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 Figs. 18.4 and 18.5 ). 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 occurs over the normal AV conduction system, and not via the BT (i.e., the ventricle is not preexcited). Orthodromic AVRT accounts for approximately 90% to 95% of AVRT episodes in patients with a manifest BT and 35% of all paroxysmal supraventricular tachycardias (SVTs).

Orthodromic and Antidromic Atrioventricular Reentrant Tachycardias (AVRTs) in a Patient With a Bidirectional Left Posteroseptal Bypass Tract (BT).

Ventricular preexcitation is evident during normal sinus rhythm (NSR) . The narrow complex tachycardia represents orthodromic AVRT using the BT as the retrograde limb of the reentrant circuit. Antidromic AVRT utilizes the BT for anterograde atrioventricular conduction, resulting in wide complex tachycardia.

Antidromic Atrioventricular Reentrant Tachycardia

Antidromic AVRT is a preexcited AVRT whereby an AV BT serves as the anterograde limb and the AVN-HPS serves as the retrograde limb of the reentrant circuit (see Figs. 18.4 and 18.5 ). 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. Other, less frequent, forms of preexcited AVRT utilize one AV BT as the anterograde conduction and a second BT for retrograde conduction or a combination of one BT plus the AVN-HPS in either direction ( eFig. 18.1 ).

Preexcited Atrioventricular Reentrant Tachycardia.

The anterograde limb of the reentry circuit in mediated by a right lateral bypass tract (BT), as indicated by the preexcited QRS morphology. The retrograde limb of the circuit is mediated by a left lateral BT, as indicated by the eccentric atrial activation sequence. A , Atrial electrogram; CS _dist , distal coronary sinus; CS _prox , proximal coronary sinus; H , His bundle potential; HRA , high right atrium; RVA , right ventricular apex.

Clinically, antidromic AVRT is much less frequent than orthodromic AVRT, occurring in less than 5% of patients with WPW syndrome, and can be induced in the electrophysiology (EP) laboratory in less than 10%. The low prevalence of antidromic AVRT is related to the EP properties of the AVN, because good retrograde ventriculoatrial (VA) conduction is required to sustain tachycardia. Clinical presentation, sex, age, and orthodromic AVRT induction appear similar in patients with and without inducible antidromic AVRT. Patients with antidromic AVRT induction more frequently have BTs with more rapid conduction properties than other WPW patients.

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 rarely part of antidromic AVRT if the other limb is the AVN and not a second free-wall BT. Up to 50% to 75% of patients with spontaneous antidromic AVRT have multiple BTs (manifest or concealed), which may or may not be utilized as the retrograde limb during the tachycardia.

Permanent Junctional Reciprocating Tachycardia

Permanent junctional reciprocating tachycardia (PJRT) is a rare form of nearly incessant 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. The incessant nature of PJRT can result in tachycardia-induced cardiomyopathy.

Atrioventricular Nodal Reentrant Tachycardia and Atrial Tachycardia

Both AVNRT and AT can use the bystander BT to transmit impulses to the ventricle (see Fig. 18.4 ). When AVNRT occurs in the WPW syndrome, the arrhythmia can be difficult to distinguish from AVRT without EP testing.

Atrial Fibrillation

The overall incidence of AF in patients with WPW syndrome varies from 12% to 39%. AF is typically paroxysmal. Persistent AF is rare in these patients. AF is most common in patients with anterogradely conducting BTs. Patients with antidromic AVRT, multiple BTs, and BTs that have a short anterograde effective refractory period (ERP) are more prone to develop AF. In individuals with WPW, AF is often preceded by AVRT that degenerates into AF ( Fig. 18.6 ).

Antidromic Atrioventricular Reentrant Tachycardia (AVRT) Converting Into Nonsustained Preexcited Atrial Fibrillation (AF) .

Normal sinus rhythm (NSR) follows. Preexcitation is mediated via a left anterior bypass tract.

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 or other predisposing factors for AF. This observation suggests that the AV BT itself can be related to the genesis of AF, supported by the fact that when the BT is ablated, AF may not recur.

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 EP 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.

AF in younger WPW patients is usually associated with the BT and is unlikely to occur after ablation; in contrast, older patients may have recurrence of AF from causes unrelated to the BT. Nonetheless, recent studies have challenged the role of BT ablation in modulating the risk of AF particularly in adult patients, and show persistently higher rates of AF in WPW patients (hazard ratio, 4.77) compared with the general population despite catheter ablation of the BT. Trends of increased risk of AF in ablated WPW patients suggest that mechanisms other than those directly related to the presence of a BT, such as underlying atrial myopathy, may play a role in AF genesis.

Atrial Flutter

About 4% of WPW patients present with AFL. AFL is the most common (60%) regular preexcited tachycardia in patients with WPW syndrome. AFL is caused by a macroreentrant 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 often 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 can potentially conduct 1:1 to the ventricles during a preexcited tachycardia, making the arrhythmia difficult to distinguish from VT ( see Fig. 12.10 ).

Ventricular Fibrillation and Sudden Cardiac Death

The mechanism of sudden cardiac death (SCD) in patients with WPW is likely the occurrence of AF or AFL with a very rapid ventricular rate, which provokes VF. Although the frequency with which AF with 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 is generally an episode of AVRT. In fact, most patients who have been resuscitated from VF secondary to preexcitation have a previous history of AVRT, AF, or both. Nonetheless, SCD can be the first manifestation of WPW syndrome.

Several factors can help identify the patient with WPW who is at increased risk for VF, including symptomatic AVRT, septal location of the BT, presence of multiple BTs, and male gender. In addition, the risk of SCD associated with WPW appears highest in the first two decades of life. 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 R-R intervals during AF or, alternatively, by measuring the anterograde ERP of the BT. If the BT has a very short anterograde ERP (less than 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 children at risk for SCD, although its positive predictive value in adults is only 19% to 38%.

