Orthodromic Atrioventricular Reentrant Tachycardia

In orthodromic AVRT, the AVN-HPS serves as the anterograde limb of the reentrant circuit (i.e., the pathway that conducts the impulse from the atria to the ventricles), whereas an AV BT serves as the retrograde limb (see Fig. 18-2). Approximately 50% of BTs participating in orthodromic AVRT are manifest (able to conduct bidirectionally) and 50% are concealed (able to conduct retrogradely only). Therefore, a WPW pattern may or may not be present on the surface ECG during NSR. When preexcitation is present, the delta wave seen during NSR is lost during orthodromic AVRT, because anterograde conduction during the tachycardia is not via the BT (i.e., the ventricle is not preexcited) but over the normal AV conduction system. Orthodromic AVRT accounts for approximately 95% of AVRTs and 35% of all paroxysmal supraventricular tachycardias (SVTs).

Antidromic Atrioventricular Reentrant Tachycardia

In antidromic AVRT, an AV BT serves as the anterograde limb of the reentrant circuit (see Fig. 18-2). Consequently, the QRS complex during antidromic AVRT is fully preexcited (i.e., the ventricles are activated totally by the BT with no contribution from the normal conduction system). The BT involved in the antidromic AVRT circuit must be capable of anterograde conduction and, therefore, preexcitation is typically observed during NSR. During classic antidromic AVRT, retrograde VA conduction occurs over the AVN-HPS. Other less frequent, nonclassic forms of antidromic AVRT can use a second BT as the retrograde limb of the reentrant circuit or a combination of one BT plus the AVN-HPS in either direction (Fig. 18-3). Antidromic AVRT occurs in 5% to 10% of patients with WPW syndrome. Susceptibility to antidromic AVRT appears to be facilitated by a distance of at least 4 cm between the BT and the normal AV conduction system. Consequently, most antidromic AVRTs use a lateral (right or left) BT as the anterograde route for conduction. Because posteroseptal BTs are in close proximity to the AVN, those BTs are less commonly part of antidromic AVRT if the other limb is the AVN and not a second free wall BT.³ Up to 50% to 75% of patients with spontaneous antidromic AVRT have multiple BTs (manifest or concealed), which may or may not be used as the retrograde limb during the tachycardia. Antidromic SVT is thus a subset of preexcited tachycardias.

FIGURE 18-3 The presence of multiple bypass tracts (BTs) is indicated by an eccentric atrial activation sequence during antidromic atrioventricular reentrant tachycardia using a right lateral BT anterogradely and a left lateral BT retrogradely. A = atrial electrogram; H = His bundle potential.

Permanent Junctional Reciprocating Tachycardia

Permanent junctional reciprocating tachycardia (PJRT) is an orthodromic AVRT mediated by a concealed, retrogradely conducting AV BT that has slow and decremental conduction properties. Conduction properties of this retrograde BT are slower than the anterograde conduction properties of the AVN and those of typical fast BTs found in patients with AVRT. The BT in PJRT is most often located in the posteroseptal region, although other portions of the AV groove can also harbor this unusual pathway. Because these BTs are almost always concealed and have slow conduction, all elements necessary for reentry are present at all times, and thus PJRT can be present much of the time (i.e., incessant), with only short interludes of sinus rhythm.

Atrioventricular Nodal Reentrant Tachycardia and Atrial Tachycardia

Physiology consistent with dual AVN physiology has been reported in 8% to 40% of patients with WPW syndrome, although spontaneous sustained AVNRT is less frequent. Both AVNRT and AT can use the bystander BT to transmit impulses to the ventricle (see Fig. 18-2). When AVNRT occurs in the WPW syndrome, the arrhythmia can be difficult to distinguish from AVRT without electrophysiological (EP) testing.

Atrial Fibrillation

Paroxysmal AF occurs in 50% of patients with WPW, and is the presenting arrhythmia in 20%. Chronic AF, however, is rare in these patients.³ Spontaneous AF is most common in patients with anterograde conduction through the BT. Patients with antidromic AVRT, multiple BTs, and BTs that have a short anterograde effective refractory period (ERP) are more liable to develop AF.³ In individuals with WPW, AF is often preceded by AVRT that degenerates into AF.

The frequency with which intermittent AF occurs in patients with the WPW syndrome is striking because of the low prevalence of coexisting structural heart disease, which is a major predisposing factor for AF in subjects without a BT. This observation suggests that the AV BT itself can be related to the genesis of AF.

The mechanisms by which AVRT precipitates AF are not well understood. The rapid atrial rate can cause disruption in atrial activation and reactivation, creating an electrophysiological substrate conducive to AF. The observation that most patients with BT and AF who undergo BT ablation are cured of both AVRT and AF is compatible with this hypothesis. Another possibility is that the complex geometry of networks of BTs predisposes to AF by fractionation of the activation wavefronts. Localized reentry has been recorded in some patients, using direct recordings of the activation of the BTs. Hemodynamic changes, atrial stretch caused by atrial contraction against closed AV valves during ventricular systole, can also play a role. Ablation of the BT can cure AF in more than 90% of patients; however, vulnerability to AF persists in up to 56%, and the response to atrial extrastimulation (AES) is also unaltered by ablation.

Atrial Flutter

AFL is the most common (60%) regular preexcited tachycardia in patients with WPW syndrome. AFL is caused by a reentrant circuit within the RA and therefore exists independently of the BT, and AFL does not have the same causal association to AV BTs as AF. In some patients with WPW syndrome who develop AFL, AVRT is the initiating event. This relationship can be mediated by contraction-excitation feedback into the atria during the AVRT.

AFL, like AF, can conduct anterogradely via a BT causing a preexcited tachycardia. Depending on the various refractory periods of the normal and pathological AV conduction pathways, AFL potentially can conduct 1:1 to the ventricles during a preexcited tachycardia, making the arrhythmia difficult to distinguish from ventricular tachycardia (VT; see Fig. 12-6).

Ventricular Fibrillation and Sudden Cardiac Death

The mechanism of sudden cardiac death (SCD) in most patients with WPW is likely the occurrence of AF with a very rapid ventricular rate that leads to VF. Although the frequency with which AF having rapid AV conduction via a BT degenerates into VF is unknown, the incidence of SCD in patients with WPW syndrome is rather low, ranging from 0% to 0.39% annually in several large case series. The trigger for AF in this population of patients (who usually are otherwise healthy individuals and are expected to have a low rate of AF) is generally an episode of SVT. In fact, most patients who have been resuscitated from VF secondary to preexcitation have previous history of AVRT, AF, or both (although in some patients, SCD may be the presenting symptom), and induction of SVT during EP testing is also predictive of clinical symptoms in some asymptomatic individuals.^7–11

Several factors can help identify the patient with WPW who is at increased risk for VF, including symptomatic SVT, septal location of the BT, presence of multiple BTs, and male gender.⁸ Nonetheless, it is clear that the most important factor for the occurrence of VF in these patients is the ability of the BT to conduct rapidly to the ventricles. This is best measured by determining the shortest and average preexcited intervals during AF or alternatively by measuring the anterograde ERP of the BT. If the BT has a very short anterograde effective refractory period (ERP <250 milliseconds), a rapid ventricular response can occur with degeneration of the rhythm to VF. A short preexcited R-R interval during AF (≤220 milliseconds) appears to be a sensitive clinical marker for identifying patients at risk for SCD in children, although its positive predictive value in adults is only 19% to 38%.^9,10,12

Drug therapy can be an additional determinant of the risk of VF in patients with preexcitation. As an example, intravenous verapamil can increase the ventricular response to AF and has resulted in VF in some patients. Several mechanisms are probably involved; hypotension produced by verapamil-induced vasodilation is followed by a sympathetic discharge that enhances BT conduction. Furthermore, verapamil slows AVN conduction directly and increases AVN refractoriness, resulting in less concealed penetration of the BT by normally conducted beats. Additionally, the increased rate, irregular rate, hypotension, and sympathetic discharge probably result in fractionation of the ventricular wavefront and VF. For these reasons, intravenous verapamil is contraindicated for the acute treatment of AF in patients with WPW. Other intravenous drugs that block the AVN also should be avoided, including beta blockers, adenosine, diltiazem, and digoxin. Both oral and intravenous digoxin has been associated with the degeneration of AF into VF in patients with preexcitation syndromes. Some of these patients had a history of previously benign AF. How digitalis might promote the development of VF is uncertain. One possible mechanism is that shortening of the atrial and BT ERP, plus increasing AVN block, results in decreased concealed retrograde penetration of the BT by normally conducted beats, thereby preventing its inactivation.

Intravenous adenosine, given appropriately to treat orthodromic AVRT, can also precipitate AF episodes. This is unusual and should not be viewed as a contraindication to adenosine use, but one should be prepared for emergency cardioversion before administering adenosine to SVT patients. Lidocaine, for reasons that are unclear, has also been associated with degeneration of AF into VF. It is occasionally used in patients with WPW who have a wide QRS complex tachycardia that might be misinterpreted as VT.

Ventricular Tachycardia

Coexisting VT is uncommon because patients with WPW syndrome infrequently have structural heart disease. Naturally, older patients are subject to coronary artery and other diseases that can cause VT.

Wolff-Parkinson-White Pattern

The prevalence of WPW pattern on the surface ECG is 0.15% to 0.25% in the general population. The prevalence is increased to 0.55% among first-degree relatives of affected patients, suggesting a familial component. The yearly incidence of newly diagnosed cases of preexcitation in the general population was substantially lower, 0.004% in a diverse population of residents from Olmsted County, Minnesota, 50% of whom were asymptomatic.¹² The incidence in men is twice that in women and highest in the first year of life, with a secondary peak in young adulthood.

The WPW pattern on the ECG can be intermittent and can even permanently disappear (in up to 40% of cases) over time. Intermittent and/or persistent loss of preexcitation may indicate that the BT has a relatively longer baseline ERP, which makes it more susceptible to age-related degenerative changes and variations in autonomic tone. Consistent with this hypothesis is the observation that, compared with patients with a persistent WPW pattern, those in whom anterograde conduction via the BT disappeared were older (50 versus 39 years) and had a longer ERP of the BT at initial EP study (414 versus 295 milliseconds). The lifetime risk of mortality related to this in asymptomatic individuals can never be accurately known but has been estimated at 0.1% annual risk, with the majority of patients identified between the ages of approximately 10 and 40 years.

In a recent report, about 90% of 293 adults who were asymptomatic at the time of diagnosis of WPW ECG pattern had no arrhythmic events, remaining totally asymptomatic over a median follow-up of 67 months, and 30% of them had disappearance of preexcitation. Only a minority of young adult patients (10%) developed a first arrhythmic event, which was potentially life-threatening in approximately 5%, but no one died. Compared with patients who experienced potentially life-threatening events, those who did not showed a characteristic EP profile (older age, lower tachyarrhythmia inducibility, longer anterograde refractory ERP of BTs, and low likelihood of baseline retrograde BT conduction or multiple BTs).¹⁰

In a similar report in 184 children (8 to 12 years of age) with WPW ECG pattern who were totally asymptomatic at the time of diagnosis (which was made incidentally in the majority of cases either at a routine medical examination or on a screening ECG before admission to sports), during a median follow-up of 57 months, no child lost preexcitation, more than 70% had no arrhythmic events, and about 30% developed a first arrhythmic event, which was potentially life-threatening in 10%. Compared with children who experienced potentially life-threatening tachyarrhythmias, those who did not showed a characteristic electrophysiological profile (lower tachyarrhythmia inducibility, longer anterograde refractory period of BTs, and low likelihood of baseline retrograde AP conduction or multiple BTs).⁹

Wolff-Parkinson-White Syndrome

The prevalence of the WPW syndrome is substantially lower than that of the WPW ECG pattern. In a review of 22,500 healthy aviation personnel, the WPW pattern on surface ECG was seen in 0.25%; only 1.8% of these patients had documented arrhythmias. In another report of 228 subjects with WPW ECG pattern followed for 22 years, the overall incidence of arrhythmia was 1% per patient-year. The occurrence of arrhythmias is related to the age at the time preexcitation was discovered. In the Olmsted County population, one-third of asymptomatic individuals younger than 40 years at the time of diagnosis of WPW eventually had symptoms, compared with none of those who were older than 40 years at diagnosis. In a recent report, of 293 asymptomatic adults with the WPW ECG pattern who underwent EP testing without ablative intervention, almost 90% remained asymptomatic over a median follow-up of 67 months, whereas 31 patients had an arrhythmic event, and 17 had a “potentially” life-threatening event (AF with mean rate of 250 beats/min or faster).¹⁰ In another report, of 188 asymptomatic children (between 8 and 12 years of age) with the WPW ECG pattern who underwent EP testing without ablative intervention, 72% remained asymptomatic over a median follow-up of 57 months, whereas 31 patients had an arrhythmic event.⁹ Symptomatic arrhythmias developed more commonly in initially asymptomatic patients with a WPW ECG pattern who had inducible SVTs in the EP laboratory compared with those with no inducible tachycardias. In one report, less than 4% of patients developed clinical SVT over a 37.7-month follow-up period, compared with 67% of those with inducible SVT on EP testing.

