Accessory pathway, bundle of Kent and Wolff-Parkinson-White syndrome
Wolff-Parkinson-White syndrome is defined by the combination of an atrioventricular pre-excitation (bundle of Kent) and paroxysmal supraventricular tachycardias preferentially occurring in young patients with a healthy heart. A bundle of Kent is a muscle structure that pierces the atrioventricular fibrous skeleton and provides a direct accessory connection between the atria and the ventricles. In the majority of cases, the heart is devoid of other lesions even if the incidence of this type of accessory pathways is increased in patients with hypertrophic cardiomyopathy or Ebstein's disease. Its frequency is probably underestimated due to the presence of intermittent pre-excitations, either atypical or minor forms as well as concealed forms. Its incidence decreases after the age of 50, mainly in conjunction with the involution of the accessory bundle.
The diagnosis is initially electrocardiographic with evidencing of:
- a P wave most often normal and sinus (in the absence of heart disease)
- a short PR interval less than 120 ms; the impulse arising from the atrium and descending via the bundle of Kent does not encounter any slow-conducting structure and thus arrives directly at the homolateral ventricle, which explains the very short delay between activation of the atrial myocardium and activation of the ventricular myocardium; the PR interval is often difficult to measure accurately with the beginning of the ventriculogram being formed by a slurring that slowly detaches from the isoelectric line; occasionally, the QRS complex may begin before the end of the P wave;
- a delta wave; the delta wave denomination is derived from the triangular pattern of the beginning of the QRS complex; the premature ventricular activation begins at the ventricular insertion of the accessory pathway; the electrical activation then propagates in the surrounding undifferentiated myocardium with a slow conduction velocity; the beginning of the QRS is therefore characteristic with a slurred pattern and slow depolarization slopes;
- a fusion between two activation fronts; the impulse arising from the atrium descends simultaneously toward the ventricles via the 2 conduction pathways (accessory and nodo-Hisian); ventricular activation begins at the accessory level but simultaneously, the impulse progresses in the atrioventricular node (nodal brake) and then rapidly into the bundle of His, the branches and the Purkinje network; the end of the QRS is mainly dependent on the activation front from the normal conduction pathways;
- a broad QRS complex and > 120 ms; on the other hand, the duration of the PJ interval (measured from the beginning of the P wave to the end of the QRS complex) remains normal, which means that the widening of the QRS complex encroaches only on the PR interval;
- repolarization disorders that are frequently associated with QRS abnormalities; the direction of the terminal phase is usually opposite that of the delta wave; these repolarization abnormalities can be attributed to abnormal activation affecting the onset of the QRS (same mechanism as for the abnormalities observed in a left bundle branch block or in a paced patient); these abnormalities can be fluctuating and thus render it difficult to interpret an exercise test or an electrocardiogram in a patient with chest pain;
The pre-excitation pattern may be fixed or can vary depending on several factors. In the bundle of Kent, the conduction velocity is almost always the same. On the other hand, in the normal pathways, the impulse descends more or less rapidly according to the state of the vago-sympathetic equilibrium at the level of the atrioventricular node, which will ultimately modulate the degree of fusion and the respective proportions of ventricular mass depolarized by either of the two pathways. A vagal maneuver slows or blocks the nodal conduction and favors the appearance of a preexcited atrial fibrillation pattern. Conversely, an injection of Atropine decreases this pattern.
Anterograde conduction is sometimes present but difficult to visualize (concealed Kent). For a left lateral pathway, the time required for the impulse to travel from the sinus node to the left atrium is longer than the transit time toward the nodo-Hisian pathway explaining the presence of a minimal delta wave. The absence of a septal q wave in leads V5-V6 should evoke an accessory pathway in a patient with palpitations. While the presence of a hidden accessory pathway (no anterograde conduction) does not expose the patient to the risk of sudden death due to rapid atrial fibrillation, this is not the case for a concealed accessory pathway; indeed, the difficulty in visualizing the accessory pathway is due to a significant distance between the sinus node and the pathway but not to a long refractory period.