremental ventricular pacing at constant rates, but delivered at progressively faster PCLs, is used for assessment of VA conduction. In particular, retrograde atrial activation pattern (via AVN vs. accessory pathway) is examined to determine the earliest atrial activation site from atrial EGMs recorded on catheters at various atrial sites (Figs. 26.17 and 26.18). The shortest cycle length at which 1:1 VA conduction occurs is recorded and the pattern of VA block at shorter cycle lengths examined. A decremental VA conduction pattern (longer VA times with faster pacing rates) that is concentric (earliest atrial activation in septal leads and later activation in lateral free wall electrodes) suggests retrograde conduction is occurring via the AVN. Retrograde conduction using an accessory pathway may cause an eccentric atrial activation pattern in the CS (earliest atrial activation in the posterior or lateral CS in left-sided accessory pathways, Fig. 26.18) or early activation away from the septum in the RA. In addition, typical accessory pathways do not display significant decremental conduction, so VA conduction times generally are constant. Exceptions occur for septal accessory pathways in which earliest activation will be at septal leads, and also for decremental accessory pathways in which VA conduction times may be longer at faster pacing rates.

Programmed Ventricular Stimulation.Premature ventricular extrastimuli. Single premature ventricular beats are delivered at one or more drive cycle lengths (e.g., 600, 400 milliseconds) to assess retrograde refractory periods, pattern and change in retrograde atrial activation patterns, site of retrograde VA block, and the presence of dual retrograde AVN pathway physiology.

Atrial Pacing.Assessment of anterograde conduction is performed with atrial pacing and programmed atrial stimulation. Baseline AH and HV intervals are assessed and evidence for decremental AVN conduction is sought. Anter-ograde conduction via the AVN is characterized by increasing AH intervals with faster atrial pacing rates. The shortest PCL at which 1:1 AV conduction occurs and the pattern of anterograde activation and block at PCL shorter than this are noted. A Wenckebach AV block pattern and a narrow QRS supports conduction occurring anterogradely through the AVN. Anterograde ventricular preexcitation by an accessory pathway may become more manifest by atrial pacing, as faster pacing rates will cause decremental, or slower, conduction through the AVN. Thus, at faster atrial pacing rates, the AVN will conduct slower, leading to later ventricular activation from the AVN–HPS. Since conduction through a typical accessory pathway does not significantly decrement with more rapid pacing rates and ventricular activation times via the accessory pathway will remain relatively constant, there is less contribution of ventricular activation that occurs via the AVN and more via the accessory pathway (Fig. 26.21). Another potential important function of burst atrial pacing is the induction of SVT for mapping and ablation.

FIGURE 26.21 Left free wall accessory pathway. In sinus rhythm (left panel), there is fusion of ventricular activation occurring via the atrial node and accessory pathway. During atrial pacing and introduction of premature atrial extrastimuli (right panel), preexcitation becomes more manifest as activation via the AVN decrements and becomes later, leaving a larger component of ventricular activation to occur via the accessory pathway.

Programmed Atrial Stimulation. Delivery of single or double atrial extrastimuli may serve to study AVN physiology, determine the presence of an accessory pathway and its refractory period, and to induce SVT. Single premature beats are delivered after fixed drive cycles (e.g., typically after eight-beat 600, 500, and/or 400 milliseconds PCL atrial drive trains). Normal AVN physiology is characterized by decremental conduction: the faster the stimulation (shorter A₁A₂ coupling intervals or faster PCLs), the slower the AVN conducts and the longer the AH interval becomes (Fig. 26.22 APD₁ and APD₂). The following are typical SVT substrates that may be demonstrated:

FIGURE 26.22 Single atrial extrastimuli. Dual AVN physiology and induction of single typical AVN echo beat. Single APD, and single APD₂: decremental AVN conduction with longer AH interval after shorter A,-A₂ coupling interval. Decremental AVN conduction is demonstrated with AH 140 and 160 milliseconds with shortening of APD coupling interval (APD, to APD₂). Single APD₃: AH jump (>50-millisecond increase in AH interval for a 10-millisecond decrease in A,-A₂ coupling interval) with single typical AV nodal echo (note atrial activation seen in the CS with a short VA interval). APD, atrial premature depolarization.

