Nodoventricular Fibers Research Articles

Electrophysiological manifestations of rare supra-ventricular tachycardias with concealed nodo-ventricular fibers.

To clarify the electrophysiological mechanism of supra-ventricular tachycardias (SVT) with concealed nodo-ventricular (NV) fibers. We studied the intra-cardiac electrograms during electrophysiological study (EPS) of three cases of SVT which concerned concealed NV fibers. Electrophysiological maneuvers including right ventricular apex entrainments, RS2 stimuli, adenosine triphosphate injection and so on were done for differential diagnosis before ablation. Among these patients, one had atrio-ventricular nodal reentrant tachycardia (AVNRT) with a bystander NV fiber; the other 2 had NV fiber mediated orthodromic reentrant tachycardias (NVRT). VA dissociation was observed during SVT in all 3 cases with an antegrade His bundle conduction sequence. Ventricular stimulation at His refractory period reset the H-H intervals and the V-V intervals sequentially, suggesting the existence of a retrogradely conductive accessory pathway. Adenosine injection could terminate these tachycardias. The cycle length of an NVRT prolonged during the status of functional right bundle branch block, suggesting that the fiber located on the right side. Multiple QRS fusion morphologies during ventricular entrainments or ventricular stimulation at His refractory period at a fixed position could be observed in these cases. Concealed NV fibers can either mediate orthodromic reentrant tachycardia or be a bystander of AVNRT. V-A dissociation usually occur during such SVTs. Dissociation of H and V due to entrainment of right ventricular apex is a newly discovered maneuver to differentiate AVNRT from NVRT.

ELECTROPHYSIOLOGICAL MANIFESTATIONS OF SUPRA-VENTRICULAR TACHYCARDIAS WITH CONCEALED NODO-VENTRICULAR FIBERS

Nodo-ventricular (NV) fibers are rare Mahaim's bundles which can mediate supraventricular tachycardias. The electrophysiological phenomena of NV fiber-related tachycardias need to be clarified. We studied the intra-cardiac electrograms during EPS of 3 cases of NV fiber. Several electrophysiological

Non-Wolf Parkinson White (WPW) Preexcitation Syndrome

Mahaim (M) accessory pathway (AP) is an endocardia atrioventricular (AV) node-like structures that connect the atrium to the ventricle. M fibers were first described as accessory connections taking off from the fascicular system to the right ventricle called fasciculoventricular (FV) or from the AV node to the right ventricle called nodoventricular fibers (NV) or connecting the AV node to the fascicles called nodo-fascicular (NF). However, the majority, if not all, of Mahaim AP are atriofascicular connecting the atrium to the fasicular system. We describe two cases with non-WPW accessory pathways and their successful ablation along with a literature review.

A Latent Atrioventricular Decrementally Conducting Accessory Pathway Mimicking a Bystander Nodoventricular Fiber

A 41-year-old woman with recurrent wide-QRS tachycardia is reported. Electrophysiologic findings were consistent with the diagnosis of a preexcited atrioventricular nodal reentrant tachycardia due to a bystander nodo-ventricular fiber. However, slow pathway ablation did not preclude tachycardia recurrence. A second electrophysiology study shed light on the correct mechanism and eventually a successful ablation was achieved.

Cryoablation of a Nodoventricular Mahaim Fiber

An 11-year old female presented with paroxysmal tachycardia and was diagnosed with a Mahaim fiber during electrophysiologic study. A preexcited tachycardia and the typical variety of AV nodal reentry tachycardia were induced at different times. During preexcited tachycardia, the His bundle electrogram followed the ventricular electrogram, and, introduction of atrial premature beats at different coupling intervals, advanced the peri-AV nodal atrial tissue, with no change in the ventricular cycle length, leading to a diagnosis of an antidromic tachycardia due to a nodoventricular fiber. Cryoablation at a mid-septal location under three-dimensional guidance successfully eliminated both tachycardias without detrimental effects to the AV node.

Pathologic Findings Following Sudden Death in an Infant with Hypertrophic Cardiomyopathy and Supraventricular Tachycardia

The cardiac conduction system from infants suddenly dying with hypertrophic cardiomyopathy has not been described. We studied by serial section examination the conduction system from a 13-month old infant also known to have had supraventricular tachycardia. At autopsy, there was cardiomegaly with asymmetric septal hypertrophy. Microscopic examination revealed myofiber disarray around an abnormally formed central fibrous body, numerous nodoventricular fibers to both sides of the ventricular septum, and fibrosis of the left bundle branch. We postulate that supraventricular tachycardia utilized a concealed pathway or the malformed AV junction. Death may have resulted from deranged hemodynamics secondary to supraventricular tachycardia.

