AVRT & WPW Syndrome
Accessory pathway-mediated tachycardia and pre-excitation syndromes
Mechanism
Atrioventricular reentrant tachycardia (AVRT) is a macroreentrant tachycardia that utilizes an accessory pathway (AP) — an anomalous muscular connection bridging the atrial and ventricular myocardium across the atrioventricular groove, bypassing the normal AV node–His-Purkinje conduction system. These pathways are congenital remnants of the fetal AV ring tissue that normally regresses during cardiac development.
In orthodromic AVRT (the most common form, ~95%), the impulse travels antegradely down the AV node and His-Purkinje system to activate the ventricles, then returns retrogradely up the accessory pathway to activate the atria, completing the circuit. The QRS is narrow because ventricular depolarization occurs via the normal conduction system. In antidromic AVRT (~5%), the circuit reverses: antegrade conduction travels down the accessory pathway (producing a maximally pre-excited, wide QRS) and returns retrogradely up the AV node. Antidromic AVRT can be difficult to distinguish from ventricular tachycardia on the surface ECG.
- Manifest AP: conducts antegradely in sinus → delta wave visible on resting ECG
- Concealed AP: conducts only retrogradely → no delta wave at baseline; only discovered during tachycardia or EP study
- WPW pattern: delta wave + short PR on ECG without symptoms
- WPW syndrome: pre-excitation pattern WITH symptomatic tachycardia
- PJRT: permanent junctional reciprocating tachycardia — incessant orthodromic AVRT via a slowly conducting, decremental posteroseptal AP; presents as long RP tachycardia, often causes tachycardia-mediated cardiomyopathy
The critical danger in WPW syndrome is the development of atrial fibrillation with rapid conduction over the accessory pathway. Unlike the AV node, which has decremental conduction and limits ventricular rates, many accessory pathways conduct in a non-decremental (all-or-none) fashion. If the AP has a short antegrade refractory period, atrial fibrillation can conduct at rates exceeding 300 bpm, producing pre-excited AF — an irregular wide-complex tachycardia that can degenerate into ventricular fibrillation and sudden cardiac death.
ECG Clues
Sinus Rhythm (Pre-excitation)
The classic WPW triad on the resting ECG consists of: (1) short PR interval (<120 ms), reflecting bypass of the normal AV nodal delay; (2) delta wave — a slurred upstroke of the QRS representing early ventricular activation via the AP; and (3) wide QRS (>120 ms) due to the fusion of pre-excited and normally conducted ventricular activation. The degree of pre-excitation depends on the relative contribution of AP vs AV node conduction and the distance of the AP from the sinus node.
- Narrow QRS (normal His-Purkinje activation)
- Heart rate 150–250 bpm, regular
- RP interval 70–120 ms — retrograde P waves visible in the ST segment
- 1:1 VA conduction (the atrium is an obligatory part of the circuit)
- P waves are inverted in the leads facing the AP location (e.g., inverted in I/aVL for left lateral AP)
- Delta wave disappears during AVRT (conduction is through AV node, not the AP antegradely)
Accessory Pathway Localization
The delta wave polarity on the 12-lead ECG provides localization of the AP around the mitral and tricuspid annuli. The Arruda algorithm is the most widely used stepwise approach, analyzing delta wave polarity in specific leads to classify pathways into ~10 anatomic locations.
| AP Location | Delta Wave Axis | Key ECG Features |
|---|---|---|
| Left lateral | Positive in V1, I, aVL | Tall R in V1; most common location (~50%) |
| Left posteroseptal | Positive in V1, negative in III/aVF | Negative delta in inferior leads; consider CS diverticulum |
| Posteroseptal | Isoelectric/negative in II, III, aVF | Mimics inferior MI; may require CS mapping |
| Right free wall | Negative in V1, positive in I | LBBB-like pre-excitation; R/S transition V3–V4 |
| Anteroseptal / para-Hisian | Negative V1, positive in II/III/aVF | Higher AV block risk with ablation; consider cryoablation |
EP Study Findings
Baseline Assessment
In manifest WPW, the baseline intracardiac recordings show a short or negative HV interval (normal: 35–55 ms). The HV is short because the ventricle is pre-excited via the AP before the His bundle activates through the normal conduction system. In maximal pre-excitation, the HV may be negative (V before H on the His catheter). The AH interval is typically normal, reflecting intact AV nodal conduction.
- Earliest ventricular activation in sinus: map the AV groove during sinus rhythm; the AP insertion shows earliest V before the delta wave onset
- Earliest retrograde atrial activation during AVRT: during orthodromic AVRT, the atrial electrogram is earliest at the AP atrial insertion; eccentric CS activation points to left-sided APs
- VA interval during tachycardia: >70 ms (unlike AVNRT, which is typically <70 ms)
- Eccentric retrograde atrial activation: earliest A at CS distal = left lateral AP; earliest A at CS os = posteroseptal AP; concentric activation may suggest a septal pathway
Key Diagnostic Maneuvers
Para-Hisian pacing is the gold standard for proving the presence of a septal AP. Pacing near the His bundle at high output captures both myocardium and the His bundle, while at low output only myocardium is captured. With an AP, retrograde atrial activation sequence and timing remain the same regardless of His capture (because the impulse reaches the atrium via the AP, not the His-AV node). Without an AP, loss of His capture produces a longer stimulus-to-A interval and the activation sequence changes to concentric (retrograde through the AV node).