AH (jump >50 milliseconds over a decrement of 10 milliseconds in A₁S₂) ⇒ dual AVN physiology (Fig. 26.22 APD₂ and APD₃).

Induction of AV nodal echo beats or AVNRT by occurrence of block typically in the fast pathway and conduction delay in the slow pathway allowing recovery for retrograde fast pathway conduction and activation of retrograde atrial depolarization (Figs. 26.22 APD₃ and 26.23)

Induction of orthodromic AVRT by causing antegrade block in the AP so it is excitable when the impulse returns to conduct retrograde to the atrium.

FIGURE 26.23 Initiation of AVNRT single APDs CS 400/250 AH jump, initiation of AVNRT.

Refractory Periods. As in the ventricle, refractory periods of the components of the anterograde conduction system can be determined and are defined as follows:

Atrial Effective Refractory Period = longest atrial coupling interval (A₁A₂) that fails to capture the atrium, measured from pacing stimulus to pacing stimulus.

Atrial Functional Refractory Period (AFRP) = shortest atrial coupling interval during premature atrial stimulation (A₁A₂), measured from EGM to EGM.

Fast AVN Pathway ERP = longest atrial coupling interval that produces an AH jump to conduction via the slow pathway, measured from EGM to EGM during atrial extrastimulus testing.

Slow AVN Pathway ERP = longest atrial coupling interval that produces a block in slow pathway conduction (if only two pathways are present and the fast pathway has already blocked, slow AVN pathway ERP = AVN ERP), measured from EGM to EGM during atrial extrastimulus testing.

Accessory Pathway Anterograde ERP = longest atrial coupling interval that produces a block in accessory pathway conduction, measured from EGM to EGM during atrial extrastimulus testing.

Accessory Pathway Retrograde ERP = longest ventricular coupling interval that produces a block in retrograde accessory pathway conduction, measured from EGM to EGM during ventricular extrastimulus testing.

Minimum Preexcited R-R during Atrial Fibrillation.Short R-R intervals suggest a short AP ERP and potential increased risk.

Activation Patterns. As discussed above, the pattern of atrial and ventricular activation is examined. The anterograde ventricular activation sequence is the sequence of ventricular activation during sinus rhythm, atrial pacing, atrial extrastimuli, or SVT. Eccentric activation of the CS suggests a left-sided accessory pathway (Fig. 26.18 left panel). The atrial activation sequence is the sequence of atrial activation during ventricular pacing, ventricular extrastimuli, or SVT. Eccentric retrograde activation of the CS suggests a left-sided accessory pathway (Figs. 26.18 right panel and 26.24).

FIGURE 26.24 Left-sided accessory pathway. Retrograde atrial activation during ventricular pacing—earliest retrograde atrial activation at CS 3 (arrows).

Inducible Supraventricular Tachyarrhythmias. Types of SVTs that may be induced include the following:

AV node reentrant tachycardia—AVNRT is usually associated with dual AV nodal pathway physiology (discontinuous AVN conduction curves; an AH “jump”) (Figs. 26.15 and 26.22). In typical AVNRT,antegrade conduction occurs via the slow AVN pathway (long AH) and retrograde conduction via the fast AVN pathway with near simultaneous atrial and ventricular activation (Figs. 26.22 and 26.23). In atypical AVNRT, antegrade conduction occurs via the fast AVN pathway (with a short PR) and retrograde conduction via the slow AVN pathway (long R-P interval).

Atrioventricular reentrant tachycardia—AVRT refers to accessory pathway-mediated reentrant tachycardia. In AVRT, there is 1:1 AV association, as the atria and the ventricles are integral components of the reentrant circuit. In orthodromic AVRT, antegrade conduction occurs via the AVN (with a narrow QRS in the absence of bundle branch block/aberration) and retrograde conduction occurs via the accessory pathway (Figs. 26.25 and 26.26). In antidromic AVRT, antegrade conduction occurs via the accessory pathway (with wide QRS) and retrograde conduction via the AVN or another accessory pathway.

FIGURE 26.25 Left-sided accessory pathway mediating orthodromic AVRT—earliest retrograde atrial activation occurs via an accessory pathway at CS 2-3 (VA interval 95 milliseconds).

FIGURE 26.26 Left free wall accessory pathway mediating orthodromic AVRT—earliest atrial activation occurs in the distal CS at CS 1-2 (arrows).

