Wolff-Parkinson-White Syndrome (WPW)
What is it?
In 1930, Doctors Wolff, Parkinson, and White reported 11 young, healthy patients with particular ECG characteristics, which included a short PR interval and a branch block-like intraventricular conduction anomaly. These patients suffered from paroxysms of SVT. This clinical picture eventually became known as Wolff-Parkinson-White syndrome (WPW). The anomalies of the QRS complex were initially thought to be related to a short PR and a branch block; Kent first proposed the presence of atrioventricular extra-nodal connections to explain ventricular pre-excitation. One of the main reasons for the interest in WPW syndrome over the years has been associated morbidity and mortality. There is a consolidated relationship between the presence of symptoms and the risk of sudden death (SD). In asymptomatic patients with WPW, the percentage of SD is low and is estimated at about 1:1,000 patient-years. In a young symptomatic patient with WPW syndrome, the incidence of SD during life was estimated at 3-4%. In some patients, ventricular fibrillation was the first manifestation of this syndrome.
Which are the symptoms?
WPW syndrome can occur in the presence of a structurally healthy heart, or it can be associated with numerous cardiac conditions, including various forms of congenital heart disease. Numerous reports outline the association of Ebstein’s anomaly with WPW syndrome, with up to 5% of patients suffering from both conditions in some series of cases. In adults, an association was observed between left accessory pathways and mitral valve prolapse. Left accessory pathways appear to be the most common, however, since mitral valve prolapse is also common in the patient population. Their association may indeed represent the coexistence of two relatively common conditions.
It is important to note that the concept of “WPW pattern” refers to the presence of ventricular pre-excitation on the surface ECG, while “WPW syndrome” is the association of WPW patterns with the symptoms due to tachyarrhythmias. Of all patients who show signs of pre-excitation on the surface ECG, only about 50% develop symptoms during their lifetime. Since WPW syndrome is characterized by the association of electrocardiographic changes and arrhythmias, it can be said that only 45-50% of patients who have pre-excitation on the 12-lead ECG suffer from WPW syndrome.
- palpitations
- dyspnea
- fatigue
- chest pain
How is it diagnosed?
The diagnosis of WPW syndrome is based on the execution of ECG or ECG according to Holter, initially for 24 hours.
Suggested exams
How is it treated?
Pre-excitation therapy has four different objectives: 1. To cure symptoms; 2. Prevent the risk of sudden death; 3. Prevent or cure, in case of chronic tachycardia, the deterioration of ventricular function; 4. Allow subjects with pre-excitement to carry out all activities that are otherwise prohibited by law when there is pre-excitement on the ECG, for example in competitive sports or jobs in professions at risk.
In other cases, therapy is not indicated. In particular, in asymptomatic subjects who present only with the WPW pattern in the absence of arrhythmic symptoms, once specific risk factors are excluded through non-invasive and possibly invasive tests, no treatment is necessary, as the risk of developing dangerous arrhythmias is very limited.
There are four different types of therapeutic approaches: antiarrhythmic drugs, transcatheter ablation of the atrio-ventricular accessory pathways, surgical ablation of the AP, electrical therapy (cardioversion, stimulation).
Radiofrequency ablation (RF) is the procedure of choice for patients with symptomatic WPW syndrome and for those who respond poorly to medical therapy. In the more experienced centers, the success rate is between 95% and 97% with a recurrence rate of 6%. The success of the ablation depends critically on the accurate location of the accessory route. The location of the preliminary route can be obtained from the delta wave and QRS morphologies (see location of accessory pathways from the surface ECG).
In general, the endocavity electrophysiological study precedes the ablation of the accessory pathway, locating its exact location. The ablation procedure is performed under local anesthesia and a mild pharmacological sedation. Multiple venous accesses (usually right femoral and left subclavian) are obtained by the Seldinger technique. If the accessory pathway has a left localization, an arterial access (right femoral artery) is also positioned in order to allow ablation by transaortic approach. Alternatively, the left heart chambers can be reached by transseptal puncture.
The quadripolar diagnostic leads are positioned at the level of the upper right atrium, the bundle of His, at the apex of the right ventricle and in the coronary sinus (cardiac vein that surrounds the left ventricular atrium sulcus and allows to record the electrical activity in the left part of the heart).
The ablation consists of administering thermal energy (radio frequency) near the accessory pathway in order to create irreversible cell damage and therefore make it electrically inert.
Where do we treat it?
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