Short PR-interval and ventricular pre-excitation

ECG: This electrocardiogram shows a typical pattern of ventricular pre-excitation: short PR-interval (< 120 ms), delta wave at QRS onset, non-prolonged PJ interval, terminal portion of the QRS with no abnormality;

 Comments: The Wolff-Parkinson-White syndrome is defined by the association of an atrioventricular pre-excitation (bundle of Kent) and paroxysmal supraventricular tachycardias occurring preferentially 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 a majority of cases, the heart is free of other lesions even though the incidence of this type of accessory pathways is increased in patients with hypertrophic cardiomyopathy or Ebstein’s anomaly. Its frequency is probably underestimated due to the presence of intermittent pre-excitations, of atypical or mild forms and of hidden forms. Its frequency decreases after the age of 50, mainly related to the involution of the accessory bundle.

Diagnosis is initially electrocardiographic with demonstration of:

• A typically normal sinus P-wave (in the absence of heart disease)
•  A short PR-interval less than 120 ms; hence the impulse originating from the atrium and descending the bundle of Kent does not encounter any slow-conducting structure and therefore arrives directly at the ipsilateral ventricle which explains the very short time frame between activation of the atrial myocardium and activation of the ventricular myocardium; the PR-interval is often difficult to measure with accuracy, the beginning of the ventriculogram being formed by a slurred pattern which slowly detaches from the isoelectric line; the QRS-complex can occasionally begin before the end of the P-wave;
• A delta wave; the delta wave is named after the triangular pattern of the upstroke of the QRS-complex; premature ventricular activation begins at the ventricular insertion of the accessory bundle; the electrical activation then spreads into 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 originating from the atrium simultaneously descends to the ventricles via two conduction pathways (accessory and nodo-Hisian); ventricular activation begins at the level of the accessory pathway while the impulse simultaneously slowly progresses into the atrioventricular node and then quickly into the bundle of His, bundle branches and the Purkinje network; thus, the end of the QRS is primarily under the dependence of the activation front originating from the normal conduction pathways;
• A wide QRS-complex greater than 120 ms; conversely, the duration of the PJ interval (measured from the beginning of the P-wave to the end of the QRS) remains normal indicating that the widening of QRS-complexes solely impinges on the PR-interval;
• Repolarization disorders that are frequently associated with the abnormal QRS; the direction of the terminal phase is usually opposite to that of the delta wave; these repolarization abnormalities can be attributed to the abnormal activation affecting the beginning of the QRS (same mechanism as for the abnormalities observed in a left bundle branch block or in a paced patient); these abnormalities can fluctuate and render interpretation of a stress test or electrocardiogram difficult in a patient with chest pain;

The pre-excitation pattern can either be fixed or vary depending on various factors. In the bundle of Kent, the conduction velocity remains virtually unchanged. On the other hand, in the normal conduction pathways, the impulse descends more or less rapidly depending on the state of the vago-sympathetic balance at the atrioventricular node which in turn will modulate the degree of fusion and the respective proportions of depolarized ventricular mass by either of the two conduction pathways. A vagal maneuver slows or blocks AV nodal conduction and promotes the emergence of a fully pre-excited pattern. In contrast, an injection of atropine decreases this pattern.

Occasionally, anterograde conduction is present but difficult to visualize (concealed bundle of Kent). For a left lateral pathway, the time taken by the impulse to travel from the sinus node to the left atrium is longer than the transit time to the nodo-Hisian pathway thus explaining the presence of a minimal delta wave. The absence of a septal q wave in leads V5-V6 should suggest an accessory pathway in a patient with palpitations. While the presence of a concealed accessory pathway (no anterograde conduction) does not expose the patient to a risk of sudden death during rapid atrial fibrillation, this is not the case for a masked accessory pathway; indeed, the difficulty in visualizing the accessory pathway stems from the significant distance between the sinus node and the pathway and not to a long refractory period.

Take-home message: The diagnosis of atrioventricular pre-excitation in sinus rhythm is based on the association between a short PR-interval, a wide QRS, a delta wave, a normal terminal QRS portion and frequent repolarization disorders.