Drug therapy can be an additional determinant of the risk of VF in patients with preexcitation. Several pharmacological agents can potentially enhance BT conduction and increase the ventricular rate during AF and, hence, increase the risk of VF (see later).

Ventricular Tachycardia

Coexisting VT is uncommon in patients with WPW syndrome because structural heart disease is very infrequent in this young patient population. Naturally, older patients are subject to coronary artery and other diseases that can cause VT.

Demonstration of Intermittent Preexcitation

Intermittent preexcitation has historically been thought to confer a lower risk of SCD than persistent preexcitation. Observation of intermittent loss of the preexcitation pattern on ambulatory monitoring or serial ECGs is generally correlated with a long BT anterograde ERP. The longer refractory period of the BT decreases the frequency of manifest preexcitation during NSR and is expected to lower the risk of mediating rapid preexcited ventricular activation during AF. Nevertheless, EP studies in symptomatic patients with intermittent preexcitation found that 10% to 24% can have BTs capable of conducting at rapid rates during AF (with anterograde ERP or shortest preexcited R-R interval less than 250 milliseconds), perhaps related to autonomic influences. However, similar findings have not yet been demonstrated in asymptomatic patients with intermittent preexcitation.

Intermittent preexcitation can be observed on ambulatory monitoring in up to 67% of patients. It is important, however, to distinguish intermittent preexcitation from inapparent preexcitation (see later) and from a bigeminal ventricular rhythm with a long coupling interval. Although intermittent preexcitation is a predictor of poor anterograde conduction through the BT, it has rarely been observed in some patients with cardiac arrest. Furthermore, the presence of intermittent preexcitation does not predict retrograde conduction properties of the BT nor preclude the development of AVRT.

Loss of Preexcitation During Exercise

Demonstration of a sudden loss of preexcitation (indicated by abrupt loss of the delta wave associated with prolongation of the PR interval and normalization of the QRS) during exercise is consistent with block in the BT and is consistent with a long BT ERP (greater than 300 milliseconds). Importantly, rapid AVN conduction during exercise can potentially mask persistent preexcitation. Therefore only abrupt and complete loss of preexcitation during exercise should be sought as a surrogate of a long anterograde ERP of the BT.

Loss of preexcitation during exercise is a good predictor that the patient is not at risk for VF even during sympathetic stimulation. However, the frequency of block in the BT during exercise is low (approximately 10% to 20%), and thus sensitivity of this test is poor. On the other hand, persistence of preexcitation during exercise stress has a sensitivity of 96% but a specificity of only 17% in predicting either a shortest preexcited R-R less than 250 milliseconds during AF or a BT ERP of less than 250 milliseconds (positive predictive value of 40% and negative predictive value of 88%).

Bypass Tract Conduction Block in Response to Antiarrhythmic Agents

When the administration of ajmaline (1 mg/kg IV over 3 minutes) or procainamide (10 mg/kg IV over 5 minutes) results in complete block of the BT during NSR, a long anterograde ERP (greater than 270 milliseconds) of the BT is likely. The shorter the BT ERP, the less likely it would be blocked by these drugs. Also, the amount of ajmaline required to block conduction over the BT correlates with the duration of the anterograde ERP of the BT. However, the incidence of BT block in response to these drugs is low and, although the occurrence of block predicts a long ERP of the BT, failure to produce block does not necessarily suggest a short ERP. Moreover, pharmacological testing is carried out at rest and therefore does not indicate what effect the drug will have on the BT ERP during sympathetic stimulation, such as exercise, emotion, anxiety, and recreational drug use. Importantly, the specificity of loss of preexcitation after administration of sodium blockers is poor compared to the shortest preexcited R-R intervals during inducible AF. Given these limitations, pharmacologic challenge is no longer routinely utilized.

Evaluation of Ventricular Response During Atrial Fibrillation

During spontaneous or induced AF, the propensity for rapid AV conduction can be judged by the interval between consecutively preexcited QRS complexes. A mean preexcited R-R interval greater than 250 milliseconds and a shortest preexcited R-R greater than 220 milliseconds predict low risk for SCD, with a negative predictive value of more than 95%; however, the positive predictive value is low (20%).

Response of Preexcitation to Transesophageal Atrial Stimulation

There is good correlation between the value of the anterograde ERP of the BT obtained during single-test programmed atrial stimulation and atrial pacing at increasing rates and the ventricular rate during AF. Programmed electrical stimulation of the atrium can be performed by the transesophageal route and the value of the anterograde ERP of the BT can be determined.

Electrophysiological Testing

Programmed atrial stimulation is used to evaluate the anterograde ERP of the BT. Because BT refractoriness shortens with decreasing pacing cycle length (PCL), the ERP should be determined at multiple PCLs (preferably ≤400 milliseconds). In addition, atrial stimulation should be performed close to the BT atrial insertion site to obviate the effect of intraatrial conduction delay. Incremental-rate atrial pacing is performed to determine the maximal rate at which 1:1 conduction over the BT occurs. Induction of AF should be performed to determine the average and the shortest R-R interval during preexcited AF. Atrial and ventricular stimulation is also performed to evaluate inducibility of AVRT as well as the number and location of BTs.

A shortest preexcited R-R interval less than 220 to 250 milliseconds during AF has been shown to be the best discriminator of those at risk of VF, with a high sensitivity (88% to 100%) and a high negative predictive value for identifying children and young adults with WPW syndrome at risk for VF. However, the positive predictive value is low (19% to 38%), largely due to the very low incidence of SCD in these patients. Also, a shortest preexcited R-R interval less than 250 milliseconds during AF has been noted in 20% to 26% of asymptomatic adults with a WPW pattern, and in up to 67% when isoproterenol is administered. Thus, although isoproterenol raises the sensitivity of invasive EP testing, it markedly reduces the specificity.

