Treatment Study of AV Node Reentry Tachycardia
Treatment Study of AV Node Reentry Tachycardia
Compare the effectiveness and safety of two techniques for modification of slow AV nodal
 pathway conduction underlying AVNRT: 1) New Ablation Technique, low voltage and wave front
 collision mapping vs. 2) the Standard Ablation Technique, an anatomical/electrogram approach.
Supraventricular tachycardia (SVT) is an arrhythmia condition that affects 1 in 250 to 1/1000
 children. While there are many different mechanisms for SVT, having an additional electrical
 pathway in the heart is the most common underlying reason. The extra electrical pathway may
 be in the form of an accessory AV pathway that bridges the atrium and ventricle or a slowing
 conducting pathway in the AV nodal region. SVT may cause significant disability from the
 sudden unexpected rapid increase in heart rate. Symptoms associated with SVT may include
 dizziness, syncope, shortness of breath, chest pain and exercise intolerance. Prolonged
 episodes that do not self terminate may require the patient to be evaluated in an emergency
 room. If left untreated, SVT may result in congestive heart failure and the potential for
 sudden cardiac arrest.

 Catheter based ablation involves the localized application of energy to the site responsible
 for the SVT, effecting a permanent cure. Ablation has become the primary mode for treating
 patients with SVT. Ablation is achieved by the focal and limited application of energy
 (either heating the tissue to temperatures beyond viability, radiofrequency energy (RF)) or
 cooling the tissue (cryoablation)) to functionally destroy the underlying myocardial tissue.
 Both energy sources are very effective in achieving this end point, and the elimination of
 arrhythmias.

 SVT involving the AV node, known as AV node reentry tachycardia (AVNRT), is one of the most
 common forms of this arrhythmia. While a conceptual construct for understanding AV node
 reentry tachycardia has evolved over the years, the subtleties of the exact pathophysiologic
 mechanism leading to its occurrence is undefined. Most of the medical literature endorses the
 concept of two (dual) inputs into the compact AV node. Circus movement or reentry
 incorporating the fast and slow pathways (two AV nodal pathways) is thought to facilitate
 this form of SVT. Current ablation practice is centered on modification of the slow AV nodal
 pathway conduction, leaving the fast AV nodal pathway intact so as to allow for a normal
 conduction interval between the atrium and ventricule, the PR interval.

 Approaches for ablation of the slow AV nodal pathway differ among pediatric centers. The two
 most used techniques for ablation of the slow AV nodal pathway to prevent AV nodal reentry
 tachycardia involve: 1) an anatomical/electrogram approach based on physical position of the
 ablation catheter and the electrogram morpholog (Standard Technique), and 2) mapping of
 electrogram voltage in the triangle of Koch to define an area of low voltage with assessment
 of the site for wave front collision of electrical activity traveling over the fast and slow
 AV nodal pathways (New Technique).
Inclusion Criteria:

 1. Weight >15 kg

 2. Age < 21 years old

 3. Simple CHD acceptable to enroll (Table 1):

 Table 1. Diagnoses in Adult Patients with Simple Congenital Heart Disease

 -  Isolated congenital aortic valve disease

 -  Isolated congenital mitral valve disease (eg, except parachute valve, cleft leaflet)

 -  Small atrial septal defect

 -  Isolated small ventricular septal defect (no associated lesions)

 -  Mild pulmonary stenosis

 -  Small patent ductus arteriosus

 -  Repaired conditions

 -  Previously ligated or occluded ductus arteriosus

 -  Repaired secundum or sinus venosus atrial septal defect without residua

 -  Repaired ventricular septal defect without residua

 Exclusion Criteria:

 1. Additional mechanism(s) for SVT in addition to AV nodal reentry tachycardia.

 2. Moderate or Complex Congenital Heart Disease, see tables 2 and 3.

 Table 2. Diagnoses in Adult Patients with Congenital Heart Disease of Moderate Complexity

 -  Aorto-left ventricular fistulas

 -  Anomalous pulmonary venous drainage, partial or total

 -  Atrioventricular septal defects (partial or complete)

 -  Coarctation of the aorta

 -  Ebstein's anomaly

 -  Infundibular right ventricular outflow obstruction of significance

 -  Ostium primum atrial septal defect

 -  Patent ductus arteriosus (not closed)

 -  Pulmonary valve regurgitation (moderate to severe)

 -  Pulmonary valve stenosis (moderate to severe)

 -  Sinus of Valsalva fistula/aneurysm

 -  Sinus venosus atrial septal defect

 -  Subvalvular AS or SupraAS (except HOCM)

 -  Tetralogy of Fallot

 -  Ventricular septal defect with:

 -  Absent valve or valves

 -  Aortic regurgitation

 -  Coarctation of the aorta

 -  Mitral disease

 -  Right ventricular outflow tract obstruction

 -  Straddling tricuspid/mitral valve

 -  Subaortic stenosis

 Table 3. Types of Adult Congenital Heart Disease - Severe Complexity

 -  Conduits, valved or nonvalved

 -  Cyanotic congenital heart (all forms)

 -  Double-outlet ventricle

 -  Eisenmenger syndrome

 -  Fontan procedure

 -  Mitral atresia

 -  Single ventricle (also called double inlet or outlet, common, or primitive)

 -  Pulmonary atresia (all forms)

 -  Pulmonary vascular obstructive disease

 -  Transposition of the great arteries

 -  Tricuspid atresia

 -  Truncus arteriosus/hemitruncus

 -  Other abnormalities of atrioventricular or ventriculoarterial connection not included
 above (ie, crisscross heart, isomerism, heterotaxy syndromes, ventricular inversion)