A recent report demonstrated that women more commonly had right-sided BTs compared with men and that Asians had right free wall BTs substantially more frequently than other races. These relationships may suggest a potential inherited component of development of the AV annuli.¹³

Associated Cardiac Abnormalities

Most patients with AV BTs do not have coexisting structural cardiac abnormalities, except for those that are age-related. Associated congenital heart disease, when present, is more likely to be right-sided than left-sided in location. Ebstein anomaly is the congenital lesion most strongly associated with the WPW syndrome. As many as 10% of such patients have one or more BTs; most of these are located in the right free wall and right posteroseptal space. An association between mitral valve prolapse and left-sided BTs has also been reported. However, this association may simply reflect the random coexistence of two relatively common conditions.

Familial Wolff-Parkinson-White Syndrome

Among patients with the WPW syndrome, 3.4% have first-degree relatives with a preexcitation syndrome. A familial form of WPW has infrequently been reported and is usually inherited as an autosomal dominant trait. The genetic cause of a rare form of familial WPW syndrome has been described.^14,15 The clinical phenotype is characterized by the presence of preexcitation on the ECG; frequent SVTs, including AF; progressive conduction system disease; and cardiac hypertrophy. Patients typically present in late adolescence or the third decade with syncope or palpitations. Premature SCD occurred in 10% of patients. Paradoxically, by the fourth decade of life, progression to advanced sinus node dysfunction or AV block (with the loss of preexcitation) requiring pacemaker implantation was common. Approximately 80% of the patients older than 50 years had chronic AF. Causative mutations in the PRKAG2 gene were identified in these families. The PRKAG2 gene encodes the gamma-2 regulatory subunit of the adenosine monophosphate (AMP)–activated protein kinase, which is a key regulator of metabolic pathways, including glucose metabolism. The penetrance of the disease for WPW syndrome was complete, but the expression was variable. The described phenotype of this syndrome is similar to the autosomal recessive glycogen storage disease, Pompe disease. Given the function of the AMP-activated protein kinase and this similarity, the PRKAG2 syndrome is likely a cardiac-specific glycogenosis syndrome. This syndrome thus belongs to the group of genetic metabolic cardiomyopathies, rather than to the congenital primary arrhythmia syndromes.

Concealed Bypass Tracts

The true prevalence of concealed BTs is unknown because, unlike the situation with the WPW ECG pattern, these BTs are concealed on the surface ECG and are only expressed during AVRT; only symptomatic patients undergo EP testing. As noted, orthodromic AVRT accounts for approximately 95% of AVRTs and 35% of all paroxysmal SVTs, and 50% of the BTs that participate in orthodromic AVRT are concealed. SVTs using a concealed BT have no gender predilection and tend to occur more frequently in younger patients than in those with AVNRT; however, significant overlap exists. PJRT most often occurs in early childhood, although clinically asymptomatic patients presenting later in life are not uncommon.

Methods for Evaluation of Bypass Tract Refractory Period

Management of Asymptomatic Patients with Preexcitation

The role of EP testing and catheter ablation in asymptomatic patients with preexcitation is still controversial. Guidelines of the American College of Cardiology and European Society of Cardiology on the management of asymptomatic WPW patients suggest restricting catheter ablation of BTs to those in high-risk occupations (e.g., school bus drivers, police, and pilots) and professional athletes.¹⁹ Catheter ablation in asymptomatic preexcitation was classified as a class IIA indication with a B level of evidence. This means essentially that it is “reasonable” to offer ablation in selected patients but is not mandated in all patients. According to the North American Society of Pacing and Electrophysiology (NASPE; now the Heart Rhythm Society [HRS]) Expert Consensus Conference, asymptomatic WPW pattern on the ECG without recognized tachycardia is a class IIB indication for catheter ablation in children older than 5 years and a class III indication in younger children.²⁰

This approach has several justifications; one-third of asymptomatic individuals younger than 40 years when preexcitation was identified eventually developed symptoms, whereas no patients in whom preexcitation was first uncovered after the age of 40 years developed symptoms. Additionally, most patients with asymptomatic preexcitation have a good prognosis; cardiac arrest is rarely the first manifestation of the disorder. The positive predictive value of invasive EP testing is considered to be too low to justify routine use in asymptomatic patients.

Some studies, however, have questioned the approach discussed above.^8,17,18 Those studies have shown that in the asymptomatic WPW population, a negative EP study with no AVRT or AF inducibility identifies subjects at very low risk for the development of spontaneous arrhythmias. Inducibility of sustained preexcited AF with a fast ventricular response, particularly in the presence of multiple BTs, may help select asymptomatic WPW subjects at definite risk for dying suddenly, and catheter ablation of the BT(s) appears to be required to prevent SCD. Because extensive studies have reported extremely rare complications from EP testing and radiofrequency (RF) ablation in experienced centers, it has been suggested that all asymptomatic patients with WPW pattern should undergo EP testing for risk stratification, and those with inducible AVRT or AF or who have a short BT ERP should be considered for catheter ablation of the BT, whereas patients who are noninducible and have a long BT ERP may be followed without treatment.^8–1021 This argument is further supported by the fact that assessment of the future VF risk in an asymptomatic patient with WPW is not easy. Noninvasive markers of lower risk such as intermittent loss of preexcitation, sudden loss of BT conduction on exercise stress testing, and loss of BT conduction after treatment with antiarrhythmic drugs are limited by inadequate sensitivity or specificity and the low incidence of future adverse events. With this approach, prophylactic ablation of BTs in high-risk subjects may be justified but is not an acceptable option for low-risk individuals. The physician involved needs to use special care and discretion in making the decision to proceed to ablation and must especially consider his or her own success and complication rates for ablation of the specific location of the BT identified.

In summary, the potential value of EP testing in identifying high-risk patients who may benefit from catheter ablation must be balanced against the approximately 2% risk of a major complication associated with catheter ablation.²² If RF catheter ablation were a totally risk-free procedure, one would logically advise such a procedure to the asymptomatic WPW patient with a short anterograde ERP. However, complications such as AV block, stroke, tamponade, and even death have been reported. It is not difficult to envision a small potential mortality benefit, if present, erased or eclipsed by a small complication rate if thousands of patients with BTs in various locations undergo ablation.¹⁶ Although complications of a diagnostic EP study are minor and non–life-threatening and are less common than those of catheter ablation, if routine EP testing of all asymptomatic WPW patients were considered, many patients would proceed immediately to RF ablation and, in others, there would be a strong temptation to ablate when catheters are in place (regardless of predicted SCD risk), especially given the fact that the criteria for ablation usually will not be black or white. This greatly increases the risk to the patient. Furthermore, invasive EP assessment has drawbacks, because no single factor has both a high sensitivity and specificity for identifying at-risk individuals. For example, a shortest preexcited R-R interval of less than 250 milliseconds during sustained induced AF is a very sensitive but not specific marker of the risk of VF in WPW patients, because approximately one-third of patients will have a shortest R-R interval of less than 250 milliseconds during induced AF. In fact, the addition of isoproterenol to the baseline study may shorten the ERP of the accessory pathway to levels of potential concern in the majority of individuals with WPW. In view of those considerations, prudence dictates that noninvasive testing with a Holter monitor and (if the Holter monitor does not show intermittent preexcitation) exercise testing should be considered before the EP study to identify the low-risk patient because of a long anterograde ERP of the BT.^21,22

For the low-risk patient, it may be appropriate to pursue a strategy of follow-up with ECGs and reevaluation at selected intervals with a high degree of suspicion for new arrhythmia symptoms. This strategy is supported by recent prospective studies of asymptomatic patients with WPW pattern; although “potentially” life-threatening arrhythmias were observed during follow-up, no patients had actually died. This observation implies that patient education about the potential risks associated with preexcitation and about the symptoms of arrhythmias that should prompt them to seek attention can prove very important at reducing the risk of mortality without necessarily exposing the patient to the risks of catheter ablation.^10,16 It is also advisable to give the patient a copy of his or her ECG and a short note about the fact that the WPW pattern is present to prevent the misdiagnosis of myocardial infarction (MI) and to explain the basis of cardiac arrhythmias in case they develop later. Patients should also be encouraged to seek medical expertise whenever arrhythmia-related symptoms occur.

In patients not showing block in their BT during noninvasive studies, esophageal pacing may be performed to determine the anterograde ERP of the BT and the ability to induce sustained arrhythmias. This procedure is neither pleasant for patients nor often definitive, but if arrhythmias can be induced, the benefits and risk of an invasive investigation and catheter ablation should be based on individual considerations such as age, gender, occupation, and athletic involvement. This should be discussed with the patient or, in the case of a child, with the parents. Because knowledge about the success and complication rate at the EP center plays a major role in decision making, that information should be made available so that the appropriate place for invasive diagnosis and treatment can be selected. If an EP study is performed for risk stratification, the combination of inducible AVRT and a shortest preexcited R-R interval during AF of less than 250 milliseconds provides the most compelling indications for ablation. The key is a clear understanding by the patient of the relative merits of each strategy. The well-informed patient needs to choose between a very small risk of potentially life-threatening arrhythmia over a long period of time and a one-time small procedural risk associated with EP testing and catheter ablation. Certain patients such as athletes and those in higher risk occupations will generally choose ablation. Others, especially patients older than 30 years, may prefer the small risk of a conservative strategy.^10,16,21,22

Management of Symptomatic Patients

Inapparent Versus Intermittent Preexcitation

Inapparent Preexcitation

With inapparent preexcitation, preexcitation is absent on the surface ECG despite the presence of an anterogradely conducting AV BT, because conduction over the AVN-HPS reaches the ventricle faster than that over the BT. In this setting, the PR interval is shorter than what the P-delta interval would be if preexcitation were present. Therefore, when preexcitation becomes inapparent, the PR interval becomes shorter, reflecting the now better AVN-HPS conduction.³

Inapparent preexcitation is usually caused by (1) enhanced AVN conduction, so that it is faster than conduction over the BT; (2) prolonged intraatrial conduction from the site of atrial stimulation to the atrial insertion site of BT (most often left lateral), favoring anterograde conduction over the AVN-HPS; and/or (3) prolonged conduction over the BT, so that it is slower than AVN-HPS conduction.

Intermittent Preexcitation

Intermittent preexcitation is defined as the presence and absence of preexcitation on the same tracing (Fig. 18-8). True intermittent preexcitation is characterized by an abrupt loss of the delta wave (independently of how fast or slow is AVN conduction), with prolongation (normalization) of the PR interval (reflecting the loss of the faster BT conduction, and the subsequent conduction over the slower AVN-HPS), and normalization of the QRS in the absence of any significant change in heart rate.

FIGURE 18-8 Intermittent preexcitation. Surface ECG leads II and V₁ and intracardiac recordings in a patient with Wolff-Parkinson-White syndrome and a right anterior bypass tract (BT). Note the intermittent abrupt loss of delta wave (stars) associated with prolongation of the PR interval and normalization of the His bundle–ventricular (HV) interval, despite the presence of a constant atrial–His bundle (AH) interval (atrioventricular node [AVN] conduction) and a stable sinus rate, indicating that loss of preexcitation is secondary to anterograde block in the BT (i.e., intermittent preexcitation) rather than enhanced AVN conduction.

Intermittent preexcitation is usually caused by (1) phase 3 (i.e., tachycardia-dependent) or phase 4 (i.e., bradycardia-dependent) block in the BT (see Chap. 10); (2) anterograde or retrograde concealed conduction produced by PVCs, premature atrial complexes (PACs), or atrial arrhythmias; (3) BTs with long ERP and the gap phenomenon in response to PACs; and/or (4) BTs with long ERP and supernormal conduction.

Intermittent preexcitation is generally a reliable sign that the AV BT has a relatively long anterograde ERP and is not capable of excessively rapid impulse conduction, such as during AF. Maneuvers that slow AVN conduction (e.g., carotid sinus massage, AVN blockers) would unmask inapparent preexcitation but would not affect intermittent preexcitation.

Preexcitation alternans is a form of intermittent preexcitation in which a QRS complex manifesting a delta wave alternates with a normal QRS complex (see Fig. 18-5). Concertina preexcitation is another form of intermittent preexcitation in which the PR intervals and QRS complex durations show a cyclic pattern; that is, preexcitation becomes progressively more prominent over a number of QRS complex cycles followed by a gradual diminution in the degree of preexcitation over several QRS cycles, despite a fairly constant heart rate.

Differentiation between intermittent preexcitation and inapparent preexcitation on an ECG showing QRS complexes with and without preexcitation can be achieved by comparing the P-delta interval during preexcitation and the PR interval when preexcitation is absent. Loss of preexcitation associated with a PR interval longer than the P-delta interval is consistent with intermittent preexcitation (see Fig. 18-8), whereas loss of preexcitation associated with a PR interval shorter than the P-delta interval is consistent with inapparent preexcitation.

Orthodromic Atrioventricular Reentrant Tachycardia

The ECG during orthodromic AVRT shows P waves inscribed within the ST-T wave segment with an RP interval that is usually less than half of the tachycardia R-R interval (i.e., RP interval < PR interval) (Fig. 18-9). The RP interval remains constant, regardless of the tachycardia CL, because it reflects the nondecremental conduction over the BT. QRS morphology during orthodromic AVRT is generally normal and not preexcited, even when preexcitation is present during NSR (Fig. 18-10). Functional bundle branch block (BBB) can be observed frequently during orthodromic AVRT (see Fig. 18-9). The presence of BBB during SVT in a young person (<40 years) should raise the suspicion of orthodromic AVRT incorporating a BT ipsilateral to the blocked bundle, because the longer conduction time through the involved ventricle engendered by the BBB facilitates orthodromic reentry by enabling all portions of the circuit enough time to recover excitability from the prior cycle. This is particularly true with left bundle branch block (LBBB), which is very uncommon in younger patients.