On the other hand, BT ERP less than 240 milliseconds appears to significantly correlate with only AVRT inducibility, but as an isolated variable, it is less predictive of life-threatening events and exhibits significant overlap between WPW patients with VF and those without VF. The presence of multiple BTs and the ability to induce sustained AVRT, especially when AVRT spontaneously degenerates into AF, have been proposed to predict risk of malignant ventricular arrhythmias. The lack of retrograde conduction over the BT appears to be at lower risk for SCD. However, the predictive value of these criteria remains limited and significant overlap exists.

Symptomatic Patients With Concealed Bypass Tracts

Patients with orthodromic AVRT utilizing a concealed BT are treated in a similar fashion as those with paroxysmal SVT. Vagal maneuvers (including Valsalva and carotid sinus massage) are the first-line intervention for acute conversion of the tachycardia; though the overall success rate is limited (approximately 28%). If SVT persists, adenosine is recommended, and it offers a success rate of 90% to 95%. For refractory tachycardia, IV diltiazem, verapamil, or beta-blockers can terminate orthodromic AVRT in the majority of patients. Synchronized cardioversion is recommended for hemodynamically unstable patients and for those refractory or intolerant to drug therapy ( Fig. 18.7 ).

Acute Treatment of Orthodromic Atrioventricular Reentrant Tachycardia (AVRT) .

^a For rhythms that break or recur spontaneously, synchronized cardioversion is not appropriate. IV, Intravenous.

(From Page RL, Joglar JA, Caldwell MA, et al. 2015 ACC/AHA/HRS guideline for the management of adult patients with supraventricular tachycardia: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. J Am Coll Cardiol . 2016;67:e27–e115.)

Symptomatic Patients With Manifest Bypass Tracts

In patients with manifest preexcitation during NSR presenting with AVRT (orthodromic or antidromic), vagal maneuvers are the first-line intervention for tachycardia termination (see Fig. 18.7 ). For persistent SVT, adenosine is recommended. Importantly, adenosine should be used with caution because it can induce AF with a rapid ventricular rate in the presence of an anterogradely conducting BT. 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.

For refractory AVRT, IV diltiazem, verapamil, or beta-blockers can be considered to block conduction in the AVN, which represents either the retrograde or anterograde limb in the AVRT circuit. AVN blocking drugs, however, are ineffective in patients with preexcited AVRT that utilizes two separate BTs for anterograde and retrograde conduction. Drug treatment directed at the BT (ibutilide, procainamide, flecainide) may also be considered. When drug therapy fails or hemodynamic instability is present, electrical cardioversion should be considered. It is important to note that IV diltiazem and verapamil can result in hemodynamic collapse if the AVRT does not terminate or AF is induced with rapid conduction over the BT degenerating to VF, and one must be prepared for immediate electrical cardioversion if that occurs (see later).

Preexcited Atrial Fibrillation

In patients with AF or AFL, ventricular preexcitation, and rapid ventricular response, prompt direct-current cardioversion is recommended, especially when hemodynamic compromise is present. IV procainamide or ibutilide to restore NSR or slow the ventricular rate may be considered in hemodynamically stable patients. Both drugs slow BT conduction.

Importantly, drugs that preferentially slow AVN conduction without prolonging BT refractoriness (such as verapamil, diltiazem, beta-blockers, adenosine, oral or IV digoxin, and IV amiodarone) can accelerate the ventricular rate and potentially precipitate hemodynamic collapse and VF in high-risk patients. Several mechanisms are probably involved; hypotension produced by some of those medications is followed by a sympathetic discharge that enhances BT conduction. Furthermore, slowing or blocking conduction through the AVN prevents competitive concealed retrograde conduction into the BT by normally conducted beats and, as a result, can potentially enhance conduction over the BT. In addition, the rapid and irregular ventricular rate, hypotension, and sympathetic discharge probably result in fractionation of the ventricular wavefront and VF. Also, digoxin increases the ventricular rate by shortening BT refractoriness. 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. Unlike the IV route of administration, chronic oral amiodarone therapy can slow or block BT conduction.

Symptomatic Patients With Concealed Bypass Tracts

Catheter ablation is considered first-line therapy (class I) for patients with paroxysmal SVT involving a concealed BT (i.e., orthodromic AVRT). However, because concealed BTs are not associated with an increased risk of SCD in these patients, catheter ablation can be presented as one of a number of potential therapeutic approaches, including pharmacological therapy and clinical follow-up alone. When pharmacological therapy is selected for patients with concealed BTs, it is reasonable to consider a trial of beta-blocker therapy, diltiazem, or verapamil ( Fig. 18.8 ). These agents are effective for preventing recurrent tachycardia in approximately 50% of patients. Antiarrhythmic agents may be considered for patients with refractory tachycardia; however, the risk and benefits of these drugs should be carefully considered.

Ongoing Management of Orthodromic Atrioventricular Reentrant Tachycardia (AVRT) .

Drugs listed alphabetically. pt, Patient; SHD, structural heart disease (including ischemic heart disease).

(From Page RL, Joglar JA, Caldwell MA, et al. 2015 ACC/AHA/HRS guideline for the management of adult patients with supraventricular tachycardia: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. J Am Coll Cardiol . 2016;67:e27–e115.)

Symptomatic Patients With Manifest Bypass Tracts

Catheter ablation is considered the treatment of choice for patients with WPW syndrome—that is, patients with manifest preexcitation along with documented arrhythmias (antidromic or orthodromic AVRT or preexcited AF) or symptoms consistent with cardiac arrhythmias. Catheter ablation is curative in more than 95% of patients with a relatively low complication rate (about 3%), and it also obviates the unwanted side effects of pharmacological therapy.

For patients with WPW syndrome who are not candidates for, or prefer not to undergo catheter ablation, antiarrhythmic drugs to block BT conduction are considered (see Fig. 18.8 ). Class IC agents such as flecainide and propafenone (in patients without structural heart disease or ischemic heart disease), and class III drugs, such as sotalol and dofetilide, may be considered. Oral amiodarone is a last resort therapy, given the associated risks of long-term therapy. In general, antiarrhythmic drug therapy can offer symptomatic improvement in up to 90% of patients, although complete disappearance of symptoms is observed in only 30%.

