Resumen

CENTURION, OA. Intrinsic vulnerability of the atrial myocardium as genesis mechanism of atrial fibrillation in the Wolff-Parkinson-White syndrome. Mem. Inst. Investig. Cienc. Salud [online]. 2012, vol.10, n.2, pp.47-62. ISSN 1812-9528.

The researchers that described Wolff-Parkinson White (WPW) syndrome for the first time already recognized the existence of an association of this syndrome with atrial fibrillation (AF). AF episodes have been documented in 30% of patients with WPW syndrome. Several histological and electrophysiological modifications of the atrial myocardium such as fibrodegenerative changes, increased dispersion of the refractory periods, delay of the impulse conduction, anisotropic conduction and interaction with the autonomic nervous system have been found associated with the induction, generation and persistence of AF. Through the programmed atrial stimulation with single extrasystole during the electrophysiological study several parameters of increased atrial vulnerability can be induced. For example, the repetitive atrial activity, the fragmented atrial activity and the delay in the interatrial conduction induced by an early extrastimulus in diastole in patients with electrophysiological abnormalities of the atrial myocardium have been used as indicators of atrial vulnerability and as important requirements of the reentry genesis and therefore of the AF. The patients with WPW syndrome and paroxysmal AF have a significantly higher number of abnormally prolonged and fragmented atrial electrograms and a significantly higher electrophysiological abnormality of the atrial muscle than patients with WPW syndrome without paroxysmal AF. These results clearly demonstrate that the pathological atrial myocardium and the intrinsic vulnerability of the atrial myocardium play an important role in the development of AF in patients with WPW syndrome.

Palabras clave : atrial vulnerability; Wolff-Parkinson-White syndrome; abnormal atrial electrogram.

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