FIGURE 18-9 Surface ECG of orthodromic atrioventricular reentrant tachycardia (AVRT) using a concealed superoparaseptal bypass tract (BT). Note the P waves (arrows) inscribed within the ST-T wave segment (short RP interval). Ischemic-appearing ST segment depression is also observed. Functional right bundle branch block occurs in the right side of the tracing, with prolongation of the RP (ventriculoatrial [VA]) interval, suggesting that retrograde VA conduction during the supraventricular tachycardia is mediated by a right-sided BT. The dashed lines denote the QRS onset and P wave onset.

FIGURE 18-10 Surface ECG of multiple supraventricular arrhythmias in a patient with a bidirectional left posteroseptal bypass tract (BT). Ventricular preexcitation is evident during normal sinus rhythm (NSR). Atrial flutter with 2:1 atrioventricular (AV) conduction over the BT results in a wide complex tachycardia. The narrow complex tachycardia represents orthodromic atrioventricular reentrant tachycardia (AVRT) using the BT as the retrograde limb of the reentrant circuit. Atrial fibrillation results in an irregularly irregular rhythm with “clumping” of the preexcited (wide) and normal QRS complexes.

Orthodromic AVRT tends to be a rapid tachycardia, with rates ranging from 150 to more than 250 beats/min. A beat-to-beat oscillation in QRS amplitude (QRS alternans) is present in up to 38% of cases and is most commonly seen when the rate is very rapid. The mechanism for QRS alternans is not clear but can partly result from oscillations in the relative refractory period of the distal portions of the HPS.

Ischemic-appearing ST segment depression also can occur during orthodromic AVRT, even in young individuals who are unlikely to have coronary artery disease. An association has been observed between repolarization changes (ST segment depression or T wave inversion) and the underlying mechanism of the tachycardia, because such changes are more common in orthodromic AVRT than AVNRT (57% versus 25%). Several factors can contribute to ST segment depression in these arrhythmias, including changes in autonomic tone, intraventricular conduction disturbances, a longer ventricular-atrial (VA) interval, and a retrograde P wave of longer duration that overlaps into the ST segment. The location of the ST segment changes can vary with the location of the BT; ST segment depression in leads V₃ to V₆ is almost invariably seen with a left lateral BT, whereas ST segment depression and a negative T wave in the inferior leads is associated with a posteroseptal or posterior BT. A negative or notched T wave in leads V₂ or V₃ with a positive retrograde P wave in at least two inferior leads suggests an anteroseptal BT. However, ST segment depression occurring during orthodromic AVRT in an older patient mandates consideration of possible coexisting ischemic heart disease.

Antidromic Atrioventricular Reentrant Tachycardia

Antidromic AVRT is characterized by a wide (fully preexcited) QRS complex, usually regular R-R intervals, and ventricular rates of up to 250 beats/min. The width of the preexcited QRS complex and the amplitude of the ST-T wave segment usually obscure the retrograde P wave on the surface ECG. When the P waves can be identified, they are inscribed within the ST-T wave segment with an RP interval that may be more than half of the tachycardia R-R interval because retrograde conduction occurs slowly via the AVN-HPS. The PR (P-delta) interval remains constant, regardless of the tachycardia CL, because it reflects nondecremental conduction over the BT.

Permanent Junctional Reciprocating Tachycardia

PJRT tends to be incessant, stopping and starting spontaneously every few beats without initiating PACs or PVCs. The heart rate is usually between 120 and 200 beats/min and the QRS duration is generally normal. Slow retrograde conduction over the BT causes the RP interval during PJRT to be long, usually more than half of the tachycardia R-R interval (Fig. 18-11). The P waves resulting from retrograde conduction are easily seen on the ECG and are inverted in leads II, III, aVF, and V₃ to V₆.

FIGURE 18-11 Surface ECG of permanent junctional reciprocating tachycardia (PJRT). Note the incessant nature of the arrhythmia, stopping and starting spontaneously every few beats without initiating atrial or ventricular ectopic beats. Slow retrograde conduction over the bypass tract causes the RP interval during PJRT to be long (long RP tachycardia). The P waves resulting from retrograde conduction are easily seen on the ECG and are inverted in the inferior leads.

Atrioventricular Nodal Reentrant Tachycardia and Atrial Tachycardia

Both AVNRT and AT can be associated with partially or fully preexcited QRS complex secondary to anterograde conduction to the ventricles over the bystander BT. When AVNRT occurs in the WPW syndrome, the arrhythmia can be difficult to distinguish from orthodromic AVRT without EP testing.

Atrial Fibrillation

There are several characteristic findings on the ECG in patients with AF conducting over a BT, so-called preexcited AF (see Fig. 18-10). The rhythm is irregularly irregular, and can be associated with very rapid ventricular response caused by the nondecremental anterograde AV conduction over the BT. However, a sustained rapid ventricular rate of more than 180 to 200 beats/min will often create pseudo-regularized R-R intervals when the ECG is recorded at 25 mm/sec. Although the QRS complexes are conducted aberrantly, resembling those during preexcited NSR, their duration can be variable and they can become normalized. This is not related to the R-R interval (i.e., it is not a rate-related phenomenon), but rather is related to the variable relationship between conduction over the BT and AVN-HPS. Preexcited and normal QRS complexes often appear “clumped” (see Fig. 18-10). This can result from concealed retrograde conduction into the BT or the AVN.

The QRS complex during preexcitation is a fusion between the impulse that preexcites the ventricles caused by rapid conduction through a BT and the impulse that takes the usual route through the AVN. The number of impulses that can be transmitted through the BT and the amount of preexcitation depend on the refractoriness of both the BT and AVN. The shorter the anterograde ERP of the BT, the more rapid is anterograde impulse conduction and, because of more preexcitation, the wider the QRS complexes. Patients who have a BT with a very short ERP and rapid ventricular rates represent the group at greatest risk for development of VF.

Anterograde block in the BT abolishes retrograde conduction into the AVN, which in turn allows the AVN to recover its excitability and conduct anterogradely. These conducted impulses through the AVN can result in retrograde concealment into the BT, causing anterograde block of the BT, thereby slowing the ventricular rate.

Atrial Flutter

AFL, like AF, can conduct anterogradely via a BT resulting in a preexcited tachycardia (see Fig. 18-10). Depending on the various refractory periods of the normal and pathological AV conduction pathways, AFL potentially can conduct 1:1 to the ventricles during a preexcited tachycardia, making the arrhythmia difficult to distinguish from VT (see Fig. 12-6).

Localization Using the Delta Wave

Careful analysis of the preexcitation pattern during sinus rhythm can potentially allow an accurate approximation of the location of the BT. This provides the electrophysiologist with important information that can guide patient counseling with regard to risks and benefits of ablation, in particular, providing some guidance about the proximity of the BT to the normal conduction system and the subsequent risk of AV block associated with an ablation attempt, as well as the need for left heart catheterization and atrial septal puncture and their potential complications. Additionally, it can also allow planning the subsequent catheter ablation, such as the use of cryoablation for septal BTs or the need for special equipment for atrial septal puncture for left-sided BTs.²⁴

The delta wave vector is helpful in approximating BT location, especially when maximal preexcitation is present. However, during NSR, only partial ventricular preexcitation is usually present, which limits the accuracy of ECG localization of the BT. Additionally, the degree of preexcitation may vary in an individual, depending on heart rate, autonomic tone, and AVN function, as well as BT location and EP characteristics. Therefore, it is important first to assess the degree of preexcitation visible throughout the entire ECG and then use only the delta wave polarity for localization (the first 40 milliseconds of the QRS in most cases, unless fully preexcited) rather than the overall QRS polarity, which may vary from each other.^25–29

Several algorithms have been developed to precisely locate a BT to a specific anatomic location, using the delta wave polarity (Table 18-1; Figs. 18-12 and 18-13).^25,26 Although these algorithms facilitate prediction of the location of a BT, they are inherently limited by biological variability in anatomy (e.g., rotation of the heart within the thorax), variable degree of preexcitation and QRS fusion, the presence of more than one manifest BT, intrinsic ECG abnormalities (such as prior myocardial infarction and ventricular hypertrophy), as well as technical variability in ECG acquisition and electrode positioning. These factors can subject all algorithms to exceptions and inaccuracies.²⁴

TABLE 18-1 Delta Wave Characteristics during Preexcitation According to Bypass Tract Location^*

Atrial Pacing and Atrial Extrastimulation During Normal Sinus Rhythm

In the presence of a manifest AV BT, atrial stimulation from any atrial site can help unmask preexcitation if it is not manifest during NSR because of fast AVN conduction. Incremental rate atrial pacing and progressively premature AES produce decremental conduction over the AVN (but not over the BT), increasing the degree of preexcitation and shortening the HV interval, until the His potential is inscribed within the QRS. The His potential is still activated anterogradely over the AVN until anterograde block in the AVN occurs; the QRS then becomes fully preexcited, and the His potential becomes retrogradely activated (see Fig. 18-4).

Atrial stimulation close to or at the AV BT insertion site results in maximal preexcitation and the shortest P-delta interval because of the lack of intervening atrial tissue whose refractoriness may otherwise limit the ability of atrial stimulation to activate the AV BT as early (Fig. 18-14). The failure of atrial stimulation to increase the amount of preexcitation can be caused by markedly enhanced AVN conduction, the presence of another AV BT, a pacing-induced block in the AV BT because of a long ERP of the BT (longer than that of the AVN), total preexcitation already present at the basal state caused by prolonged or absent AVN-HPS conduction, and/or decremental conduction in the BT. Atrial pacing can reveal the presence of multiple BTs (Fig. 18-15). Rare cases of catecholamine-dependent BTs have been reported that require isoproterenol infusion to manifest preexcitation that is absent at baseline.

FIGURE 18-14 Effect of site of pacing on preexcitation. A, In the presence of a manifest left lateral bypass tract (BT), pacing from the high right atrium at a cycle length (CL) of 600 milliseconds produces minimal preexcitation. The degree of preexcitation increases with premature stimulation because of delay in atrioventricular nodal conduction. B, In the same patient, pacing at the same CLs from the distal coronary sinus (CS), close to or at the BT insertion site, results in a larger degree of preexcitation and shorter P-delta interval because of the lack of intervening atrial tissue whose refractoriness might otherwise limit the ability of atrial stimulation to activate the BT as early.

FIGURE 18-15 Surface ECG and intracardiac recordings during coronary sinus (CS) pacing (S) in a patient with both right and left lateral BTs. The first two complexes show a left lateral preexcitation pattern (red arrows), whereas this pathway fails to conduct on the last two complexes, which show a right lateral preexcitation pattern (blue arrows).

Ventricular Pacing and Ventricular Extrastimulation During Normal Sinus Rhythm

In the presence of a retrogradely conducting AV BT (whether manifest or concealed), ventricular extrastimulation (VES) during NSR can result in VA conduction over the BT, AVN, both, or neither (Fig. 18-16). Conduction over the BT alone is the most common pattern at short pacing CLs or short VES coupling intervals. In this setting, the VA conduction time is fairly constant over a wide range of pacing CLs and VES coupling intervals, in the absence of intraventricular conduction abnormalities or additional BTs. On the other hand, retrograde conduction over the BT and HPS-AVN is especially common when RV pacing is performed in the presence of a left-sided BT at long pacing CLs or long VES coupling intervals. This occurs because it is easier to engage the right bundle branch (RB) and conduct retrogradely through the AVN than it is to reach a distant left-sided BT. In this setting, the atrial activation pattern depends on the refractoriness and conduction times over both pathways and usually exhibits a variable degree of fusion. In addition, VA conduction can proceed over the HPS-AVN alone, resulting in a normal pattern of VA conduction, or can be absent because of block in both the HPS-AVN and BT, which is especially common with short pacing CLs and very early VES.

FIGURE 18-16 Retrograde conduction during ventricular extrastimulation (VES) in a patient with a bidirectional left lateral bypass tract (BT). A, The ventricular pacing drive is conducted retrogradely over the atrioventricular node (AVN) with a concentric atrial activation sequence. The VES is conducted over both the AVN and BT (atrial fusion). B, An earlier VES encounters delay in the His-Purkinje system (HPS)–AVN and conducts solely over the BT with an eccentric atrial activation sequence. C, An early-coupled VES blocks retrogradely in the BT and conducts solely over the AVN. D, The VES conducts only over the HPS-AVN with more pronounced ventriculoatrial (VA) delay, which allows recovery of the BT and anterograde conduction, initiating antidromic atrioventricular reentrant tachycardia (AVRT). The VA delay is provided by conduction delay, not only within the AVN but also within the HPS. Note that the VES encounters retrograde block in the right bundle branch (RB), and His bundle (HB) activation is mediated by retrograde conduction over the left bundle branch (LB). Consequently, the His potential is visible after the ventricular electrogram. Note that despite the fact that the H₁-H₂ interval following VES approximates the H-H interval during supraventricular tachycardia (SVT), the His bundle–atrial (HA) interval following the initiating VES is shorter than that during the SVT, which favors antidromic AVRT over preexcited atrioventricular nodal reentrant tachycardia (AVNRT) as the mechanism of the SVT.