Chronic oral beta-blocker, verapamil, and diltiazem may be used for the treatment of patients with WPW syndrome, particularly if their BT has been demonstrated to be incapable of rapid anterograde conduction. However, these agents must be used with caution and after a discussion with the patient concerning the potential risk of rapid conduction over the BT if AF develops. Digoxin, on the other hand, should be avoided because it can shorten the refractory period of the BT and, hence, is potentially harmful in patients with manifest BTs.

Asymptomatic Patients With Manifest Bypass Tracts

Asymptomatic young WPW patients have about 30% risk of becoming symptomatic, and a very small, but definite risk of life-threatening arrhythmias and SCD. Therefore, in the recent Pediatric and Congenital Electrophysiology Society (PACES) and the Heart Rhythm Society (HRS) expert consensus document on treatment of asymptomatic young WPW subjects, risk stratification is recommended to identify a potential subgroup of patients with BTs with “high-risk” properties that may confer an increased risk for lethal cardiac arrhythmias and in whom the risk-to-benefit ratio favors prophylactic ablation ( Fig. 18.9 ).

Management Algorithm for Young Asymptomatic Patients With Wolf-Parkinson-White Electrocardiogram Pattern.

^a Patients unable to perform an exercise stress test should undergo risk stratification with an electrophysiological study. ^b Prior to invasive testing, patients and their parents/guardians should be counseled on the risks and benefits of proceeding with invasive studies, risks of observation only, and risks of medication strategy. ^c Patients participating at moderate- to high-level competitive sports should be counseled concerning the risk-benefit of ablation. ^d In the absence of inducible atrial fibrillation, the shortest preexcited R-R interval determined by rapid atrial pacing is a reasonable surrogate. SPERRI, Shortest pre-excited R-R interval SVT, supraventricular tachycardia.

(From Cohen MI, Triedman JK, Cannon BC, et al. PACES/HRS expert consensus statement on the management of the asymptomatic young patient with a Wolff-Parkinson-White [WPW, ventricular preexcitation] electrocardiographic pattern. Heart Rhythm . 2012;9:1006–1024.)

Initial risk stratification utilizes noninvasive testing (e.g., Holter monitoring, exercise stress testing) to ascertain true loss of preexcitation at physiological heart rates. Complete and abrupt loss of preexcitation during exercise testing or intermittent loss of preexcitation during ECG or ambulatory monitoring, indicate long anterograde ERP of the BT and help identify patients at low risk of rapid conduction over the BT and SCD ( Box 18.1 ).

Inability to clearly demonstrate absolute loss of ventricular preexcitation on noninvasive testing warrants consideration for transesophageal or intracardiac EP testing. However, the benefits and risk of invasive risk stratification should be based on individual considerations such as age, gender, occupation, and athletic involvement, and should be thoroughly discussed with the patient or, in the case of a child, with the parents. Given the low risk associated with invasive EP testing (0.1% to 1%), it is reasonable to consider this approach for risk stratification in asymptomatic WPW patients. Several EP findings help identify high-risk patients who may benefit from catheter ablation, including: (1) shortest preexcited R-R interval less than 250 milliseconds during induced AF; (2) the presence of multiple BTs; (3) spontaneous degeneration of induced AVRT into preexcited AF; and (4) BT anterograde ERP less than 240 milliseconds. The critical obligatory condition for VF is the presence of a short anterograde functional refractory period of the BT, which is best reflected in the shortest R-R interval between preexcited beats in AF. Although the ability to induce sustained AVRT has been considered by some as a potential risk factor, this has not been supported by recent studies.

The role of isoproterenol challenge during EP testing has not yet been clearly defined. Isoproterenol administration can significantly shorten the shortest preexcited R-R interval and, as a result, increase the proportion of asymptomatic patients in the “high-risk” category. Thus some investigators suggested the use of a more stringent threshold for the shortest preexcited R-R interval (≤220 milliseconds) instead of the threshold adopted by the 2012 PACES/HRS Guidelines (≤250 milliseconds) for definition of “high-risk” BTs when EP testing is performed under the influence of isoproterenol.

In low-risk patients, as determined by noninvasive or invasive testing, it is 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 should incorporate patient education about the potential risks associated with preexcitation and the symptoms of arrhythmias that should prompt them to seek medical attention. 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 help prevent the misdiagnosis of MI and to explain the basis of cardiac arrhythmias in case they develop later. Importantly, WPW patients most susceptible to SCD are symptomatic. Thus the evolution of the clinical status from an asymptomatic state to symptoms (e.g., syncope or palpitations) likely portends a higher risk for SCD. Once WPW patients become symptomatic, catheter ablation may be considered, regardless of the prior risk assessment.

In patients with high-risk BT characteristics, prophylactic catheter ablation is reasonable. A combination of inducible AVRT and short R-R interval during preexcited AF provides the best indication for ablation. Catheter ablation of the BT, regardless of BT characteristics, is also reasonable in asymptomatic patients with high-risk occupations (e.g., school bus drivers, police, and pilots), and is probably reasonable in: (1) patients involved in moderate- to high-intensity competitive sports; (2) patients with structural heart disease; (3) patients with ventricular dysfunction secondary to dyssynchronous contractions; and (4) patients with BT locations associated with lower risk of procedural complications (such as AV block or coronary artery injury), which can counterbalance the potential benefit of ablation. However, because knowledge about the success and complication rates plays a major role in decision-making, the physician must consider his or her own success and complication rates for ablation of the specific location of the BT identified, and that information should be made available to the patient.

It is important to recognize that the majority of adult patients with asymptomatic preexcitation have a benign course with few clinically significant arrhythmic events occurring over time; the risk of SCD is low, is seen mainly in children, and is rarely the initial clinical manifestation. Hence, observation without further evaluation or treatment remains a reasonable option in these patients, even when noninvasive low-risk markers are not evident. 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.

