Babak Nazer1, Tomos E Walters2, Thomas A Dewland1, Aditi Naniwadekar3, Jacob S Koruth4, Mohammed Najeeb Osman5, Anselma Intini5, Minglong Chen6, Jurgen Biermann7, Johannes Steinfurt7, Jonathan M Kalman8, Ronn E Tanel9, Byron K Lee2, Nitish Badhwar10, Edward P Gerstenfeld2, Melvin M Scheinman2. 1. Knight Cardiovascular Institute, Oregon Health & Sciences University, Portland (B.N., T.A.D.). 2. Cardiology Division (T.E.W., B.K.L., E.P.G., M.M.S.), University of California San Francisco. 3. Division of Cardiology, East Carolina University; Greenville, NC (A.N.). 4. Cardiology Division, Mount Sinai Medical Center; New York (J.S.K.). 5. Division of Cardiology, Louis Stokes Cleveland Veterans Affairs Medical Center & Case Western Reserve University, OH (M.N.O., A.I.). 6. Department of Cardiology, The First Affiliated Hospital of Nanjing Medical University, China (M.C.). 7. Department of Cardiology and Angiology, Heart Center Freiburg University, Germany (J.B., J.S.). 8. Department of Cardiology, Royal Melbourne Hospital, Parkville, Australia (J.M.K.). 9. Pediatric Cardiology Division (R.E.T.), University of California San Francisco. 10. Division of Cardiology, Stanford University, CA (N.B.).
Abstract
BACKGROUND: Nodofascicular and nodoventricular (NFV) accessory pathways connect the atrioventricular node and the Purkinje system or ventricular myocardium, respectively. Concealed NFV pathways participate as the retrograde limb of supraventricular tachycardia (SVT). Manifest NFV pathways can comprise the anterograde limb of wide-complex SVT but are quite rare. The purpose of this report is to highlight the electrophysiological properties and sites of ablation for manifest NFV pathways. METHODS: Eight patients underwent electrophysiology studies for wide-complex tachycardia (3), for narrow-complex tachycardia (1), and preexcitation (4). RESULTS: NFV was an integral part of the SVT circuit in 3 patients. Cases 1 to 2 were wide-complex tachycardia because of manifest NFV SVT. Case 3 was a bidirectional NFV that conducted retrograde during concealed NFV SVT and anterograde causing preexcitation during atrial pacing. NFV was a bystander during atrioventricular node re-entrant tachycardia, atrial fibrillation, atrial flutter, and orthodromic atrioventricular re-entrant tachycardia in 4 cases and caused only preexcitation in 1. Successful NFV ablation was achieved empirically in the slow pathway region in 1 case. In 5 cases, the ventricular insertion was mapped to the slow pathway region (2 cases) or septal right ventricle (3 cases). The NFV was not mapped in cases 5 and 7 because of its bystander role. QRS morphology of preexcitation predicted the right ventricle insertion sites in 4 of the 5 cases in which it was mapped. During follow-up, 1 patient noted recurrent palpitations but no documented SVT. CONCLUSIONS: Manifest NFV may be critical for wide-complex tachycardia/manifest NFV SVT, act as the retrograde limb for narrow-complex tachycardia/concealed NFV SVT, or cause bystander preexcitation. Ablation should initially target the slow pathway region, with mapping of the right ventricle insertion site if slow pathway ablation is not successful. The QRS morphology of maximal preexcitation may be helpful in predicting successful right ventricle ablation site.
BACKGROUND:Nodofascicular and nodoventricular (NFV) accessory pathways connect the atrioventricular node and the Purkinje system or ventricular myocardium, respectively. Concealed NFV pathways participate as the retrograde limb of supraventricular tachycardia (SVT). Manifest NFV pathways can comprise the anterograde limb of wide-complex SVT but are quite rare. The purpose of this report is to highlight the electrophysiological properties and sites of ablation for manifest NFV pathways. METHODS: Eight patients underwent electrophysiology studies for wide-complex tachycardia (3), for narrow-complex tachycardia (1), and preexcitation (4). RESULTS:NFV was an integral part of the SVT circuit in 3 patients. Cases 1 to 2 were wide-complex tachycardia because of manifest NFV SVT. Case 3 was a bidirectional NFV that conducted retrograde during concealed NFV SVT and anterograde causing preexcitation during atrial pacing. NFV was a bystander during atrioventricular node re-entrant tachycardia, atrial fibrillation, atrial flutter, and orthodromic atrioventricular re-entrant tachycardia in 4 cases and caused only preexcitation in 1. Successful NFV ablation was achieved empirically in the slow pathway region in 1 case. In 5 cases, the ventricular insertion was mapped to the slow pathway region (2 cases) or septal right ventricle (3 cases). The NFV was not mapped in cases 5 and 7 because of its bystander role. QRS morphology of preexcitation predicted the right ventricle insertion sites in 4 of the 5 cases in which it was mapped. During follow-up, 1 patient noted recurrent palpitations but no documented SVT. CONCLUSIONS: Manifest NFV may be critical for wide-complex tachycardia/manifest NFV SVT, act as the retrograde limb for narrow-complex tachycardia/concealed NFV SVT, or cause bystander preexcitation. Ablation should initially target the slow pathway region, with mapping of the right ventricle insertion site if slow pathway ablation is not successful. The QRS morphology of maximal preexcitation may be helpful in predicting successful right ventricle ablation site.