Clinical, electrophysiological, molecular, and genetic characteristics of patients with Wolf–Parkinson–White syndrome: literature review

The Wolf–Parkinson–White (WPW) syndrome is a condition with early excitation of the heart ventricles due to the conduction of an electrical pulse along the atrioventricular pathway, such as the Kent, James bundle, and Mahaim fibers; the pulse is usually accompanied by supraventricular tachycardia, atrioventricular reciprocal tachycardia in 95% of cases, and fibrillation, atrial flutter, and other supraventricular tachycardia in other cases. WPW syndrome can be observed in patients of any age, approximately 1–30 per 10,000 people, with male predominance. The disease affects 0.15–0.25% of the population. Sudden cardiac death occurs in one patient per 1000 annually, and sometimes this is the first "business card" of the disease. This is mainly due to the lightning-fast formation of life-threatening arrhythmias, for example, with the transformation of atrial fibrillation into ventricular fibrillation. The morphological substrate is an additional atrioventricular connection. Currently, transcatheter radiofrequency ablation is the standard of the interventional treatment of WPW syndrome. WPW syndrome has a diverse etiology. Numerous studies reported that genetics play a significant role in the development of WPW syndrome. Several genetic predictors of WPW syndrome are presented in the modern literature, which may be relevant in predicting and diagnosing hidden forms of this syndrome, such as course, development of symptoms and manifestations, and reduction of the risks of sudden cardiac death.