It is important to note that both invasive and noninvasive EP markers, despite their high sensitivity and negative predictive value, lack specificity for identifying patients at risk of life-threatening ventricular arrhythmias, largely due to the very low incidence of SCD. The great majority of individuals with WPW, even with a shortest preexcited R-R interval less than 250 milliseconds during AF, will not experience SCD; thus the positive value of predicting SCD remains very low. Therefore the management of asymptomatic patients with a WPW pattern remains controversial.

The ability of noninvasive risk stratification to identify low-risk patients is low (less than 20%). Hence, according to the 2012 PACES/HRS Guidelines, invasive EP evaluation would be recommended for the majority of young asymptomatic WPW patients, and the majority of those would undergo catheter ablation. A recent report retrospectively examined the consequences of following the published guidelines in 85 asymptomatic patients (less than 18 years old) with ventricular preexcitation ECG pattern persisting at peak exercise, to assess the outcomes of invasive risk stratification applying current guidelines. Approximately 38% of the patients exhibited adverse BT properties at EP study, fulfilling either the class IIA indication (shortest preexcited R-R interval less than 250 milliseconds during AF) or class IIB indication (AVRT inducibility) for catheter ablation. The use of isoproterenol infusion during EP testing shifted an additional 36% of those tested into one of these two indication classes. About 69% of young patients subjected to risk stratification underwent BT ablation as a result of the evaluated BT properties or patient/parental decision.

Although complications of a diagnostic EP study are generally minor and not life-threatening, the risks associated with an ablation procedure are likely at least similar to the risk of SCD in asymptomatic WPW patients. In three large series, procedure-related complications occurred in 1.8% to 8.2% of cases, and death as a consequence of ablation occurred in 0.07% to 0.19%. If routine EP testing were to be performed in the majority of asymptomatic WPW patients, many patients would proceed immediately to catheter 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, which can potentially nullify the benefit of elimination of SCD risk achieved by BT ablation. A recent study using decision analysis software to construct a risk-benefit decision tree for a target population of 20- to 40-year-old asymptomatic patients with WPW, found the decision to ablate resulted in a reduction of 10-year mortality risk of 8.8 patients for 1000 patients. The study suggested that it is necessary to treat 112 asymptomatic patients with WPW to save one life over 10 years.

Finally, the physician and the patient must have a shared understanding of the value of invasive EP study for risk stratification, rather than as a therapeutic tool. These issues have to be resolved before proceeding with invasive measures, and the risks and benefits of proceeding with ablation of BT found not to have high-risk characteristics should be discussed thoroughly with patients in advance of the EP procedure.

Wolff-Parkinson-White Patients and Sports Participation

WPW syndrome accounts for approximately 1% of deaths in athletes. Although many of the cases of SCD with WPW are associated with exercise, training does not alter the EP properties in WPW.

Catheter ablation is the treatment of choice for symptomatic WPW patients (whether or not engaged in athletics). For asymptomatic WPW patients engaged in moderate- to high-level competitive sports, noninvasive and, if needed, invasive risk stratification is advisable. For those with high-risk BT characteristics, ablation of the BT is recommended before clearance for competitive sports because of risk for life-threatening arrhythmias. In low-risk patients, as determined by noninvasive or invasive testing, BT ablation may still be appropriate, but competitive sports may be allowed without ablation, especially when BT ablation confers an unacceptable potential risk (e.g., AV block in the setting of midseptal or superoparaseptal BTs).

Inapparent Versus Intermittent Preexcitation

Intermittent preexcitation.

Intermittent preexcitation is defined as the presence and absence of preexcitation on serial ECGs or ambulatory cardiac monitoring ( Fig. 18.11 ). True intermittent preexcitation is characterized by an abrupt loss of the delta wave (regardless of how fast or slow AVN conduction is), with prolongation (normalization) of the PR interval (reflecting the loss of the faster BT conduction, and the subsequent conduction over the slower AVN), and normalization of the QRS in the absence of any significant change in heart rate.

Intermittent Preexcitation.

Surface electrocardiogram leads II and V1 and intracardiac recordings in a patient with Wolf-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 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. A, Atrial electrogram; CS _dist , distal coronary sinus; CS _prox , proximal coronary sinus; H, His bundle potential; HRA, high right atrium; RVA, right ventricular apex.

The mechanism of intermittent preexcitation is poorly understood, but is likely related to the BT refractory period and cellular connectivity within the BT. Potential mechanisms include (1) phase 3 (i.e., tachycardia-dependent) or phase 4 (i.e., bradycardia-dependent) block in the BT ( see Chapter 10 ); (2) anterograde or retrograde concealed conduction produced by PVCs, premature atrial complexes (PACs), or atrial arrhythmias; (3) BTs with a long ERP and the gap phenomenon in response to PACs; and (4) BTs with a long ERP and supernormal conduction.

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. 18.10 ). 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. 18.11 ), whereas loss of preexcitation associated with a PR interval shorter than the P-delta interval is consistent with inapparent preexcitation. Furthermore, maneuvers that slow AVN conduction (e.g., carotid sinus massage, AVN blockers) would unmask inapparent preexcitation but would not affect intermittent preexcitation.

Orthodromic Atrioventricular Reentrant Tachycardia

The ECG during orthodromic AVRT shows retrograde 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. 18.12 ). The RP interval remains constant, regardless of the tachycardia cycle length (TCL), because it reflects nondecremental retrograde conduction over the BT. QRS morphology during orthodromic AVRT is generally normal and not preexcited, even when preexcitation is present during NSR (see Fig. 18.5 ). Functional bundle branch block (BBB) can be observed frequently during orthodromic AVRT at fast rates (see Fig. 18.12 ). The presence of BBB during SVT in a young person (less than 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.

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.

