4. Preexcitation syndromes, diagnosis and treatment

Page created on August 8, 2021. Last updated on October 30, 2022 at 15:50

Preexcitation syndromes

Preexcitation syndromes are characterised by earlier-than-normal depolarisation of the ventricles due to an accessory conduction pathway which bypasses part of the conduction system. The most important one is Wolff-Parkinson-White syndrome (WPW), but others exist as well, like Lown-Ganong-Levine syndrome. Only WPW will be discussed here.

Wolff-Parkinson-White syndrome

Introduction

The WPW pattern is characterised by the presence of an accessory conduction pathway which bypasses the AV node, called the bundle of Kent. The AV node delays the conduction to the ventricles, but people with WPW have this accessory pathway which doesn’t have this built-in delay, so this accessory pathway causes the depolarisation of the ventricles to occur earlier. This is apparent on the ECG as the “delta wave”, which is where the QRS complex gets a small “head start” at the expense of the PQ interval. The delta wave causes the QRS complex to be wider than normal. However, the delta wave pattern on the ECG may be intermittent. As such, the characteristic ECG findings are the follows:

• Shortened PQ/PR interval (< 120 ms)
• Presence of delta wave
• Widened QRS complex

WPW syndrome is characterised by the presence of WPW pattern and the occurrence of paroxysmal tachycardia. WPW syndrome occurs in as little as 2% of people with WPW pattern. The remaining 98% are asymptomatic.

Treatment

Asymptomatic people with WPW pattern rarely require treatment, although treatment should be considered if they develop an episode of paroxysmal tachycardia. For acute management of tachycardia, see below.

Once terminated, the patient should receive therapy to prevent recurrence of the paroxysmal tachycardia. The first choice is catheter ablation of the accessory pathway. Oral flecainide or propafenone are second line options.

AVRT

The paroxysmal tachycardia is usually an atrioventricular reciprocating/reentry tachycardia (AVRT) or an Afib. AVRT refers to the formation of a re-entry circuit consisting of the AV node and the accessory pathway, usually precipitated by a premature atrial beat. AVRT may be orthodromic, which is the case in 95% of cases, or antidromic, in the remaining cases.

In orthodromic AVRT, the antegrade conduction (from atria to ventricles) occurs through the AV node and the signal travels back from the ventricles to the atria (retrograde conduction) through the accessory pathway. This creates a re-entry circuit which sustains itself, maintaining the tachycardia. Orthodromic AVRT is a narrow-complex tachycardia. There may be retrograde P waves (after the QRS complex), and no delta-wave is visible.

Orthodromic AVRT is treated acutely by the same algorithm as other narrow-complex tachycardias. Haemodynamically unstable paroxysmal tachycardias should be treated with synchronised electrical cardioversion. In stable patients, vagal manoeuvres or IV adenosine can terminate the tachycardia, by blocking the conduction through the AV node, breaking the re-entry circuit.

In antidromic AVRT, the conduction circuit goes the opposite direction. The antegrade conduction is through the accessory pathway, while the retrograde conduction is through the AV node. Antidromic AVRT is a wide-complex tachycardia, and it’s often difficult to distinguish from ventricular tachycardia on an ECG. The delta wave may be visible.

Because antidromic AVRTs can be impossible to distinguish from VT, it should be treated similarly as other wide-complex tachycardias. Haemodynamically unstable paroxysmal tachycardias should be treated with synchronised electrical cardioversion. Stable patients should receive antiarrhythmics. AV-nodal blocking agents like adenosine are contraindicated as they may precipitate pre-excited atrial fibrillation, detailed below.

Pre-excited atrial fibrillation

Atrial fibrillation (or atrial flutter, or other atrial tachycardias) in the setting of WPW (preexcited Afib) is dangerous as the accessory pathway allows atrial impulses to be conducted to the ventricles in a 1:1 ratio without the AV-node’s delay, causing a ventricular rate of 300 bpm or more, which can degenerate into ventricular fibrillation. The patient is usually haemodynamically unstable.

AV-nodal blocking agents are strictly contraindicated in wide-complex tachycardias if one cannot rule out the presence of an accessory pathway for this exact reason. Treatment is by cardioversion or non-AV-blocking antiarrhythmics.