Ventricular stimulation during NSR also helps prove the presence of a retrogradely conducting AV BT. Ventricular stimulation resulting in retrograde VA conduction not consistent with normal conduction over the AVN (i.e., eccentric atrial activation sequence; see Fig. 18-16) and a VES delivered when the HB is refractory that results in atrial activation are indicators of the presence of a retrogradely conducting AV BT. However, if a VES delivered when the HB is refractory does not result in atrial activation, this does not necessarily exclude the presence of a retrogradely conducting AV BT, because such a VES can be associated with retrograde block in the BT itself (see Fig. 18-16). Additionally, the lack of such a response does not exclude the presence of unidirectional (anterograde-only) AV BTs. A VES that conducts to the HB and results in an atrial activation that either precedes HB activation (Fig. 18-17) or is associated with an apparent His bundle–atrial (HA) interval shorter than that during drive complexes indicates the presence of a BT. Ventricular pacing can also reveal the presence of multiple BTs (Fig. 18-18).

FIGURE 18-17 Ventricular pacing with a single ventricular extrastimulus (S₂) showing the presence of a bypass tract (BT). A retrograde His potential is present on both drive complexes (S₁) as well as following the extrastimulus (arrows); although atrial activation also follows each stimulus, it occurs (dashed line) before the inscription of the His potential on the extrastimulus complex. Thus, a BT is present because atrial activation is not dependent on His bundle–atrioventricular (HB-AVN) activation.

FIGURE 18-18 Surface ECG and intracardiac recordings in a patient with both right and left free wall bypass tracts (BTs). The first complex shows sinus rhythm with preexcitation, showing a left free wall pattern. Four complexes of right ventricular pacing follow, the first two of which show fusion of retrograde activation over both a left lateral BT (red arrows), which is present in each complex, as well as a right lateral BT (blue arrows) that is present in the first two paced complexes but fails to conduct on the last two complexes. Dashed lines aid in comparison of activation sequences.

During the delivery of progressively premature single VESs, an abrupt increase in the VA conduction interval is often observed. This may be due to a variety of reasons including a change in activation from a BT block to the AVN or a change from fast to slow pathway conduction; or it may be the result of an abrupt change when the refractory period of the RB has been reached. Retrograde right bundle branch block (RBBB) occurs frequently during VES testing, and can be diagnosed by observing the retrograde His potential during the drive train and its abrupt delay following the VES. Often, however, it is difficult to visualize the retrograde His potential during the pacing train; nevertheless, the sudden appearance of an easily distinguished retrograde His potential, separate from the ventricular electrogram following the VES, may be sufficient to recognize retrograde RBBB. Prolongation of the V-H interval is observed on development of retrograde RBBB, because conduction must traverse the interventricular septum (which requires approximately 60 to 70 milliseconds in normal hearts), enter retrograde via the left bundle branch (LB), and ascend to reach the HB. Although an increase in the V-H interval necessarily occurs with retrograde RBBB, whether a similar increase occurs in the VA interval depends on the nature of VA conduction. Measurement of the effect of retrograde V-H and VA intervals on the development of retrograde RBBB during VES can help the distinction between retrograde AVN and BT conduction. In the absence of a BT, the AVN can be activated in a retrograde fashion only after retrograde activation of the HB; as a consequence, VA activation will necessarily be delayed with retrograde RBBB, and the increase in the VA interval will be at least as much as the increase in the V-H interval. On the other hand, when retrograde conduction is via a BT, there will be no expected increase in the VA interval when retrograde RBBB is induced. Thus, the increase in the VA interval is minimal and always less than the increase in the V-H interval.³²

During retrograde conduction over the BT, the VA interval may increase slightly in response to incremental rate ventricular pacing or progressively premature VES. At short ventricular pacing CLs or VES coupling intervals, intramyocardial conduction delay can occur, resulting in prolongation in the VA interval; however, the local VA interval at the BT location remains unchanged. Furthermore, short ventricular pacing CLs or VES coupling intervals can encroach on the BT refractoriness, causing some decremental conduction, with a consequent increase in total and local VA intervals. The VA interval can also change with changing the site of ventricular stimulation, because the VA interval represents the sum of conduction time over the BT and conduction time through the ventricular tissue intervening between the site of stimulation and ventricular insertion site of the BT. BTs with retrograde decremental conduction properties can also exhibit prolongation of conduction time and VA interval with ventricular pacing or VES.

The absence of VA conduction (at long pacing CLs) or the presence of decremental VA conduction at baseline makes the presence of a retrogradely conducting BT unlikely, except for the rare catecholamine-dependent BTs that require isoproterenol infusion for demonstration.

Initiation by Atrial Extrastimulation or Atrial Pacing

Orthodromic Atrioventricular Reentrant Tachycardia: Manifest Atrioventricular Bypass Tract

In the presence of a manifest AV BT, initiation of orthodromic AVRT with an AES requires the following: (1) anterograde block in the AV BT; (2) anterograde conduction over the AVN-HPS; and (3) slow conduction over the AVN-HPS, with adequate delay to allow for the recovery of the atrium and AV BT and subsequent retrograde conduction over the BT (see Fig. 3-10).³ The reason this occurs is that, whereas the BT conducts more rapidly than the AVN, it has a longer ERP, so the early atrial impulse blocks anterogradely in the BT but conducts over the AVN. The site of AV delay is less important; it is most commonly in the AVN, but it can occur also in the HB, bundle branches, or ventricular myocardium. Because the coupling intervals of the AES required to achieve anterograde block in the BT are usually short, sufficient AVN delay is usually present so that orthodromic AVRT is initiated once anterograde BT block occurs. The presence of dual AVN physiology can facilitate the initiation of orthodromic AVRT by providing adequate AV delay by mediating anterograde conduction over the slow AVN pathway. BBB ipsilateral to the AV BT provides an additional AV delay that can facilitate tachycardia initiation.

Induction of orthodromic AVRT is easier with atrial stimulation at a site in close proximity to the AV BT insertion site; the closer the stimulation site to the BT, the easier it is to encroach on the refractory period of the BT and achieve block, because it is not limited by the refractoriness of intervening atrial tissue. Furthermore, the earlier the atrial insertion of the BT is activated, the more likely it will recover before arrival of the retrograde atrial activation wavefront to the BT atrial insertion site, thereby facilitating reentry. Thus, one may actually require less anterograde AV delay if recovery of excitability is shifted earlier in time. In addition, different sites of atrial stimulation can produce different AVN conduction velocities and refractoriness (even at the same AES coupling intervals).

If SVT induction fails, the use of multiple AESs, rapid atrial pacing, and pacing closer to the BT would achieve block in the BT and produce adequate AV delay.

AES can also result in a 1:2 response caused by conduction over both the AV BT and the AVN-HPS (i.e., a single AES resulting in two ventricular complexes; the first is fully preexcited and the second is normal). For this response to occur, significant delay in AVN-HPS conduction should be present to allow for recovery of the ventricle after its activation via the BT. AES can also produce sinus nodal or AVN echo beats that in turn may block in the BT and achieve adequate AV delay to initiate orthodromic AVRT.

Orthodromic Atrioventricular Reentrant Tachycardia: Concealed Atrioventricular Bypass Tract

Orthodromic AVRT in patients with concealed BTs is identical to that in patients with WPW. The only difference is that in patients with concealed BTs anterograde block in the BT is already present. Consequently, the only condition needed to induce orthodromic AVRT is adequate AV delay (in the AVN or HPS) to allow for recovery of the atrium and atrial insertion site of the AV BT. Therefore, orthodromic AVRT initiation requires less premature coupling intervals of the AESs in patients with concealed BTs than in patients with WPW.

Orthodromic Atrioventricular Reentrant Tachycardia: Slowly Conducting Concealed Atrioventricular Bypass Tract (Permanent Junctional Reciprocating Tachycardia)

PJRT is usually incessant and is initiated by spontaneous shortening of the sinus CL, without a triggering PAC or PVC. The tachycardia can be transiently terminated by PACs or PVCs but usually resumes after a few sinus beats (Fig. 18-19). This phenomenon has three potential mechanisms: a rate-related decrease in the retrograde ERP of the BT, a rate-related decrease in atrial refractoriness that allows the impulse to reactivate the atrium retrogradely over the BT, or a concealed Wenckebach block with block at the atrial-BT junction terminating the Wenckebach cycle, relieving any anterograde concealed conduction that may have prevented retrograde conduction up the BT. The latter is the most likely mechanism, because such slow BTs actually demonstrate decremental conduction at rapid rates and, in most cases, the atrial ERP at the atrial-BT junction is shorter than the RP (VA) interval. Thus, some sort of anterograde concealment during NSR in the BT must be operative, preventing tachycardia from always occurring.³ Late-coupled AESs can also readily initiate PJRT.

FIGURE 18-19 Two surface ECG leads are shown during permanent junctional reciprocating tachycardia. Carotid sinus pressure is applied at left, resulting in termination of supraventricular tachycardia (SVT) caused by block in the bypass tract (the SVT terminates with a QRS). Several escape and sinus complexes follow, and then the SVT resumes. This phenomenon gives rise to the use of the term permanent or incessant.

Antidromic Atrioventricular Reentrant Tachycardia

The initiation of classic antidromic AVRT by an AES requires the following: (1) intact anterograde conduction over the BT; (2) anterograde block in the AVN or HPS; and (3) intact retrograde conduction over the HPS-AVN once the AVN resumes excitability following partial anterograde penetration (see Fig. 18-4). The latter is usually the limiting factor for the initiation of antidromic AVRT. A delay of more than 150 milliseconds between atrial insertion of the BT and HB is probably required for the initiation of antidromic AVRT.³

Several mechanisms of antidromic AVRT initiation can be operative.³ The AES may block in the AVN with anterograde conduction down the BT and subsequent retrograde conduction over the HPS-AVN. In this setting, ventricular–His bundle (V-H) delay is required to allow recovery of the AVN. Because antidromic AVRTs have relatively short VA intervals, this mechanism of initiation is probably uncommon, except with left-sided BTs, which would potentially provide sufficient V-H delay to allow retrograde conduction. Tachycardia initiation can be facilitated by a short retrograde AVN ERP, a common finding in patients with these SVTs. Alternatively, the AES may block in the AVN, with anterograde conduction down the BT and subsequent retrograde conduction over a different BT. Subsequent complexes can conduct retrogradely over the AVN-HPS or the second BT. Changing tachycardia CL (and VA interval) may relate to whether retrograde conduction proceeds over the AVN-HPS or the second BT. A third potential mechanism for the initiation of antidromic AVRT involves AES conduction over the BT and simultaneously over the slow pathway of a dual AVN pathway situation, with anterograde block in the fast AVN pathway. Conduction beyond the HB to the ventricle is not possible because of ventricular refractoriness, yet an AVN echo to the atrium may occur, which in turn may conduct anterogradely over the BT, when the ventricle would have recovered excitability, and subsequently back up the now-recovered AVN, initiating antidromic AVRT. AVN reentry may not persist or may be preempted by retrograde conduction up the fast AVN pathway because of the premature ventricular activation over the BT. In this scenario, the location of the His potential will depend on whether or not it was anterograde or retrograde.

In general, if atrial stimulation induces antidromic AVRT, multiple BTs are often operative. Whether or not they are operative throughout the SVT depends on the relative retrograde activation times over the additional BTs and HPS-AVN and the varying degree of anterograde and/or retrograde concealment into the additional BTs, HPS-AVN, or both during the SVT.

The site of atrial stimulation plays an important role in inducibility of AVRT, and can also determine the type of AVRT initiated in patients with bidirectional BTs. The closer the stimulation site to the BT, the more likely anterograde block in the BT will occur and orthodromic AVRT will result. Conversely, antidromic AVRT is more likely to occur with atrial stimulation close to the AVN.

Initiation by Ventricular Extrastimulation or Ventricular Pacing

Orthodromic Atrioventricular Reentrant Tachycardia: Manifest or Concealed Atrioventricular Bypass Tract

Ventricular stimulation is usually able to induce orthodromic AVRT (inducibility rate of 60% with VES and 80% with ventricular pacing), and is similar in patients with manifest or concealed BTs (Fig. 18-20). Initiation of orthodromic AVRT by ventricular stimulation requires the following: (1) retrograde block of the ventricular impulse in the HPS-AVN; (2) retrograde conduction only over the AV BT; and (3) adequate VA conduction delay to allow for recovery of the AVN-HPS from any concealment produced by ventricular stimulation, so it can support anterograde conduction of the reentrant impulse. Because the BT retrograde ERP is usually very short, the prime determinant of orthodromic AVRT initiation is the extent of retrograde conduction and/or concealment in the HPS-AVN.³

FIGURE 18-20 Induction of an orthodromic atrioventricular reentrant tachycardia (AVRT) using a concealed posteroseptal bypass tract with ventricular pacing. Note that although the ventricular pacing cycle length (CL) approximates the supraventricular tachycardia (SVT) CL, the ventriculoatrial (VA) interval (dashed lines) during ventricular pacing is only slightly longer than that during SVT, which favors orthodromic AVRT over atrioventricular nodal reentrant tachycardia (AVNRT) as the mechanism of the SVT. Additionally, the atrial–His bundle interval of the first SVT complex is longer than that of subsequent beats, indicating retrograde concealment in the AVN produced by the last ventricular stimulus.