Orthodromic AVRT tends to be a rapid tachycardia, with rates ranging from 150 to more than 250 beats/min, generally faster in younger people. 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 ( Fig. 18.13 ). The mechanism for QRS alternans is not clear but may partly result from oscillations in the relative refractory period of the distal portions of the HPS.

Electrocardiogram (ECG) of Orthodromic Atrioventricular Reentrant Tachycardia Showing QRS Alternans in Multiple ECG Leads.

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% vs. 25%). Several factors can contribute to ST segment depression in these arrhythmias, including changes in autonomic tone, intraventricular conduction disturbances, a longer 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 (see Fig. 18.5 ). 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 TCL, because it represents nondecremental anterograde 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. 18.14 ). 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.

Surface Electrocardiogram (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. The rhythm is irregularly irregular, and can be associated with very rapid ventricular response caused by the nondecremental anterograde AV conduction over the BT ( Fig. 18.15 ). However, a sustained rapid ventricular rate of more than 180 to 200 beats/min will often create R-R intervals that appear to be regular when the ECG is recorded at 25 mm/s. 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.” This can result from concealed retrograde conduction into the BT or the AVN ( Fig. 18.16 ).

Electrocardiogram of Sinus Rhythm Atrial Fibrillation With Ventricular Preexcitation.

Ventricular preexcitation by the same right superoparaseptal bypass tract. Note the fast ventricular rate during preexcited atrial fibrillation (exceeding 100 beats/min).

Preexcited Atrial Fibrillation.

Note the “clumping” of preexcited and normal QRS complexes, likely due to concealed retrograde conduction into the bypass tract or the atrioventricular node.

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 the BT and AVN. The shorter the anterograde ERP of the BT, the more rapid is the anterograde impulse conduction over the BT 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 during AF abolishes retrograde concealment into the AVN, which in turn allows the AVN to recover its excitability and conduct anterogradely. In turn, these conducted impulses through the AVN can result in retrograde concealment into the BT, causing anterograde block of the BT and, thereby, slowing the ventricular rate.

Atrial Flutter

AFL, like AF, can conduct anterogradely via a BT resulting in a preexcited tachycardia. Depending on the various refractory periods of the normal and pathological AV conduction pathways, AFL can potentially conduct 1:1 to the ventricles during a preexcited tachycardia, making the arrhythmia difficult to distinguish from VT ( see Fig. 12.10 ).

Localization Using the Delta Wave

Delta wave morphology reflects the ventricular insertion site of the BT and, hence, is helpful in approximating the BT location, especially when maximal preexcitation is present. However, during NSR, only partial ventricular preexcitation is usually observed, which limits the accuracy of BT localization based on the surface ECG. In addition, the degree of preexcitation can vary in an individual, depending on heart rate, autonomic tone, and AVN function, as well as the location and EP characteristics of the BT. Therefore it is important first to assess the degree of preexcitation visible throughout the entire ECG and then use only delta wave polarity for localization (the first 20 to 60 milliseconds of the QRS in most cases, unless fully preexcited) rather than the overall QRS polarity, which may vary from each other.

Several algorithms have been developed to predict the anatomic location of manifest BTs based on delta wave polarity on the surface ECG ( Box 18.2 ; Figs. 18.17–18.20 ). 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 MI and ventricular hypertrophy), patient body habitus, and technical variability in ECG acquisition and electrode positioning. The accuracy of these algorithms in more recent studies has not reached the accuracy previously reported by their designers. Therefore these algorithms should be regarded as an orientation rather than a precise localization tool. No single published algorithm offers extremely high sensitivity and specificity for all BT locations. The algorithms appear most accurate in predicting left free-wall BT locations and least accurate in predicting midseptal or right anteroseptal BT locations. Hence, it may be more realistic to initially identify a general area in which the BT is located, and then to apply more subtle criteria from one or more of the algorithms to attempt a more precise localization. This can be achieved by applying some basic rules while maintaining a mental 3-D representation of the mitral and tricuspid annuli and their anatomical relationships to adjacent structures as they lie within the chest (i.e., “attitudinally correct orientation”) while analyzing the ECG and predicting morphology of the preexcited QRS.

Algorithm for Localization of Bypass Tract Using Delta Wave Morphology on the Surface Electrocardiogram.

+, Positive delta wave; ±, isoelectric delta wave; −, negative delta wave; AS, right anteroseptal; CS/MCV, coronary sinus/middle cardiac vein; LAL, left anterolateral; LL, left lateral; LP, left posterior; LPL, left posterolateral; LPS, left posteroseptal; MS, midseptal; PPV, positive predictive value; RA, right anterior; RAL, right anterolateral; RAP, right anterior paraseptal; RL, right lateral; RP, right posterior; RPL, right posterolateral; RPS, right posteroseptal; R/S, R-S wave ratio; Sens., sensitivity; Spec., specificity.

(From Arruda M, Wang X, McClelland J. ECG algorithm for predicting sites of successful radiofrequency ablation of accessory pathways [abstract]. Pacing Clin Electrophysiol . 1993;16:865.)

Stepwise Algorithm for Localization of the Bypass Tract (BT) by Delta Wave Polarity.

Numbers indicate the accuracy of the algorithm for each BT location. LAL, Left anterolateral; LL, left lateral; LP, left posterior; LPL, left posterolateral; LPS, left posteroseptal; MS, midseptal; RA, right anterior; RAL, right anterolateral; RAS, right anteroseptal; RL, right lateral; RP, right posterior; RPL, right posterolateral; RPS, right posteroseptal; R/S, R-S wave ratio.

(From Chiang CE, Chen SA, Teo WS, et al. An accurate stepwise electrocardiographic algorithm for localization of accessory pathways in patients with Wolf-Parkinson-White syndrome from a comprehensive analysis of delta waves and R/S ratio during sinus rhythm. Am J Cardiol . 1995;6:40.)

Algorithm of Bypass Tract Localization Based on Delta Wave Morphology on the Surface Electrocardiogram.

