Wolff-Parkinson-White Syndrome

Anatomical basis and mechanism of development

Normally, an electrical impulse originating in the atria passes through the atrioventricular (AV) node, where its natural physiological delay occurs. In WPW syndrome, a patient has an additional conduction pathway connecting the atria and ventricles directly from birth. This specific muscular bridge is called the Kent bundle.

The electrophysiological essence of the syndrome is that the Kent bundle conducts excitation significantly faster than the AV node. The nerve impulse bypasses the normal AV delay, resulting in premature ventricular excitation—almost immediately after atrial depolarization ends.

The phenomenon of dual conduction occurs. The ventricular myocardium depolarizes in a combined manner: one part is excited pathologically fast via the anomalous Kent bundle, while the remaining part undergoes excitation slightly later—when the impulse that traveled the normal pathway through the AV junction reaches it.

Clinical course and symptoms

The presence of an accessory conduction pathway does not always indicate a severe disease. The condition can present in two ways:

• Asymptomatic course. In this case, the syndrome becomes an entirely incidental finding during a routine electrocardiogram in a practically healthy individual.
• Manifestation of arrhythmias. Most often, the syndrome makes itself known in childhood or adolescence. The main clinical manifestation is paroxysms (attacks) of supraventricular tachycardia.

The development of such attacks is based on the re-entry mechanism—the formation of a pathological impulse circulation loop in which the accessory bundle actively participates. In rarer situations, attacks of atrial fibrillation or flutter may occur.

ECG diagnosis: classical triad

The diagnosis of WPW syndrome is established exclusively using electrocardiography. Characteristic changes consist of three main features:

1. Shortening of the P-Q (P-R) interval. Its duration is less than 0.12 seconds. The reason lies in the fact that the impulse traveling through the Kent bundle does not experience physiological delay in the AV node.
2. Alteration of the QRS complex. The complex becomes widened. A specific notch—the $\Delta$ wave (delta wave)—appears on its initial upslope. It graphically reflects the very same premature depolarization of a section of the ventricles via the Kent bundle. The rest of the QRS complex is formed by the normal impulse that passed through the AV junction with a delay.
3. Secondary repolarization abnormalities. Displacement of the ST segment and a change in T wave polarity are observed. The syndrome is characterized by discordance—meaning the T wave and ST segment are directed opposite to the direction of the main vector of the widened QRS complex.

Topographic diagnostics (typing)

The ECG allows not only making the diagnosis but also presuming the exact anatomical location of the accessory conduction pathway. For this, the polarity of the delta wave in chest lead $V_1$ is evaluated:

• Type A: the $\Delta$ wave in lead $V_1$ is directed upward (positive).
• Type B: the $\Delta$ wave in lead $V_1$ is directed downward (negative).

Briefly: answers to topical questions

Class and exam questions

What else to study on this topic

• Clerg-Levy-Cristesco (CLC) syndrome and its ECG criteria
• Electrophysiological mechanism of re-entry in tachycardias
• Features of atrial fibrillation and flutter with accessory pathways
• Differential diagnosis of supraventricular tachyarrhythmias

Other topics in the "Cardiovascular system" section

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