Multiple modes of initiation of orthodromic AVRT can be present, depending on the pacing CL or VES coupling interval, conduction velocities, and refractoriness of the HPS-AVN and BT, as well as the site of ventricular stimulation.³ Ventricular pacing at a CL or a VES with a coupling interval shorter than the ERP of the AVN but longer than that of the HPS and AV BT would block retrogradely in the AVN and conduct over the AV BT to initiate orthodromic AVRT. Block in the AVN, which is more likely to occur with rapid ventricular pacing or VES delivered after a short pacing drive CL, can cause concealment and subsequent delay in anterograde conduction of the first SVT impulse over the AVN, resulting in longer AH and PR intervals of the first SVT beat compared with subsequent beats (see Fig. 18-20). On the other hand, a VES with a coupling interval or ventricular pacing at a CL shorter than the ERP of the HPS, but longer than that of the AV BT, would block retrogradely in the HPS and conduct over the AV BT to initiate orthodromic AVRT. When block occurs in the HPS, which is more likely to occur with a VES delivered during NSR or after a long pacing drive CL, the first SVT beat will approach a fully recovered AVN and conduct with short AH and PR intervals equal to subsequent SVT beats. In this case, adequate prolongation of the HV interval may be required to allow for the recovery of ventricular refractoriness for the ventricle to be activated and support reentry, because AVN delay may have not been sufficient. When HV interval prolongation is required to initiate orthodromic AVRT, it is almost invariably associated with LBBB. A short-coupled VES, especially following a pacing drive with a long CL, that blocks retrogradely in both the AV BT and RB and conducts transseptally and then retrogradely over the LB, can result in a bundle branch reentrant (BBR) beat that conducts to the ventricle down the RB, and then retrogradely to the atrium over the AV BT, mediating the initiation of orthodromic AVRT. The long HV interval often associated with BBR beats, plus the LBBB pattern, facilitate the induction of orthodromic AVRT using a left-sided BT (Fig. 18-21).

FIGURE 18-21 Induction of an orthodromic atrioventricular reentrant tachycardia (AVRT) using a concealed left posteroseptal bypass tract (BT) with ventricular extrastimulation (VES). The VES conducts retrogradely over the BT, but also results in a bundle branch reentrant (BBR) beat, which in turn conducts to the atrium over the BT and initiates orthodromic AVRT. Note that right bundle branch block (RBBB) develops shortly after initiation of the SVT; however, the ventriculoatrial (VA) interval (dashed lines) remains constant, regardless of the presence or absence of RBBB, because the BT is in the contralateral ventricle.

Orthodromic Atrioventricular Reentrant Tachycardia: Slowly Conducting Concealed Atrioventricular Bypass Tract (Permanent Junctional Reciprocating Tachycardia)

Ventricular stimulation is less effective in initiating PJRT because of the already impaired conduction in the BT, such that an early VES produces block in the BT. A late-coupled VES (when the HB is refractory) can initiate SVT in some cases.

Antidromic Atrioventricular Reentrant Tachycardia

Initiation of classic antidromic AVRT by ventricular pacing and VES requires the following: (1) retrograde block in the BT; (2) retrograde conduction over the AVN or HPS; and (3) adequate VA delay to allow for recovery of the atrium and BT so it can support subsequent anterograde conduction (see Fig. 18-16).³

When induction of the SVT is achieved by ventricular pacing at a CL similar to the tachycardia CL or by a VES that activates the HB at a coupling interval (i.e., H₁-H₂ interval) similar to the H-H interval during the SVT, the HA interval following the initiating ventricular stimulus is always equal to or shorter than that during the antidromic AVRT. This is because the His potential and atrium are activated in sequence during antidromic AVRT and in parallel during ventricular stimulation. Therefore, an HA interval of the initiating ventricular stimulus longer than the HA interval during SVT favors AVNRT and excludes antidromic AVRT (see Fig. 18-16). Moreover, because the AVN usually exhibits greater decremental conduction with repetitive engagement of impulses than to a single impulse at a similar coupling interval, the more prolonged the HA interval with the initiating ventricular stimulus, the more likely that the SVT is AVNRT.

Orthodromic Atrioventricular Reentrant Tachycardia: Manifest or Concealed Atrioventricular Bypass Tract

Atrial Activation Sequence

The initial site of atrial activation during orthodromic AVRT depends on the location of the AV BT, but is always near the AV groove and without multiple breakthrough points. The atrial activation sequence during orthodromic AVRT should be identical to that during ventricular pacing at comparable CLs when VA conduction occurs exclusively over the AV BT. However, retrograde conduction during ventricular pacing may proceed over the AVN or over both the BT and AVN, resulting in fusion of atrial activation, depending on the site of ventricular stimulation relative to the BT and HPS, and on retrograde conduction and refractoriness of the HPS-AVN.

Atrial–Ventricular Relationship

Conduction time over the classic (fast) BTs is approximately 30 to 120 milliseconds. Therefore, the RP interval during orthodromic AVRT is short, but longer than that during typical AVNRT, because in the setting of orthodromic AVRT the wavefront has to activate the ventricle before it reaches the AV BT ventricular insertion site at the AV groove and subsequently conduct to the atrium. Consequently, a very short VA interval (<70 milliseconds) or V–high RA interval (<95 milliseconds) largely excludes orthodromic AVRT, and is consistent with typical AVNRT.³³ The RP and VA intervals remain constant during orthodromic AVRT regardless of oscillations in tachycardia CL from whatever cause or changes in the PR interval (AH interval); as a consequence, the tachycardia CL is most closely associated with the PR interval (i.e., anterograde slow conduction) and the RP/PR ratio may vary (Fig. 18-22).

FIGURE 18-22 Spontaneous termination of orthodromic atrioventricular reentrant tachycardia (AVRT) using a concealed superoparaseptal bypass tract. Note that the supraventricular tachycardia (SVT) terminates with an atrial complex not followed by a QRS, consistent with anterograde block in the atrioventricular node (AVN). Also, note the oscillation in the SVT cycle length (CL) preceding termination. Changes in H-H and V-V intervals precede the subsequent changes in A-A intervals, and the ventriculoatrial (VA) interval remains constant despite oscillation of the CL. This indicates that the variability in the tachycardia CL is secondary to changes in the anterograde conduction over the AVN, whereas VA conduction over the retrograde limb of the reentrant circuit (the bypass tract) remains constant.

A 1:1 A-V relationship is a prerequisite for maintenance of AVRT, because parts of both the atrium and the ventricle are essential components of the reentrant circuit. If an SVT persists despite the presence of AV block, orthodromic AVRT is excluded.

When dual AVN pathways are present, the slow AVN pathway functions in most cases as the anterograde limb during orthodromic AVRT. An AH interval of more than 180 milliseconds during orthodromic AVRT suggests a slow AVN pathway mediating the anterograde limb of the reentrant circuit, whereas an AH interval of less than 160 milliseconds suggests a fast AVN pathway mediating anterograde conduction. Obviously, orthodromic AVRT using the slow pathway will have a longer tachycardia CL.

Slow-slow AVNRT is associated with an RP interval and P wave morphology similar to that during orthodromic AVRT using a posteroseptal AV BT. However, although both SVTs have the earliest atrial activation in the posteroseptal region, conduction time from that site to the HB region is significantly longer in AVNRT than in orthodromic AVRT, resulting in a significantly longer RP interval in lead V₁ and a larger difference in the RP interval between lead V₁ and the inferior leads. Therefore, a ΔRP interval (V₁ – III) longer than 20 milliseconds suggests slow-slow AVNRT with a sensitivity of 71%, specificity of 87%, and positive predictive value of 75%.

Effects of Bundle Branch Block

The presence of BBB during SVT is much more common in orthodromic AVRT than AVNRT or AT (90% of SVTs with sustained LBBB are orthodromic AVRTs). Two reasons have been proposed to explain why prolonged aberration occurs less commonly during AVNRT than orthodromic AVRT. First, the induction of AVNRT requires significant AVN delay, which makes the H₁-H₂ interval longer and makes aberration unlikely, whereas in orthodromic AVRT, AVN conduction need not be slow, resulting in a shorter AH interval and an impulse encroaching on HPS refractoriness, in turn resulting in BBB. Second, LBBB facilitates the induction of orthodromic AVRT when a left-sided AV BT is present.³⁴

BBB is more common when AVRT is initiated by an AES that is delivered during NSR or after long-drive CLs, whereby HPS refractoriness is longest and AVN conduction and refractoriness are shortest. When AVRT is induced by atrial stimulation, RBBB is more common than LBBB (2:1). In contrast, when AVRT is induced by ventricular stimulation, LBBB is much more common than RBBB (because of concealment in the LB). Additionally, the incidence of BBB is more common in AVRTs induced by ventricular stimulation than those induced by atrial stimulation (75% versus 50%).

BBB ipsilateral to the AV BT results in prolongation of the surface VA interval because more time is needed for the impulse to travel from the AVN down the HB and contralateral bundle branch, and transseptally to the ipsilateral ventricle to reach the AV BT and then activate the atrium (Fig. 18-23). However, the local VA interval (measured at the site of BT insertion) remains constant. On the other hand, the tachycardia CL usually increases in concordance with the increase in the surface VA interval as a result of ipsilateral BBB, because of the now larger tachycardia circuit; however, because the time the wavefront spends outside the AVN is now longer, AVN conduction may improve, resulting in shortening of the AH interval (PR interval), which can be sufficient to overcome the prolongation of the VA interval. This can consequently result in shortening of the tachycardia CL. Thus, the surface VA interval and not the tachycardia CL should be used to assess the effects of BBB on the SVT (Fig. 18-24; and see Fig. 18-23).

FIGURE 18-23 Schematic illustration of the effect of bundle branch block (BBB) on the reentrant circuit during orthodromic atrioventricular reentrant tachycardia (AVRT) using a left-sided bypass tract (BT). Block in the left bundle branch (LB) (ipsilateral to the BT) results in prolongation of the reentrant pathway and, therefore, prolongation of the ventriculoatrial interval. In contrast, block in the right bundle branch (RB) (contralateral to the BT) has no effect on the reentrant circuit. AVN = atrioventricular node; HB = His bundle; LBBB = left bundle branch block; RBBB = right bundle branch block.

FIGURE 18-24 Effect of right bundle branch block (RBBB) on orthodromic atrioventricular reentrant tachycardia (AVRT). RBBB is initially present during an orthodromic AVRT using a concealed superoparaseptal bypass tract (BT). Introduction of a ventricular extrastimulus (S₂) from the right ventricular apex during the tachycardia is followed by resolution of RBBB (peeling of refractoriness). Note that the loss of RBBB is associated with shortening of the ventriculoatrial (VA) interval (by 21 milliseconds) and a milder degree of shortening of the tachycardia cycle length (by 8 milliseconds), indicating the presence and participation of a septal BT in the reentrant circuit.

Prolongation of the surface VA interval during SVT in response to BBB by more than 35 milliseconds compared to that with normal QRS or contralateral BBB indicates that an ipsilateral free wall AV BT is present and is participating in the SVT (i.e., diagnostic of orthodromic AVRT). On the other hand, prolongation of the surface VA by more than 25 milliseconds suggests a septal AV BT (posteroseptal AV BT in association with LBBB, and superoparaseptal AV BT in association with RBBB; see Fig. 18-24). In contrast, BBB contralateral to the AV BT does not influence the VA interval or tachycardia CL (because the contralateral ventricle is not part of the reentrant circuit; see Figs. 18-21 and 18-23). Prolongation of the VA interval by more than 45 milliseconds in response to RV pacing entraining the orthodromic AVRT is also diagnostic of a left-sided BT, whereby RV pacing results in effects analogous to those created by LBBB and, as a consequence, VA interval prolongation.

Oscillations in the Tachycardia Cycle Length

Oscillation of the tachycardia CL during orthodromic AVRT can occur and generally is caused by changes in the anterograde conduction over the AVN (see Fig. 18-22). Because retrograde conduction through the BT is much less variable, the changes in ventricular CL that result from variability in the anterograde AVN conduction precede the subsequent changes in atrial CL, and changes in atrial CL do not predict changes in subsequent ventricular CL (similar to observations during typical AVNRT). Contrariwise, changes in atrial CL predict the changes in subsequent ventricular CL during atypical AVNRT and AT.³⁵

Additionally, orthodromic AVRT in the presence of dual AVN physiology can be associated with anterograde conduction alternating over the slow and fast AVN pathways, resulting in a regular irregularity of the tachycardia CL (alternating long and short cycles). Alternatively, the presence of dual AVN pathways can lead to two separate stable tachycardia CLs. In either setting, the RP interval during the SVT remains constant.

QRS Alternans

Alternans of the QRS complex amplitude during relatively slow SVTs is almost always indicative of orthodromic AVRT (Fig. 18-25). On the other hand, although QRS alternans during fast SVTs is most commonly seen in orthodromic AVRT, it can also be seen with other types of SVTs.

FIGURE 18-25 Surface 12-lead ECG of orthodromic atrioventricular reentrant tachycardia showing QRS alternans in multiple ECG leads.