LBBB, Left bundle branch block-type pattern (QRS ≥90 milliseconds in lead I with an rS pattern in leads V1 or V2); LL, left lateral; PS, posteroseptal; RL, right lateral; RAS, right anteroseptal; QRS > 30°, QRS axis >+30°.

(From Fox DJ, Klein GJ, Skanes AC, Gula LJ, Yee R, Krahn AD. How to identify the location of an accessory pathway by the 12-lead ECG. Heart Rhythm . 2008;5:1763–1766.)

Stepwise Electrocardiogram Algorithm for the Determination of Bypass Tract Location.

LA, Left anterior; LL, left lateral; LP, left posterior; LPL, left posterolateral; MS, midseptal; PS, posteroseptal; RA, right anterior; RAS, right anteroseptal; RL, right lateral; RP, right posterior; RPL, right posterolateral.

(From Taguchi N, Yoshida N, Inden Y, et al. A simple algorithm for localizing accessory pathways in patients with Wolff-Parkinson-White syndrome using only the R/S ratio. J Arrhythmia . 2014;30:439–443.)

Of note, the mere presence and the degree of preexcitation can sometimes help in predicting the location of the BT. Posteroseptal and right-sided BTs tend to be associated with a prominent degree of preexcitation because of the proximity to the sinus node, whereas left lateral BTs are often associated with subtle preexcitation. Nevertheless, when preexcitation is prominent, the accuracy of surface ECG localization of manifest BTs tends to be higher for the diagnosis of left free-wall BTs than for BTs in other locations.

On the surface ECG, analysis of delta wave polarity and amplitude progression in precordial leads, and frontal plane horizontal and vertical axes, are valuable for predicting the site of origin of manifest BTs ( Fig. 18.21 ).

Delta Wave Morphology on the Surface Electrocardiogram (ECG) During Ventricular Preexcitation.

Representative surface 12-lead ECG of delta wave morphology (top panels) with the corresponding location of the successful ablation site around the valvular annulus on an anatomic illustration (bottom) . (A) left anterolateral (LAL) ; (B) left lateral (LL); (C) left posterolateral (LPL) ; (D) left posterior (LP) ; (E) left posteroseptal (LPS) ; (F) right posteroseptal (RPS) ; (G) midseptal (MS) ; (H) right anteroseptal (superoparaseptal, RAS ); (I) right lateral (RL) . MV, Mitral valve; TV, tricuspid valve.

(Anatomic illustration of mitral and tricuspid annuli is shown at the bottom [from Netter Images { www.netterimages.com } with permission].)

Localization Using Polarity of the Retrograde P Wave Morphology

The polarity of the retrograde P waves during orthodromic AVRT is dependent on the location of the atrial insertion of the BT, and is helpful in localizing the BT. However, the P wave is usually inscribed within the ST segment and its morphology may not be easily determined.

In general, P wave morphology in leads I and V1 and in the inferior leads is most helpful ( Fig. 18.22 ). A negative P wave vector in lead I is highly suggestive of left free-wall BTs, whereas a positive vector is suggestive of right free-wall BTs. On the other hand, a negative P wave in lead V1 predicts right-sided BTs. P wave polarity in the inferior leads, positive or negative, suggests superior or inferior location of the BT, respectively.

Stepwise Algorithm for Predicting Bypass Tract Location Based on Retrograde P Wave Morphology During Orthodromic Atrioventricular Reentrant Tachycardia.

The accuracy of the algorithm is indicated based on results of a prospective study in 164 patients. The denominator is the total number of patients in that group; the numerator is the number of patients with correct predictions. AVNRT, Atrioventricular nodal reentrant tachycardia; INF, inferior leads (II, III, aVF); LA, left anterior; LL, left lateral; LP, left posterior; LPS, left posteroseptal; RA, right anterior; RAS, right anteroseptal; RMS, right midseptal; RP, right posterior; RPS, right posteroseptal.

(From Tai CT, Chen SA, Chiang CE, et al. A new electrocardiographic algorithm using retrograde P waves for differentiating atrioventricular node reentrant tachycardia from atrioventricular reciprocating tachycardia mediated by concealed accessory pathway. J Am Coll Cardiol . 1997;29:394–402.)

Left free-wall BTs have positive P waves in lead V1 and negative P waves in leads I and aVL. If the retrograde P wave is negative in all three inferior leads, the BT is located at the inferoposterior mitral annulus. As the BT location moves to the lateral mitral annulus, the P wave becomes isoelectric or biphasic in one of the three inferior leads. The P wave becomes positive in all inferior leads for left anterior/anterolateral BTs. Thus, as the BT moves from posterior to anterior locations along the mitral annulus, the positive P wave is seen initially in lead III, followed by lead aVF and lead II.

For right free-wall BTs, the P wave is negative in lead V1 and positive or isoelectric in lead I. If the P wave is positive in all inferior leads, the BT is located in the anterior wall. If the P wave is negative in all inferior leads, the BT is located in the posterior wall. However, moving from the posterior to the anterior location, the positive P wave is seen initially in lead II, followed by lead aVF and lead III.

Posteroseptal BTs display positive P waves in leads V1, aVR, and aVL, and isoelectric or biphasic P waves in lead I. P waves are negative in all inferior leads (II, III, aVF). Left posterior BTs also have negative P waves in the inferior leads, but the P waves are more negative in lead II than in lead III and are more positive in lead aVR than in lead aVL. Discrimination between left and right posteroseptal BTs based on P wave morphology is limited. In contrast, anteroseptal BTs display positive P waves in inferior leads and biphasic P waves in lead V1.

Programmed Atrial Stimulation During 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 remains 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 ( Fig. 18.23 ).

Effect of Atrial Extrastimulation (AES) on Preexcitation.

