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Partial atrioventricular septal defect associated with wolff-parkinson-white syndrome: Perioperative dysrhythmias during the intracardiac repair.

ABSTRACT: Wolff-Parkinson-White syndrome (WPW) is rarely seen in association with atrioventricular septal defect. Although paroxysm's of palpitation due to supraventricular tachycardia can occur in these patients, rare, fatal, ventricular dysrhythmias can also occur. Herein, we report the case of a 20-year-old male patient with partial atrioventricular septal defect and WPW syndrome for intracardiac repair, developing intraoperative Torsades de pointes and postoperative cardiac arrest, adding to the difficulty in overall patient management.

SUBMITTER: Mammen A

PROVIDER: S-EPMC8617382 | biostudies-literature | 2021 Oct-Dec

REPOSITORIES: biostudies-literature

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Partial atrioventricular septal defect associated with wolff-parkinson-white syndrome: Perioperative dysrhythmias during the intracardiac repair.

Mammen Anand A Tewari Prabhat P Horo Pallavi P Pande Shantanu S

Annals of cardiac anaesthesia 20211001 4

Wolff-Parkinson-White syndrome (WPW) is rarely seen in association with atrioventricular septal defect. Although paroxysm's of palpitation due to supraventricular tachycardia can occur in these patients, rare, fatal, ventricular dysrhythmias can also occur. Herein, we report the case of a 20-year-old male patient with partial atrioventricular septal defect and WPW syndrome for intracardiac repair, developing intraoperative Torsades de pointes and postoperative cardiac arrest, adding to the diffi ...[more]

PMID: 34747759

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Project description:While Drs Wolff, Parkinson, and White fully described the syndrome in 1930, prior case reports had described the essentials. Over the ensuing century this syndrome has captivated the interest of anatomists, clinical cardiologists, and cardiac surgeons. Stanley Kent described lateral muscular connections over the atrioventricular (AV) groove which he felt were the normal AV connections. The normal AV connections were, however, clearly described by His and Tawara. True right-sided AV connections were initially described by Wood et al., while Öhnell first described left free wall pathways. David Scherf is thought to be the first to describe our current understanding of the pathogenesis of the WPW syndrome in terms of a re-entrant circuit involving both the AV node-His axis as well as the accessory pathway. This hypothesis was not universally accepted, and many theories were applied to explain the clinical findings. The basics of our understanding were established by the brilliant work of Pick, Langendorf, and Katz who by using careful deductive analysis of ECGs were able to define the basic pathophysiological processes. Subsequently, Wellens and Durrer applied invasive electrical stimulation to the heart in order to confirm the pathophysiological processes. Sealy and his colleagues at Duke University Medical Center were the first to successfully surgically divide an accessory pathway and ushered in the modern era of therapy for these patients. Morady and Scheinman were the first to successfully ablate an accessory pathway (posteroseptal) using high-energy direct-current shocks. Subsequently Jackman, Kuck, Morady, and a number of groups proved the remarkable safety and efficiency of catheter ablation for pathways in all locations using radiofrequency energy. More recently, Gollob et al. first described the gene responsible for a familial form of WPW. The current ability to cure patients with WPW is due to the splendid contributions of individuals from diverse disciplines throughout the world.

Project description:BackgroundPatients with an accessory pathway (AP) have an increased propensity to develop atrial fibrillation (AF), but the mechanism is unknown.ObjectiveThe purpose of this study was to identify crucial risk factors and to test the hypothesis that reflection and/or microreentry of atrial impulses propagating into the AP triggers AF.MethodsFive hundred thirty-four patients successfully treated with radiofrequency ablation of AP at two university hospitals were evaluated. Patients were separated into those with concealed vs those with manifest AP in terms of their propensity to develop AF. To investigate AF triggering mechanisms, linear and branched two-dimensional models of atrium-to-ventricle propagation across a heterogeneous 1 x 6 AP using human ionic kinetics were simulated.ResultsA history of AF was twice as common in patients with manifest AP vs concealed AP irrespective of AP location. AF was more likely to occur in older males and in patients with larger atria. There was no correlation between AF history and AP refractory measures. However, the electrophysiologic properties of APs seemed to fulfill the prerequisites for reflection and/or microreentry of atrially initiated impulses. In the linear AP model, repetitive atrial stimulation resulted in progressively larger delay of atrium-to-ventricle propagation across the passive segment. Eventually, sufficient time for repolarization of the atrial segment allowed for reflection of an impulse that activated the entire atrium and by wavefront-wavetail interaction with a new atrial stimulus AF reentry was initiated. Simulations using the branched model showed that microreentry at the ventricular insertion of the AP could also initiate AF via retrograde atrial activation as a result of unidirectional block at the AP-ventricle junction.ConclusionPropensity for AF in patients with an AP is strongly related to preexcitation, larger atria, male gender, and older age. Reflection and microreentry at the AP may be important for AF initiation in patients with manifest (preexcited) Wolff-Parkinson-White syndrome. Similar mechanisms also may trigger AF in patients without an AP.

Dataset Information

Partial atrioventricular septal defect associated with wolff-parkinson-white syndrome: Perioperative dysrhythmias during the intracardiac repair.

Publications

Partial atrioventricular septal defect associated with wolff-parkinson-white syndrome: Perioperative dysrhythmias during the intracardiac repair.

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