Editorial
Volume 5 Issue 9 - 2018
Sudden Cardiac Death Associated to Auriculoventricular Accessory Pathways: Sleeping with the Enemy
Osmar Antonio Centurión1,2*, Judith María Torales1,2 and Laura Beatriz García1,2
1Department of Health Sciences Investigation, Sanatorio Metropolitano, Fernando de la Mora, Paraguay
2Cardiology Department, Clinic Hospital, Asunción National University (UNA), San Lorenzo, Paraguay
*Corresponding Author: Osmar Antonio Centurión, Professor of Medicine, Department of Health Sciences Investigation, Asuncion National University (UNA), Sanatorio Metropolitano, Fernando de la Mora, Paraguay.
Received: July 25,2018; Published: August 14, 2018
Citation: Osmar Antonio Centurión., et al. “Sudden Cardiac Death Associated to Auriculoventricular Accessory Pathways: Sleeping with the Enemy”. EC Cardiology 5.9 (2018): 612-615.
It may be a life-threatening situation when paroxysmal atrial fibrillation (AF) develops in patients with manifested Wolff-Parkinson- White (WPW) syndrome, that is, those who have anterograde conduction via the accessory pathway (AP) [1-4]. In this case, the ventricular rate may fastly accelerate if the AP has a short refractory period leading to ventricular fibrillation. Indeed, the presence of a high risk AP denotes the presence of an undeniable killer, and it is a red alert situation to a probable episode of sudden cardiac death (SCD). Since we do not want to sleep with the enemy, there are several diagnostic and therapeutic maneuvers that should be performed in order to localize and destroy the enemy to overcome a fatal situation caused by the AP [5-9].
A conventional electrocardiogram (ECG) is probable one of the cheapest diagnostic auxiliary method that is easily and widely available in the clinical setting. We can make the diagnosis of manifested WPW syndrome with a simple ECG when we found a short PR interval, a delta wave, and a wide QRS complex. Although, the diagnosis is easily made with the ECG, we still do not know if we are dealing with a high risk AP. At that time, we still do not know the predisposition to develop paroxysmal AF that will lead to fast ventricular response developing ventricular fibrillation and SCD. There are various mechanisms dealing with the development of paroxysmal AF in WPW patients. For example, the convertion of a macroreentrant tachycardia into AF is one of them, specially the antidromic tachycardia. The existence of a functional AP and inducible atrioventricular tachycardia in the electrophysiological laboratory has been found to play an important role in triggering AF in the WPW syndrome. It was demonstrated that these tachycardias can increase the vulnerability of the atrial myocardium due to the fast atrial rate, the augmented sympathetic tone and the stretching of atrial walls. In addition, the electrical properties of the AP and the presence of several AP are distinct mechanisms. It was mentioned that intermittent retrograde conduction over a second AP with faster conduction caused early atrial depolarization as a mechanism of premature atrial contraction that initiates atrial repetitive firing or intratrial reentry in the vulnerable period of the atrium during reciprocating tachycardia or during incremental right ventricular pacing [9]. Moreover, the effects of AP on atrial architecture, and the intrinsic abnormalities of the atrial muscle generating atrial vulnerability are other mechanisms [10-18].
Copyright: © 2018 Osmar Antonio Centurión., et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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