Termination and Response to Physiological and Pharmacological Maneuvers

Spontaneous termination of orthodromic AVRT is usually caused by gradual slowing and then block in the AVN (see Fig. 18-22), sometimes causing initial oscillation in the tachycardia CL, with alternate complexes demonstrating a Wenckebach periodicity before block. However, termination with block in the AV BT without any perturbations of the tachycardia CL can occur during very rapid AVRT or following a sudden shortening of the tachycardia CL.

Carotid sinus massage can terminate orthodromic AVRT by gradual slowing and then block in the AVN. Adenosine, digoxin, calcium channel blockers, and beta blockers terminate orthodromic AVRT by block in the AVN; therefore, the SVT terminates with a P wave not followed by a QRS. Verapamil rarely produces block in the AV BT and, when it does, block is usually preceded by oscillation in the tachycardia CL produced by changes in AVN conduction, leading to long-short sequences. Class IA and IC antiarrhythmic agents can produce block in the AV BT with variable effect on the AVN-HPS. Amiodarone can terminate AVRT by block in the AVN, HPS, or AV BT. Sotalol affects the AVN with little or no effect on the AV BT.

Orthodromic Atrioventricular Reentrant Tachycardia: Slowly Conducting Concealed Atrioventricular Bypass Tract (Permanent Junctional Reciprocating Tachycardia)

Atrial Activation Sequence

The initial site of atrial activation is most often in the posteroseptal part of the triangle of Koch near the CS os, similar to that in atypical AVNRT (Fig. 18-26).

FIGURE 18-26 Ventricular extrastimulation (VES) during permanent junctional reciprocating tachycardia. The supraventricular tachycardia has a stable baseline cycle length (522 milliseconds). A single VES (S₂) introduced during His bundle refractoriness retards the timing of the next atrial complex (538 milliseconds) (postexcitation). The anticipated timing of the high RA electrogram is indicated by the dashed line.

Atrial–Ventricular Relationship

Because the retrograde limb of the reentry circuit is the slow BT (which conducts more slowly than the AVN), the RP interval is longer than the PR interval, similar to atypical AVNRT (see Figs. 18-11 and 18-26). In contrast to the classic fast BTs, the RP interval during PJRT is not fixed, because the BT serving as the retrograde limb of the reentrant circuit has decremental properties. Similar to all types of AVRTs, a 1:1 A-V relationship is a prerequisite to sustenance of the tachycardia.

Oscillations in the Tachycardia Cycle Length

The tachycardia rate typically fluctuates (100 to 220 beats/min) in response to autonomic tone and physical activity, and the rate changes result from modulation of the PR and RP intervals. The tachycardia CL is often just longer than the shortest CL at which the BT can conduct retrogradely.

Effects of Bundle Branch Block

BBB affects PJRT in a manner analogous to that described for orthodromic AVRT.

Termination and Response to Physiological and Pharmacological Maneuvers

Carotid sinus massage and AVN blockers (adenosine, digoxin, calcium channel blockers, and beta blockers) usually terminate PJRT by block in the AVN (two-thirds) or in the BT (one-third) (see Fig. 18-19). Although the mode of tachycardia termination by adenosine has been suggested to distinguish between PJRT and atypical AVNRT, one report has shown that termination of atypical AVNRT with adenosine can also result from block in the fast AVN pathway and therefore its value in distinguishing between atypical AVNRT and PJRT is questionable.

Antidromic Atrioventricular Reentrant Tachycardia

Atrial Extrastimulation and Atrial Pacing During Supraventricular Tachycardia

Orthodromic Atrioventricular Reentrant Tachycardia

Atrial pacing at a CL slightly shorter than the tachycardia CL generally can entrain orthodromic AVRT (Fig. 18-27). If the P waves on the surface ECG can be seen, which usually is not the case, they may appear to be fusion beats resulting from intraatrial collision of the impulse propagating from the paced site with the one emerging from the BT. In general, when pacing is initiated orthodromically to the zone of slow conduction (the AVN in this case), conduction time within the area of slow conduction is long enough to allow a wide atrial antidromic wavefront to generate surface ECG fusion (see Fig. 18-27).

FIGURE 18-27 Atrial entrainment of orthodromic atrioventricular reentrant tachycardia (AVRT) using a left lateral bypass tract (BT). Atrial fusion (between the paced and tachycardia wavefronts; compare shaded areas) is observed during entrainment, which is consistent with AVRT and excludes both focal atrial tachycardia and atrioventricular nodal reentrant tachycardia. Note that the ventriculoatrial (VA) interval (dashed lines) of the return cycle after cessation of atrial pacing is similar to that of the supraventricular tachycardia (V-A linking), because retrograde VA conduction of the last entrained QRS is mediated by the BT.

The initial atrial complex following cessation of atrial pacing entraining orthodromic AVRT is linked to, and cannot be dissociated from, the last captured ventricular complex. As a consequence, the VA intervals of the return cycle after cessation of atrial pacing are fixed and similar to those during tachycardia (with <10 milliseconds of variation) after different attempts at SVT entrainment (see Fig. 18-27). The post-pacing VA intervals typically remain constant regardless of the site, duration, or CL of the entraining atrial pacing drive because retrograde VA conduction of the last entrained QRS is mediated by the BT, which is fixed and constant. VA linking can also be observed in typical AVNRT but not AT.^33,36

It is difficult for AES not to affect the SVT because of the large size and large excitable gap of the reentrant circuit. However, this can be influenced by the distance between the site of atrial stimulation and the atrial region incorporated in the AVRT circuit (i.e., atrial myocardium between the BT and the AVN). Because only parts of the atrium ipsilateral to the BT are requisite components of the orthodromic AVRT circuit, AES delivered in the contralateral atrium may not affect the circuit, whereas AESs delivered at sites in close proximity to the BT or the AVN have the highest success at resetting the reentrant circuit.

AES over a wide range of coupling intervals can reset orthodromic AVRT via conduction down the AVN-HPS. In this setting, atrial activation is a fusion of the AES and the SVT impulse traveling retrogradely up the AV BT. The next QRS can be early or late, depending on the degree of slowing of conduction of the AES anterogradely down the AVN (i.e., the degree of prolongation of the A₂-H₂ interval).

An early-coupled AES can terminate the SVT, usually by block in the AVN-HPS. In this setting, the SVT terminates with an AES not followed by a QRS (i.e., AV block). Alternatively, the AES can render the atrium refractory to the SVT impulse traveling retrogradely up the AV BT, in which case the SVT terminates with an AES followed by a QRS (i.e., VA block). The AES can also anterogradely penetrate the AV BT and collide with the retrogradely traveling SVT wavefront (VA block). Lastly, the AES can conduct down the AVN-HPS and advance the next QRS, which then blocks in the still-refractory AV BT or atrium (VA block).

Antidromic Atrioventricular Reentrant Tachycardia

AES is of value in distinguishing antidromic AVRT from preexcited AVNRT. A late-coupled AES, delivered close to the BT atrial insertion site during SVT when the AV junctional atrium is refractory (i.e., when the atrial electrogram is already manifest in the HB recording at the time of AES delivery) that advances (accelerates) the timing of both the next ventricular activation as well as the subsequent atrial activation, proves that the SVT is an antidromic AVRT using an AV BT anterogradely, and excludes preexcited AVNRT (Fig. 18-28A). Because the AV junctional atrium is refractory at the time of the AES, the AES cannot penetrate the AVN, and resetting of the SVT by such an AES is therefore incompatible with AVNRT.

FIGURE 18-28 Atrial extrastimulation (AES) during antidromic atrioventricular reentrant tachycardia (AVRT) using a left lateral bypass tract (BT). A, A late-coupled AES delivered when the atrioventricular (AV) junction is refractory (as indicated by lack of advancement of the timing of the local atrial electrogram recording by the His bundle catheter) resets both the next ventricular activation and the subsequent atrial activation. This proves that the supraventricular tachycardia (SVT) is an antidromic AVRT using an AV BT anterogradely, and excludes preexcited atrioventricular nodal reentrant tachycardia (AVNRT). Additionally, the reset ventricular activation occurs at a coupling interval identical to the AES coupling interval (i.e., exact coupling phenomenon), and the ventriculoatrial (VA) interval following the AES remains similar to that during SVT, which is consistent with antidromic AVNRT. B, Late-coupled AES delivered when the AV junction is refractory advances the subsequent QRS and terminates the SVT by retrograde block in the His-Purkinje system–atrioventricular node. C, An earlier AES terminates the SVT without conduction to the ventricle (i.e., anterograde block in the BT). The AES advances the timing of AV junctional atrial activation.

Also, an AES delivered during the SVT that advances ventricular activation and does not influence the VA interval excludes preexcited AVNRT and is diagnostic of antidromic AVRT (see Fig. 18-28A). The VA interval should change in the setting of preexcited AVNRT because the AES penetrates the AVN, producing slower conduction down the AVN before resumption of the tachycardia, which, in the presence of a fixed AV interval (caused by conduction down the BT) in response to the AES, would lead to a longer VA interval. In addition, the advanced QRS could invade and capture the HB retrogradely and conduct up the fast AVN pathway and reset the AVN circuit. Then the V-H interval of the advanced QRS plus the HA interval in response to this QRS should add up to the same VA interval on an undisturbed AVNRT, which is clearly unlikely.

Exact atrial and ventricular capture by an AES delivered when the AV junction is depolarized excludes AVNRT (see Fig. 18-28A). An AES that captures the ventricle at the same coupling interval as that of the AES indicates that the atrial stimulation site is inside the reentrant circuit, because if there were intervening atrial tissue between the stimulation site and the tachycardia circuit (as is the case during AVNRT), the AV interval would increase, and consequently, the V-V interval would exceed the AES coupling interval.³

The presence of a fixed and short V-H interval during entrainment of the SVT with atrial pacing suggests antidromic AVRT, and makes AVNRT unlikely (but does not exclude AVNRT). Moreover, failure of entrainment by atrial pacing to influence the VA interval during SVT excludes preexcited AVNRT.

An early-coupled AES can terminate the SVT by retrograde block in the AVN-HPS (the SVT terminates with an AES followed by a QRS; i.e., VA block; Fig. 18-28B) or by anterograde block in the BT (the SVT terminates with an AES not followed by a QRS; i.e., AV block; Fig. 18-28C).

Ventricular Extrastimulation and Ventricular Pacing During Supraventricular Tachycardia

Orthodromic Atrioventricular Reentrant Tachycardia: Manifest or Concealed Atrioventricular Bypass Tract

VES and ventricular pacing can easily reset, entrain, and may terminate orthodromic AVRT (Fig. 18-29).³³ However, the ability of the VES to affect the SVT depends on the distance between the site of ventricular stimulation to the ventricular insertion site of the BT and on the VES coupling interval. Because only parts of the ventricle ipsilateral to the BT are requisite components of the orthodromic AVRT circuit, a VES delivered in the contralateral ventricle may not affect the circuit.

FIGURE 18-29 Ventricular extrastimulation (VES) during orthodromic atrioventricular reentrant tachycardia (AVRT) using a left lateral bypass tract (BT). A, A late-coupled VES delivered when the His bundle (HB) is refractory, as indicated by lack of advancement of the timing of the His potential, fails to reset the supraventricular tachycardia (SVT). B, An earlier VES fails to advance the timing of the HB but advances the subsequent atrial activation, indicating orthodromic AVRT and excluding atrioventricular nodal reentrant tachycardia (AVNRT). Note that the reset atrial impulse is followed by a prolonged atrial–His bundle (AH) interval caused by decremental anterograde conduction in the atrioventricular node (AVN). However, the local ventriculoatrial (VA) interval (retrograde BT conduction) remains constant. C, An earlier VES delivered before the HB is refractory resets the subsequent atrial activation and terminates the SVT by anterograde atrioventricular (AV) block in the AVN. D, A more premature VES terminates the SVT by retrograde VA block in the BT, excluding atrial tachycardia (AT), but can still occur in AVNRT because the VES is delivered before anterograde activation of the HB and could potentially penetrate the AVN.

The preexcitation index analyzes the coupling interval of the VES (delivered from the RV) that resets orthodromic AVRT as a percentage of the tachycardia CL. A relative preexcitation index (the ratio of the coupling interval to the tachycardia CL) more than 90% of a VES that advances atrial activation during orthodromic AVRT suggests that the BT is close to the site of ventricular stimulation (i.e., RV or septal BT). An absolute preexcitation index (tachycardia CL minus VES coupling interval) of at least 75 milliseconds suggests a left free wall BT, an index of less than 45 milliseconds suggests a septal BT, and an index of 45 to 75 milliseconds is indeterminate.

Resetting and/or Entrainment with Manifest Ventricular Fusion

The relative proximity (conduction time) of the pacing site, the site of entrance to a reentrant circuit, and the site of exit from the circuit to the paced chamber is critical for the occurrence of fusion during resetting and/or entrainment. A requirement for the presence of fusion, independent of the pacing site, is spatial separation between the sites of entrance to and exit from the reentrant circuit. In orthodromic AVRT, the entrance and exit of the reentrant circuit (to and from ventricular tissue) are separated from each other, the entrance being from the HPS and the exit being at the ventricular insertion site of the BT. Therefore, pacing at a site closer to the BT ventricular insertion site (e.g., left ventricular [LV] pacing in the setting of left free wall BTs, and RV pacing in the setting of right-sided or septal BTs) than the entrance of the reentrant circuit to ventricular tissue (i.e., the HPS) would result in fusion of QRS morphology between baseline morphology during orthodromic AVRT and that of fully paced QRS (Fig. 18-30). Manifest ventricular fusion during entrainment is proof that the ventricle is a part of the SVT circuit because fusion is due to collision of the antidromic stimulated wavefront with the orthodromic wavefront from the preceding beat occurring within ventricular myocardium. On the other hand, such phenomena cannot occur during AVNRT because of the lack of spatial separation of the entrance and exit to the AVNRT circuit and because the ventricles are not an obligatory part of the AVNRT circuit.