Atrial flutter—In type I (typical) atrial flutter, right atrial activation proceeds in a counterclockwise activation pattern through the posterior isthmus between the inferior vena cava and tricuspid annulus. There may also be clockwise activation utilizing the isthmus. Type II (atypical) atrial flutter refers to atrial flutter using non–isthmus-dependent flutter circuits.

Atrial tachycardia—Atrial tachycardias may be macroreentrant in mechanism, including most incisional or scar-related atrial tachycardias, or due to ectopic (to the sinus node) foci and/or automatic mechanisms.

Atrial fibrillation—This most common sustained clinical arrhythmia typically initiates from pulmonary vein ostial or other focal triggering sites or microreentrant circuits. It may sustain with multiple wandering reentrant circuits.

Sinus node reentrant tachycardia—This tachycardia is characterized by a similar P wave morphology to sinus rhythm and may be induced and terminated with premature extrastmuli.

Inappropriate sinus tachycardia—Inappropriate sinus tachycardia (IST) is characterized by an inappropriately high resting sinus rate and enhanced sensitivity to adrenergic stimulation.

Evaluation during tachycardia. Once a tachycardia is induced, various observations and maneuvers can be performed to help determine the SVT mechanism. These include:

Morphology: Narrow complex, RBBB or LBBB aberrant conduction, or preexcited

Atrial activation sequence

Ventricular activation sequence

HA or VA interval—short HA interval (<100 milliseconds) suggests AVNRT, longer HA intervals (>100 milliseconds) suggests orthodromic AVRT mediated by an accessory pathway.

Single ventricular premature extrastimuli during SVT (Fig. 26.27)—If single ventricular premature extrastimuli delivered during His refractoriness advances retrograde atrial activation, then a retrogradely conducting or concealed accessory pathway is present. However, this only demonstrates the presence of an accessory pathway. It does not prove that the pathway is an integral part of the circuit, as it could be a bystander pathway.

Bundle branch block aberration in SVT (Figs. 26.28 to 26.30)—VA interval prolongation during aberration in SVT indicates a retrogradely conducting accessory pathway ipsilateral to the bundle branch block. On a surface ECG recording, this may be manifest by a longer cycle length (slower rate) during the wide complex tachycardia/aberration than during narrow complex conduction (Fig. 26.28). The prolongation of the cycle length occurs due to a prolongation of VA conduction times. Bundle branch block aberration ipsilateral to the accessory pathway results in longer retrograde (VA) activation times due to additional time required for transseptal myocardial conduction (Figs. 26.28 to 26.30). Demonstration of such a change in VA time with aberration demonstrates the presence of the accessory pathway ipsilateral to the bundle branch blocked and also indicates that the accessory pathway is a component of the reentrant circuit.

FIGURE 26.27 Orthodromic AVRT with single VPD introduced during His refractoriness. The single ventricular extrastimulus delivered during His bundle refractoriness advances retrograde atrial activation, suggesting the presence of a ret-rogradely conducting accessory pathway, in this case located in the right posteroseptal region.

FIGURE 26.28 A: Conversion of wide complex to narrow complex tachycardia with longer RR interval during wide complex tachycardia. This is diagnostic for AVRT with an accessory pathway ipsilateral to the bundle branch block. B: Orthodromic AVRT with ipsilateral BBB. BBB aberration ipsilateral to the accessory pathway results in longer retrograde (VA) activation times as a result of additional time required for transseptal myocardial conduction.

FIGURE 26.29 Initiation of orthodromic AVRT with initial LBBB aberration. Retrograde VA activation times are longer during LBBB aberration, indicating participation of a left-sided accessory pathway. Local VA time measured nearest the accessory pathway (CS distal 55 milliseconds) is similar, but earliest ventricular to atrial activation is longer with LBBB aberration.

FIGURE 26.30 RBBB aberration during AVRT utilizing a right posteroseptal accessory pathway. Retrograde VA activation times are longer during RBBB aberration, confirming the presence of a right-sided accessory pathway.