(A) Preexcitation is manifest during normal sinus rhythm and atrial pacing associated with a short His bundle–ventricular (HV) interval (−11 milliseconds). AES produces decremental conduction over the atrioventricular node (AVN) (with prolonged atrial–His bundle interval) but not over the bypass tract (constant P-delta interval), increasing the degree of preexcitation with the His potential inscribed within the QRS (HV interval of −64 milliseconds). (B) An earlier coupled AES produces more pronounced preexcitation and an HV interval of −93 milliseconds. (C) A more premature AES produces full preexcitation with the His bundle activated retrogradely (H′) , followed by ventriculoatrial conduction over the AVN and an echo beat (atrioventricular reentry). A, Atrial electrogram; CS _dist , distal coronary sinus; CS _prox , proximal coronary sinus; H, His bundle potential; HRA, high right atrium; RVA, right ventricular apex.

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. 18.24 ). Atrial pacing can reveal the presence of multiple BTs ( eFig. 18.4 ). Rare cases of catecholamine-dependent BTs have been reported that require isoproterenol infusion to manifest preexcitation that is absent at baseline.

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, 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. CS _dist , Distal coronary sinus; CS _prox , proximal coronary sinus; HRA, high right atrium; RVA, right ventricular apex.

Atrial Pacing in the Presence of Two Bypass Tracts (BTs).

Surface electrocardiogram and intracardiac recordings during coronary sinus 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) . CS _dist , Distal coronary sinus; CS _prox , proximal coronary sinus; His _dist , distal His bundle; His _mid , middle His bundle; His _prox , proximal His bundle; HRA, high right atrium; RVA, right ventricular apex.

The failure of atrial stimulation to increase the amount of preexcitation can be caused by: (1) markedly enhanced AVN conduction; (2) the presence of another AV BT; (3) pacing-induced block in the AV BT because of a long ERP of the BT (longer than that of the AVN); (4) total preexcitation already present at the basal state caused by prolonged or absent AVN-HPS conduction; (5) decremental conduction in the BT; or (6) the presence of a fasciculoventricular BT rather than an AV BT.

Programmed Ventricular Stimulation During Sinus Rhythm

Retrograde atrial activation sequence.

In the presence of a retrogradely conducting AV BT (whether manifest or concealed), VES during NSR can result in VA conduction over the BT, AVN, both, or neither ( Fig. 18.25 ). Conduction over the BT alone is the most common pattern at short PCLs or short VES coupling intervals. In this setting, the VA conduction time is fairly constant over a wide range of PCLs and VES coupling intervals (given the absence of intraventricular conduction abnormalities or additional BTs). On the other hand, retrograde conduction over both the BT and HPS-AVN is especially common when RV pacing is performed at long PCLs or long VES coupling intervals and in the presence of a left-sided BT. This occurs because it is easier to engage the 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 PCLs and very early VES.

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, and His bundle activation is mediated by retrograde conduction over the left bundle branch. 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 interval following the initiating VES is shorter than that during the SVT, which favors antidromic AVRT over preexcited atrioventricular nodal reentrant tachycardia as the mechanism of the SVT. CS _dist , Distal coronary sinus; CS _prox , proximal coronary sinus; HRA, high right atrium; RVA, right ventricular apex.

Ventricular stimulation resulting in eccentric retrograde atrial activation sequence not consistent with normal conduction over the AVN is consistent with VA conduction over an AV BT (see Fig. 18.25 ). Ventricular pacing can also reveal the presence of multiple BTs ( Fig. 18.26 ). However, a concentric retrograde atrial activation sequence does not exclude the presence of a septal or paraseptal BT or a free-wall BT when VA conduction is mediated by the AVN. In addition, AVN slow pathway conduction can be associated with an eccentric atrial activation sequence in the CS. Accurate analysis of an atrial activation sequence frequently requires the use of multielectrode catheters around the tricuspid annulus and deep in the CS.

Ventricular Pacing Revealing the Presence of Multiple Bypass Tracts (BTs).

The first complex shows sinus rhythm with preexcitation, showing a left free-wall pattern. Four complexes of right ventricular apical (RVA) pacing follow, the first two paced complexes (S) show fusion of retrograde activation over both a left lateral BT (red arrows) , which is present in each complex, and a right lateral BT (blue arrows) . The last two paced complexes conduct over the left lateral BT. Dashed lines aid in comparing activation sequences. CS _dist , Distal coronary sinus; CS _prox , proximal coronary sinus; His _dist , distal His bundle; His _mid , middle His bundle; His _prox , proximal His bundle; HRA, high right atrium.

VES during HB refractoriness.

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 results in atrial activation is diagnostic of the presence of a retrogradely conducting BT. Because the HPS-AVN is already refractory and cannot mediate VA conduction, retrograde atrial activation from ventricular stimulation has to be mediated by a BT.

Furthermore, an early coupled VES that results in an atrial activation that either precedes HB activation ( Fig. 18.27 ) or is associated with an apparent HA interval shorter than that during drive complexes indicates “atrial preexcitation” via an AV BT.

Ventricular Extrastimulation Revealing the Presence of a Bypass Tract (BT).

A retrograde His potential is present on both drive complexes (S1) and following the extrastimulus (arrows) . Although atrial activation also follows each stimulus, it occurs (dashed line) before the inscription of the His potential on the ventricular extrastimulus (S2) . Thus a BT is present because atrial activation is not dependent on His bundle–atrioventricular activation. CS _dist , Distal coronary sinus; CS _mid , middle coronary sinus; CS _prox , proximal coronary sinus; His _dist , distal His bundle; His _mid , middle His bundle; His _prox , proximal His bundle; HRA, high right atrium; RVA, right ventricular apex.

Importantly, 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. 18.25 ). In addition, the lack of such a response does not exclude the presence of unidirectional (anterograde-only) AV BTs.

Differential-site RV pacing.

The response of the VA interval (i.e., the stimulus-to-atrial [SA] interval) and atrial activation sequence to differential-site RV pacing (i.e., RV basal versus RV apical pacing) can help demonstrate or exclude the presence of a retrogradely conducting septal AV BT ( Fig. 18.28 ).

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