The shortest pre-excited RR interval (SPERRI) during induced atrial fibrillation is the primary measure of AP conduction capability and sudden death risk. A SPERRI of <250 ms indicates a high-risk pathway capable of conducting at >240 bpm during AF, with significant risk for degeneration to VF. This is a Class I indication for ablation regardless of symptoms. SPERRI 250–300 ms is intermediate risk; >300 ms suggests lower risk.
Additional maneuvers include the PVC during His refractoriness test: during SVT, a PVC delivered when the His bundle is refractory that advances or resets the next atrial electrogram proves the existence of an AP (the PVC can only reach the atrium via the AP since the His-AV node pathway is refractory). This is the single most definitive maneuver to confirm AVRT over AVNRT.
Ablation Targets & Strategy
Catheter ablation of the accessory pathway is the definitive treatment for AVRT/WPW, with overall success rates of approximately 95% and a major complication rate of 1–3%. The approach depends on the AP location around the AV groove.
Left-Sided Pathways
Left-sided APs (left lateral, left posterior, left posteroseptal) are the most common (~50–60%). Access is achieved via retrograde aortic approach (catheter advanced retrograde through the aortic valve and curled under the mitral annulus) or transseptal approach (crossing the interatrial septum to reach the left atrium and map the mitral annulus from the atrial side). The target is the earliest ventricular activation during sinus rhythm or the earliest atrial activation during AVRT at the AV groove. Ablation at the mitral annulus typically achieves excellent tissue contact and high success rates (>95%).
Right-Sided Pathways
Right free wall pathways are ablated along the tricuspid annulus. These pathways have lower success rates (~90%) and higher recurrence rates compared to left-sided pathways, partly due to unstable catheter contact along the tricuspid valve and the thinner tissue at the right AV groove. A steerable sheath often improves stability.
Septal and Para-Hisian Pathways
Anteroseptal and para-Hisian pathways pose the greatest challenge because of their proximity to the compact AV node and His bundle. The risk of AV block is 2–5% for anteroseptal pathways. Cryoablation is strongly preferred in this location, allowing cryomapping at −30°C to confirm AP elimination without permanent damage before creating a definitive lesion at −80°C.
- Loss of pre-excitation: disappearance of the delta wave with normalization of PR and QRS
- Bidirectional block: no antegrade or retrograde AP conduction confirmed by pacing maneuvers
- Non-inducibility: AVRT no longer inducible with programmed stimulation ± isoproterenol
- Waiting period: 30-minute observation to confirm no recurrence of conduction (particularly important for cryoablation)
Posteroseptal and Epicardial Pathways
Posteroseptal APs may have epicardial connections via the coronary sinus (CS) or its branches, including coronary sinus diverticula. If ablation from the endocardial surface at the CS os and posteroseptal tricuspid annulus is unsuccessful, mapping within the CS or its branches (particularly the middle cardiac vein) is required. A CS venogram can identify diverticula. Ablation within the CS carries a risk of coronary artery injury (circumflex artery courses along the CS) and cardiac tamponade.
Key References
- Jackman WM, Wang X, Friday KJ, et al. Catheter ablation of accessory atrioventricular pathways (Wolff-Parkinson-White syndrome) by radiofrequency current. N Engl J Med. 1991;324(23):1605–1611. DOI: 10.1056/NEJM199106063242301
- Arruda MS, McClelland JH, Wang X, et al. Development and validation of an ECG algorithm for identifying accessory pathway ablation site in Wolff-Parkinson-White syndrome. J Cardiovasc Electrophysiol. 1998;9(1):2–12. DOI: 10.1111/j.1540-8167.1998.tb00861.x
- Pappone C, Vicedomini G, Manguso F, et al. Wolff-Parkinson-White syndrome in the era of catheter ablation: insights from a registry study of 2169 patients. Circulation. 2014;130(10):811–819. DOI: 10.1161/CIRCULATIONAHA.114.011154
- Page RL, Joglar JA, Caldwell MA, et al. 2015 ACC/AHA/HRS Guideline for the management of adult patients with supraventricular tachycardia. J Am Coll Cardiol. 2016;67(13):e27–e115. DOI: 10.1016/j.jacc.2015.08.856
- Brugada J, Katritsis DG, Arbelo E, et al. 2019 ESC Guidelines for the management of patients with supraventricular tachycardia. Eur Heart J. 2020;41(5):655–720. DOI: 10.1093/eurheartj/ehz467