Mapping During Ablation

A diagnostic EP study is critical to confirmation and definition of arrhythmia substrate prior to ablation of most SVTs and VTs. Currently, various mapping techniques based on determination of earliest activation sites include the utilization of electrophysiologic recordings and various electroanatomic, contact catheter and noncontact mapping systems that can graphically tag and record activation times in three-dimensional space with computer generation of a display of activation or voltage maps. Although ablation of some arrhythmias is based on anatomic locations (e.g., slow pathway region for AVNRT or pulmonary vein antral isolation for atrial fibrillation ablation), successful ablation of other tachycardias often requires determination of the earliest site of activation, which helps to determine the location of the targeted arrhythmia substrate. An example is shown Figure 26.31, which demonstrates the fusion of atrial and ventricular EGMs on the ablation catheter at the site of an accessory pathway. Ablation here using radiofrequency energy resulted in prompt ablation of the pathway, loss of ventricular preexcitation, and restoration of normal AV conduction.

FIGURE 26.31 Left-sided accessory pathway. A: Successful ablation site. B: Radiofrequency ablation.

SUMMARY

This chapter aims to summarize the components of a comprehensive diagnostic EP study. For users of this book aiming for cardiovascular board exam review, I would suggest focusing upon:

Recognition of the His bundle EGM and determination of the sites of AV block (AV nodal vs. infra-Hisian block);

Recognition of VA dissociation during wide complex tachycardia using intracardiac EGMs, indicating the rhythm is most likely VT;

Recognition of the initiation of AVNRT with demonstration of an “AH jump” and induction of an SVT with near simultaneous atrial and ventricular activation;

Recognition of a left free wall accessory pathway with abnormal, eccentric early activation via a more distal CS location (e.g., rather than the normal earliest activation at the septum and later activation in the lateral CS/left atrial or ventricular free wall);

Recognition that bundle branch block that manifests during SVT with a longer cycle length or longer VA time indicates the presence of an accessory pathway ipsilateral to the bundle branch block.

REFERENCES

1. Epstein AE, DiMarco JP, Ellenborgen KA, et al. ACC/AHA/HRS 2008 Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the ACC/AHA/NASPE 2002 Guideline Update for Implantation of Cardiac Pacemakers and Antiarrhythmia Devices) Developed in Collaboration With the American Association for Thoracic Surgery and Society of Thoracic Surgeons. J Am Coll Cardiol.2008;51;e1–e62; originally published online May 15, 2008.

2. Blomstrom-Lundqvist C, Scheinman MM, Aliot EM, et al. ACC/AHA/ESC guidelines for the management of patients with supraventricular arrhythmias—executive summary. a report of the American college of cardiology/American heart association task force on practice guidelines and the European society of cardiology committee for practice guidelines (writing committee to develop guidelines for the management of patients with supraventricular arrhythmias) developed in collaboration with NASPE-Heart Rhythm Society. J Am Coll Cardiol.2003;42:1493–1531.

3. Tracy CM, Akhtar M, DiMarco JP, et al. American College of Cardiology/American Heart Association clinical competence statement on invasive electrophysiology studies, catheter ablation, and cardioversion. A report of the American College of Cardiology/American Heart Association/American College of Physicians—American Society of Internal Medicine Task Force on clinical competence. J Am Coll Cardiol. 2006;114:1654–1668.

4. Buxton AE, Lee KL, Fisher JD, et al. A randomized study of the prevention of sudden death in patients with coronary artery disease. Multicenter Unsustained Tachycardia Trial Investigators. N Engl J Med. 1999;341:1882–1890.

5. Moss AJ, Hall WJ, Cannom DS, et al. Improved survival with an implanted defibrillator in patients with coronary disease at high risk for ventricular arrhythmia. Multicenter Automatic Defibrillator Implantation Trial Investigators. N Engl J Med. 1996;335:1933–1940.

6. Moss AJ, Zareba W Hall WJ, et al. Prophylactic implantation of a defibrillator in patients with myocardial infarction and reduced ejection fraction. N Engl J Med. 2002;346:877–883.

7. Kadish A, Dyer A, Daubert JP, et al. Prophylactic defibrillator implantation in patients with nonischemic dilated cardiomyopathy. N Engl J Med. 2004;350:2151–2158.

8. Bardy GH, Lee KL, Mark DB, et al. Amiodarone or an implantable cardioverter-defibrillator for congestive heart failure. N Engl J Med. 2005;352:225–237.