FIGURE 18-30 Ventricular entrainment of an orthodromic atrioventricular reentrant tachycardia (AVRT) using a concealed superoparaseptal bypass tract. Note that the ΔVA interval (ventriculoatrial interval during ventricular pacing minus VA interval during supraventricular tachycardia [SVT]) is less than 85 milliseconds and the post-pacing interval minus SVT cycle length [PPI – SVT CL] is less than 115 milliseconds, both of which favor orthodromic AVRT over atrioventricular nodal reentrant tachycardia (AVNRT). Additionally, ventricular fusion (between the paced and tachycardia wavefronts) is observed during entrainment (right, pure paced QRS morphology), which is consistent with AVRT and excludes AVNRT. Comparing the His bundle–atrial (HA) interval during the SVT (left) with that during ventricular pacing during normal sinus rhythm at the tachycardia CL (right) demonstrates that the ΔHA interval (HA interval during ventricular pacing minus HA interval during SVT) is −43 milliseconds, which favors orthodromic AVRT over AVNRT; the HA interval is measured from the end of the His potential to the atrial electrogram in the high RA.

Entrainment by Right Ventricular Apical Pacing

This technique can help differentiate orthodromic AVRT with a right lateral or septal BT from AVNRT. The VA interval during ventricular pacing is compared with that during SVT. The ventricle and atrium are activated in sequence during orthodromic AVRT and during ventricular pacing, whereas during AVNRT the ventricle and atrium are activated in parallel. Therefore, the VA interval during orthodromic AVRT approximates that during ventricular pacing. On the other hand, the VA interval during AVNRT is much shorter than that during ventricular pacing (see Fig. 18-30). Therefore, a ΔVA interval (VA interval during ventricular pacing minus VA interval during SVT) of more than 85 milliseconds is consistent with AVNRT, whereas a ΔVA interval of less than 85 milliseconds is consistent with orthodromic AVRT. In addition, evaluation of the post-pacing interval (PPI) versus the tachycardia CL is of value. In AVNRT (typical or atypical), the PPI reflects conduction time from the RV pacing site through the RV muscle and HPS, once around the reentry circuit and back. Therefore, the [PPI – tachycardia CL] difference represents twice the sum of the conduction time through the RV muscle and HPS. In orthodromic AVRT using a septal BT, the PPI reflects the conduction time through the RV to the septum, once around the reentry circuit and back. Hence, the PPI more closely approximates the tachycardia CL in orthodromic AVRT using a septal BT compared with AVNRT (see Fig. 18-30). Therefore, a [PPI – tachycardia CL] difference of more than 115 milliseconds is consistent with AVNRT, whereas a [PPI – tachycardia CL] difference of less than 115 milliseconds is consistent with orthodromic AVRT. For borderline values, ventricular pacing at the RV base can help exaggerate the difference between the PPI and tachycardia CL in the setting of AVNRT, but without significant changes in the setting of orthodromic AVRT, because the site of pacing at the RV base is farther from the AVNRT circuit than the RV apex, but is still close to an AVRT circuit using a septal BT (and in fact is closer to the ventricular insertion of the BT).³⁷

However, there are several potential pitfalls to the criteria discussed above. The tachycardia CL and VA interval are often perturbed for a few cycles after entrainment. For this reason, care should be taken not to measure unstable intervals immediately after ventricular pacing. In addition, spontaneous oscillations in the tachycardia CL and VA intervals can be seen. The discriminant points chosen may not apply when the spontaneous variability is greater than 30 milliseconds. Also, it is possible to mistake isorhythmic VA dissociation for entrainment if the pacing train is not long enough or the pacing CL is too close to the tachycardia CL. Furthermore, this test is less reliable and should be used with caution in patients with left lateral BTs. Additionally, these criteria may not apply to BTs with significant decremental properties, although small decremental intervals are unlikely to provide a false result.

A relatively common phenomenon encountered during entrainment of orthodromic AVRT by ventricular pacing is the prolongation of the AH interval because of either decremental conduction properties of the AVN or (in the presence of dual AVN physiology) a jump of anterograde conduction from the fast pathway to the slow pathway. The prolonged AH interval on the last entrained beat will contribute to prolongation of the PPI that is not reflective of the distance of the pacing site from the circuit. Thus, the [PPI – SVT CL] differences obtained after entrainment of orthodromic AVRT employing a septal BT can actually overlap with those observed after entrainment of AVNRT. Subtracting the increment in AVN conduction time in the first PPI (post-pacing AH interval minus pre-pacing AH interval) from the [PPI – SVT CL] difference (“corrected” [PPI – SVT CL]) has been found to improve the accuracy of this criterion. The difference between AV intervals (post-pacing AV interval minus pre-pacing AV interval) can be taken for the latter adjustment when a His deflection is not clearly visible (assuming the HV interval remains constant). In a study of patients with both typical and atypical forms of AVNRT, as well as orthodromic using septal and free wall BTs, a corrected [PPI – SVT CL] difference of less than 110 milliseconds was found more accurate in identifying orthodromic AVRT from AVNRT than the uncorrected [PPI – SVT CL] difference. The use of change in the VA interval is of course not influenced by prolongation of the AV interval during pacing and does not require correction.^38–40

Differential Right Ventricular Entrainment

As discussed in Chapter 17, differential-site RV entrainment (from RV apex versus RV base) can help distinguish AVNRT from orthodromic AVRT. In orthodromic AVRT, in which the ventricles are an obligatory part of the circuit, the basal pacing site relative to the RV apex is variably related to the circuit, being closer than the RV apex with septal BTs and equidistant with free wall BTs, but the paced wavefront from either RV apex or RV base tends to have, on average, approximately equal access and proximity (electrophysiologically) to the reentrant circuit involved in orthodromic AVRT and, therefore, the time taken to reach the circuit (and hence the PPI) tends to be similar, irrespective of the location of the BT. Conversely, the base of the RV is electrically more distant than the RV apex (where the His-Purkinje network directly inserts) from the AVNRT circuit. Hence, following ventricular entrainment of AVNRT, the difference in PPI from RV base versus RV apex will largely be composed of the extra time required to reach the circuit from the base versus the apex (approximately 30 milliseconds).

Correction of the PPI (to avoid potential error introduced by decremental conduction within the AVN during ventricular pacing) increases the accuracy of this method. The “corrected PPI” is obtained by subtracting any increase in the AV interval of the return cycle beat (as compared with the AV interval during SVT). A differential corrected [PPI – SVT CL] difference of more than 30 milliseconds after transient entrainment was found to be consistent with AVNRT (i.e., corrected [PPI – SVT CL] difference following pacing from the RV base was consistently at least 30 milliseconds longer than that following pacing from the RV apex), and a corrected [PPI – SVT CL] difference of less than 30 milliseconds was observed in all cases of orthodromic AVRT. Additionally, a differential VA interval (ventricular stimulus-to-atrial interval during entrainment from RV base versus RV septum) of more than 20 milliseconds was consistent with AVNRT, whereas a differential VA interval of less than 20 milliseconds was consistent with orthodromic AVRT.⁴¹

Length of Pacing Drive Required for Entrainment

As discussed in Chapter 17, assessing timing and type of response of SVT to RV pacing also can help differentiate orthodromic AVRT from AVNRT with high positive and negative predictive values. In the setting of orthodromic AVRT, once ventricular capture is achieved during RV pacing, the paced wavefront propagates to the ventricular insertion site of the BT quickly and resets the tachycardia. In the setting of AVNRT, on the other hand, where the pacing wavefront has to penetrate the HPS followed by AVN tissue prior to resetting the tachycardia, resetting of the tachycardia is delayed as compared with orthodromic AVRT. When resetting of the SVT occurs after a single paced beat orthodromic AVRT is suggested and AVNRT is generally excluded. On the contrary, if resetting occurs only after at least two beats AVNRT is suggested.⁴²

Atrial Resetting During the Transition Zone

Similar to the concept discussed earlier for entrainment with manifest QRS fusion, perturbation (at least 15 milliseconds) of atrial timing during “transition zone” on initiation of RV pacing (the zone during which the pacing train fuses with anterograde ventricular activation) indicates the presence of a retrogradely conducting BT, and cannot occur in AT or AVNRT unless a bystander retrogradely conducting BT is present (see Chap. 17).⁴³

Termination

Termination of orthodromic AVRT by VES can occur secondary to block of the VES retrogradely in the AV BT, conduction of the VES retrogradely over the AVN-HPS with or without conduction up the BT, or retrograde conduction of the VES up the BT and preexcitation of the atrium and subsequent anterograde block in the AVN-HPS (the most common mechanism) (see Fig. 18-29). Termination of SVT with a single VES strongly suggests orthodromic AVRT as the mechanism of SVT in three settings: when the VES is late-coupled (>80% of tachycardia CL), when the tachycardia CL is less than 300 milliseconds, and when the VES is delivered during HB refractoriness and is associated with no atrial activation.

Maneuvers to Prove Presence of an Atrioventricular Bypass Tract

When VES or ventricular pacing results in eccentric atrial activation sequence, the presence of a BT is strongly suggested. A VES delivered when the HB is refractory (i.e., when the His potential is already manifest or within 35 to 55 milliseconds before the time of the expected His potential) that advances (accelerates) the next atrial activation is diagnostic of the presence of a retrogradely conducting BT. Such a VES has to conduct and advance atrial activation via an AV BT because the HPS-AVN is already refractory and cannot mediate retrograde conduction of the VES to the atrium (see Fig. 18-29). Although such an observation excludes AVNRT, it does not exclude AT or prove orthodromic AVRT, and the preexcited atrial activation can reset or even terminate an AT, whereby the AV BT is an innocent bystander. However, if this VES advances atrial activation with an activation sequence identical to that during the SVT, this suggests that the SVT is orthodromic AVRT and the AV BT is participating in the SVT, although it does not exclude the rare case of an AT originating at a site close to the atrial insertion site of a bystander AV BT. Furthermore, a VES delivered when the HB is refractory may not affect the next atrial activation if the ventricular stimulation site is far from the BT. Conduction from the ventricular stimulation site to the BT, local ventricular refractoriness, and the tachycardia CL all determine the ability of a VES to reach the reentrant circuit before ventricular activation over the normal AVN-HPS.³³

Maneuvers to Prove Presence and Participation of Atrioventricular Bypass Tract in the Supraventricular Tachycardia

One maneuver is a VES delivered when the HB is refractory that delays the next atrial activation. Although such a VES can advance atrial activation during AT through fast retrograde conduction over a bystander BT, it should not be able to delay an AT beat by conduction over the AV BT. Such delay indicates that the VES was conducted with some delay over the AV BT and that the next atrial activation was dependent on this slower conduction; thus, the AV BT is participating in the SVT, proving orthodromic AVRT as the mechanism of the tachycardia. Similarly, a VES delivered when the HB is refractory that terminates the SVT without atrial activation is diagnostic of AVRT. Furthermore, entrainment of the SVT by ventricular pacing that results in prolongation in the surface VA interval indicates that the SVT is orthodromic AVRT mediated by an AV BT in the ventricle contralateral to the site of ventricular pacing; this is analogous to the influence of ipsilateral BBB on the VA interval during orthodromic AVRT (see Fig. 18-30). Exact and paradoxical capture phenomena are also diagnostic of AVRT. VES that captures the atrium at the same coupling interval as that of the VES (exact capture phenomenon) indicates that the ventricular stimulation site is inside the reentrant circuit, because if there were intervening tissue involved, the VA interval would increase and, subsequently, the A-A interval would exceed the VES coupling interval. Similarly, a VES that captures the atrium at a shorter coupling interval than that of the VES (paradoxical capture phenomenon) indicates that the ventricular stimulation site is not only inside the reentrant circuit but also closer to the ventricular insertion site of the AV BT than the initial site of ventricular activation over the AVN-HPS during the SVT, so that the VA interval following the VES is shorter than that during the SVT. This is easier to demonstrate with RV apical pacing during orthodromic AVRT mediated by a right-sided BT.³

Orthodromic Atrioventricular Reentrant Tachycardia: Slowly Conducting Concealed Atrioventricular Bypass Tract (Permanent Junctional Reciprocating Tachycardia)

A VES delivered during PJRT can produce decremental conduction in the BT and prolongation of the VA interval, resulting in possible delay of the next atrial activation (i.e., postexcitation or delay of excitation; see Fig. 18-26). Such a response excludes AT, and when this occurs in response to a VES delivered when the HB is refractory, it is diagnostic of orthodromic AVRT, and excludes both AT and AVNRT. Additionally, a late-coupled VES introduced when the HB is refractory frequently blocks retrogradely in the BT and reproducibly terminates the tachycardia without reaching the atrium, again excluding both AT and AVNRT.

The ability to preexcite the atrium with a VES introduced when the HB is refractory is difficult to demonstrate in PJRT because of the long conduction time over the BT, the decremental conduction properties of the BT, and the fact that the tachycardia CL is just longer than the shortest length at which the BT is capable of retrograde conduction. This can be facilitated by introduction of the PVC at a site closer to the BT ventricular insertion.

Antidromic Atrioventricular Reentrant Tachycardia

Failure of entrainment by ventricular pacing to influence the surface VA interval during SVT excludes AVNRT. In addition, when a VES introduced during the SVT results in retrograde RBBB (i.e., blocks retrogradely in the RB), such RBBB will not change the timing of the next atrial activation in the setting of AVNRT. However, in antidromic AVRT using a right-sided BT, such RBBB will increase the size of the reentrant circuit, because the impulse cannot reach the HB through the RB and has to travel transseptally and then retrogradely over the LB. This results in prolongation in the VA interval and delay in the timing of the next atrial activation. The increment in the VA interval is caused by prolongation of the V-H interval and, if RBBB persists, the SVT will have a long V-H interval.

Antidromic AVRT usually can be terminated by ventricular pacing. Termination occurs by retrograde invasion and concealment in the BT, resulting in anterograde block over the BT following conduction to the atrium through the AVN.

Atrial Pacing at the Tachycardia Cycle Length

Under comparable autonomic tone, 1:1 AV conduction over the AVN should be maintained during atrial pacing at a CL similar to the tachycardia CL. If AV block develops during atrial pacing, AT and orthodromic AVRT are less likely, and AVNRT is the likely mechanism of the SVT. Additionally, the PR and AH intervals during atrial pacing at a CL similar to the tachycardia CL should be comparable to those during orthodromic AVRT. These findings are also observed in the setting of AT. In contrast, the AH and PR intervals during atrial pacing would be longer than those during tachycardia in the setting of AVNRT, assuming the slow pathway has been engaged.

Ventricular Pacing at the Tachycardia Cycle Length

Under comparable autonomic tone status, 1:1 VA conduction over the AVN should be maintained during ventricular pacing at a CL similar to the tachycardia CL. If VA block develops during ventricular pacing, orthodromic AVRT is unlikely, and AT and AVNRT are favored.

It is important to recognize that the atrial activation sequence during ventricular pacing can be mediated by retrograde conduction over the BT, over the AVN, or a fusion of both, and consequently it can be similar to or different from that during orthodromic AVRT.

Ventricular pacing during NSR at a CL similar to the tachycardia results in HA and VA intervals that are shorter than those during orthodromic AVRT, because the HB and atrium are activated sequentially during orthodromic AVRT but in parallel during ventricular pacing (see Fig. 18-30). To help distinguish between orthodromic AVRT and AVNRT, the HA interval is measured from the end of the His potential (where the impulse leaves the HB to enter the AVN) to the atrial electrogram in the high RA recording and the ΔHA interval (HA interval during ventricular pacing minus HA interval during SVT) is calculated. In the setting of orthodromic AVRT the ΔHA interval is typically less than –10 milliseconds. In contrast, in the setting of AVNRT the ΔHA interval is more than –10 milliseconds. This criterion has 100% specificity and sensitivity and positive predictive accuracy for differentiation between AVNRT and orthodromic AVRT. The main limitation of the ΔHA interval criterion is the ability to record the retrograde His potential during ventricular pacing. Retrograde His potential generally appears before the local ventricular electrogram in the HB tracing, and can be verified by the introduction of a VES that causes the His potential to occur after the local ventricular electrogram. Moreover, pacing from different sites (e.g., midseptum) may allow earlier penetration into the HPS and facilitate observation of a retrograde His potential. When the retrograde His potential is not visualized, using the ΔVA interval instead of the ΔHA interval is not as accurate in discriminating orthodromic AVRT from AVNRT. Another limitation is that VA conduction during ventricular pacing may not occur over the BT but propagates preferentially over the HPS-AVN, leading to earlier atrial activation over this pathway than over the BT. If this were the case, the HA interval during ventricular pacing would be shorter than that observed if the atrium were activated via the BT. This would yield a more negative ΔHA interval.

Para-Hisian Pacing During Normal Sinus Rhythm

Technique

Ideally, two quadripolar catheters (one for pacing and one for recording) or a single octapolar catheter (for both pacing and recording) is placed at the distal His bundle–right bundle branch (HB-RB) region. Alternatively, a single quadripolar HB catheter (which is typically used during a diagnostic EP study) is used, taking into account that such an approach would limit the ability to record the retrograde His potential and HA interval.⁴⁴

Overdrive ventricular pacing is performed (from the pair of electrodes on the HB catheter that records activation of the distal HB-RB) at a long pacing CL (>500 milliseconds) and high output. During pacing, direct HB-RB capture is indicated by narrowing of the paced QRS width. The pacing output and pulse width are then decreased until the paced QRS widens, which is associated with a delay in the timing of the retrograde HB potential, indicating loss of HB-RB capture. The pacing output is increased and decreased to gain and lose HB-RB capture, respectively, while local ventricular capture is maintained. Occasionally, the HB can be captured uniquely (without myocardial capture), resulting in a QRS identical to the patient’s normally conducted QRS.⁴⁴

Concept of Para-Hisian Pacing

The para-Hisian pacing site is unique because it is anatomically close but electrically distant from the HB. Para-Hisian pacing at high output simultaneously captures the HB or proximal RB, as well as the adjacent ventricular myocardium. At lower output, direct HB-RB capture is lost and retrograde activation of the HB is delayed because the HB and RB are insulated from the adjacent myocardium and the peripheral inputs to the Purkinje system are located far from the para-Hisian pacing site. By maintaining local ventricular capture while intermittently losing HB-RB capture, retrograde VA conduction can be classified as dependent on the timing of local ventricular activation (BT), HB activation (AVN), or both (fusion).

Para-Hisian pacing can result in capture of the ventricle (indicated by a wide paced QRS), the atrium (indicated by atrial activation in the HB region immediately following the pacing artifact), the HB (indicated by narrow paced QRS), or any combination of these (Fig. 18-31).⁴⁴ Careful attention must be given to minimize the atrial signal seen on the recording from the pacing electrode pair to ensure that local atrial capture does not occur during pacing.

FIGURE 18-31 Para-Hisian pacing in a patient with concealed midseptal bypass tract and right bundle branch block (RBBB). The first complex is a sinus beat with RBBB. The second complex shows capture of the atrium, ventricle, and His bundle–right bundle branch (HB-RB). Atrial capture is indicated by immediate inscription of atrial electrogram following the pacing artifact. It is important to identify this occurrence to avoid erroneous interpretation of the results of para-Hisian pacing. The third and fourth complexes show right ventricle (RV)–only capture, and the last two complexes show RV and HB-RB capture but without atrial capture. Note that the atrial activation sequence and stimulus-atrial (SA) intervals remain unchanged, regardless of whether HB-RB capture occurs, because retrograde ventriculoatrial (VA) conduction occurs over the bypass tract in either case. During RV-only capture, the HB activation occurs after atrial activation, indicating that VA conduction is independent of the atrioventricular node (AVN). Note that para-Hisian pacing could be performed successfully even in the presence of RBBB if capture of the HB-RB is achieved proximal to the site of block. NSR = normal sinus rhythm.

Response to Para-Hisian Pacing

When the ventricle and HB are captured simultaneously, the wavefront activates the ventricles over the HPS and results in a relatively narrow QRS. The wavefront can also travel retrogradely over the AVN to activate the atrium with an S-A interval (i.e., the interval from the pacing stimulus to the atrial electrogram) that represents conduction time over the proximal part of the HB and AVN (i.e., S-A interval = HA interval) because the onset of ventricular activation occurs simultaneously to that of HB activation (i.e., S-H interval = 0).

When the ventricle is captured but not the atrium or HB, the wavefront activates the ventricles by muscle-to-muscle conduction, resulting in a wide QRS with LBBB morphology caused by pacing in the RV. Once the wavefront reaches the RV apex, it conducts retrogradely up the RB and then over the HB and AVN to activate the atrium. In this setting, the S-A interval represents the conduction time from the RV base to the HB (S-H interval) plus the conduction time over the HB and AVN (HA interval). Thus, normally (in the absence of a retrogradely conducing BT), para-Hisian pacing results in a shorter S-A interval when the HB (or HB plus RV) is captured than the S-A interval when only the ventricle is captured (because of the delayed conduction of the impulse to the HB [i.e., S-H interval] when only the RV is captured).

In the presence of a septal AV BT, the S-A interval usually remains fixed regardless of whether or not the HB is being captured, because in both situations the paced impulse travels retrogradely over the AV BT, with constant conduction time to the atrium as long as local ventricular myocardium is being captured. Atrial activation in this setting can be secondary to activation over the BT, especially when only the ventricle is captured, or a result of fusion of conduction over both the AV BT and AVN, especially when both the ventricle and the HB are captured. Nevertheless, because VA conduction time over the BT is faster than that over the AVN, the timing of the earliest atrial activation remains constant (i.e., the S-A and local VA intervals), regardless of whether or not HB-RB capture occurs and regardless of whether or not atrial activation occurs exclusively over the AV BT or as a fusion of conduction over both the AV BT and AVN.

Seven patterns of response to para-Hisian pacing can be observed (Table 18-3 and Fig. 18-32; and see Fig. 18-31). In patients with retrogradely conducing AV BTs, in whom retrograde conduction occurs over both the AVN and BT during para-Hisian pacing, the amount of atria activated by each of the two pathways (atrial fusion) is dependent on four variables: (1) the magnitude of delay in retrograde activation of the HB (i.e., S-H interval); (2) retrograde conduction time over the AVN (HA interval); (3) intraventricular conduction time from the para-Hisian pacing site to the ventricular end of the BT (S-V_BT); and (4) retrograde conduction time over the BT (V-A_BT). The first two variables (S-H plus HA) form the S-A interval resulting from retrograde VA conduction over the AVN, and the latter two variables (S-V_BT plus V-A_BT) form the S-A interval resulting from retrograde VA conduction over the BT. The amount of the atria activated by the AVN is greater during HB-RB capture, secondary to a minimal S-H interval (i.e., S-A interval = HA interval). Loss of HB-RB capture results in prolongation of the S-H interval and, therefore, an increase in the amount of atria activated by the BT, resulting in a change in the retrograde atrial activation sequence. Consequently, a change in the retrograde atrial activation sequence with loss of HB-RB capture always indicates the presence of retrograde conduction over both the BT and AVN. There are four such patterns (patterns 4 through 7). In patterns 4 and 5, HB-RB capture is associated with activation of the atria exclusively by retrograde conduction over the AVN. In patterns 6 and 7, HB-RB capture results in atrial activation over both the AVN and the BT.⁴⁴

TABLE 18-3 Response Patterns to Para-Hisian Pacing

Pattern 1 (AVN/AVN Pattern)

• Retrograde conduction occurs exclusively over the AVN regardless of whether the HB-RB is captured. • Loss of HB-RB capture results in an increase in the S-A interval in all electrograms equal to the increase in the S-H interval, with no change in the atrial activation sequence. The HA interval remains essentially the same. • This response indicates that retrograde conduction is dependent on HB activation and not on local ventricular activation. • This pattern is observed in all patients with AVNRT and is not observed in any patient with a septal or right free wall BT. However, this pattern can be observed in some patients with a left free wall BT or PJRT, in which case retrograde AVN conduction masks the presence of retrograde BT conduction.

Pattern 2 (BT-BT Pattern)

• Retrograde conduction occurs exclusively over a single BT.

• The S-A interval is identical during HB-RB capture and noncapture, indicating that retrograde conduction is dependent on local ventricular activation and not on HB activation.

• This pattern does not exclude the presence of retrograde conduction over the AVN with longer conduction time or a second BT with longer conduction time or located far from the pacing site.

Pattern 3 (BT-BT_L Pattern)

• Retrograde conduction occurs exclusively over a BT.

• Loss of HB-RB capture is associated with a delay in the timing of ventricular activation close to the BT. This results in an increase in the S-A interval in all electrograms, with no change in the atrial activation sequence. The local VA interval, recorded close to the BT, remains approximately the same. The increase in S-A interval is less than the increase in the S-H interval. Therefore, the HA interval is shortened with loss of HB-RB capture, indicating that retrograde conduction cannot be occurring over the AVN. Two mechanisms have been identified accounting for the delay in timing of ventricular activation close to the BT.

• Activation of the HPS results in earlier ventricular activation near some BTs located far from the para-Hisian pacing site, such as left lateral or anterolateral BTs.

• Decreasing the pacing output to lose HB-RB capture occasionally results in a small delay in ventricular activation close to the pacing site.

• Pattern 3 is referred to as the BT-BT_L pattern, where BT_L refers to a lengthening of the S-A interval with loss of HB-RB capture.

Pattern 4 (AVN-BT Pattern)

• Loss of HB-RB capture is associated with atrial activation exclusively over the BT.

• Loss of HB-RB capture results in an increase in S-A and local VA intervals in all electrograms, with the least increase occurring in the electrogram closest to the BT.

• The HA interval shortens, indicating that the atrium near the AVN is activated by the BT before retrograde conduction over the AVN is complete.