Radiofrequency ablation for supraventricular and ventricular tachycardia in young patients

Radiofrequency ablation therapy was conducted in 86 consecutive children and young patients with a mean age of 14 ± 3 years (range = 3–18). Fifty-two patients had Wolff-Parkinson-White syndrome, one had re-entry tachycardia incorporating a nodoventricular fiber, 22 had atrioventricular node re-entry tachycardia, two had atrial tachycardia and nine had idiopathic ventricular tachycardia. Radiofrequency ablation was successful in 50 of the 52 patients (96%) with Wolff-Parkinson-White syndrome and the one with nodoventricular fiber. Radiofrequency modification of the atrioventricular node using the inferior approach was successful in eliminating atrioventricular node re-entry tachycardia in 20 of the 22 patients (91%). Radiofrequency ablation in the two patients with atrial tachycardia was unsuccessful. Of the nine patients with idiopathic ventricular tachycardia, eight from the left ventricle and one from the right ventricular outflow tract, eight were successfully ablated (88%). Follow-up over a period ranging from 1 to 46 months (21 ± 13) revealed a recurrence of tachycardia in seven patients; a late electrophysiological study in 38 patients revealed the induction of tachycardia in 11 patients (seven with accessory pathway-mediated tachycardia, three with atrioventricular node re-entry tachycardia and one with idiopathic ventricular tachycardia). All 11 patients were successfully ablated by a second trial. In conclusion, radiofrequency ablation therapy is effective and safe in pediatric patients with supraventncular and ventricular tachycardia and should be considered as the therapy of choice in this group of patients.

Diagnosis and Surgical Treatment of Tachycardias in Patients with Nodoventricular Fibers

From May, 1982 to April, 1991 25 patients were examined and 23 had open heart surgery for tachycardia with nodoventricular fibers (NVF) participation. All patients suffered tachycardia for more than 5 years. Most patients had syncope. The patients had: true NVF tachycardia (11), atrioventricular node reentry tachycardia (5), orthodromic atrioventricular tachycardia (AVT) (5), and atrial flutter (1) all with passive propagation through NVF, pseudonodoventricular tachycardia (AVT with slow accessory pathways) two patients. In 18 out of the 23 who had surgery there were no signs of preexcitation or tachycardia events in the follow-up period.

Hypothesis Testing as an Approach to the Analysis of Complex Tachycardias-an Illustrative Case of a Preexcitation Variant

The correct elucidation of the electrophysiological substrate and mechanism(s) responsible for a complex arrhythmia requires a systematic approach to the analysis of the electrophysiological data. One approach calls for the formulation of a set of hypotheses that could explain the data obtained during the study. The hypotheses are then tested for compatibility with phenomena observed and the one that agrees with the majority of the findings would represent the most tenable explanation. We present the case of a young girl with a wide QRS complex tachycardia and a history of ventricular preexcitation that illustrates this approach. The complexities were resolved only after intraoperative analysis and surgical ablation of a right-sided accessory pathway with decremental properties, and provides further insight into our understanding of the nodoventricular Mahaim fiber.

Epicardial mapping in patients with “nodoventricular” accessory pathways

Some patients with electrophysiologic features suggesting nodoventricular fibers have been shown to have right parietal atrioventricular (AV) accessory pathways with decremental conduction properties intraoperatively. The experience with 11 patients (7 women and 4 men, mean age ± standard deviation 25 ± 5 years) who had electrophysiologic features consistent with a nodoventricular pathway and who underwent operative correction was reviewed. At electrophysiologic study, all patients had absent or minimal preexcitation in sinus rhythm. During atrial pacing and extrastimulus testing, maximal preexcitation with left bundle branch block morphology developed and the AH and AV intervals progressively prolonged. Preexcited tachycardia was initiated in all patients (AV reentrant tachycardia in 10 patients and AV node reentrant tachycardia in 1 patient). At operation all patients had a right parietal accessory pathway demonstrated. Intraoperative mapping demonstrated the earliest site of ventricular activation during anterograde preexcitation to be at the midanterior right ventricle, consistent with insertion of these pathways into the right bundle branch system, in 7 patients. The ventricular insertion was at the AV groove in 4 patients, in keeping with the typical Wolff-Parkinson-White syndrome. Retrograde conduction over the pathway was not demonstrated in any patient. Two patients had evidence of a second accessory AV pathway in the left paraseptal region. Operative AV node ablation was electively performed in 2 patients without affecting preexcitation in either case. In 1 of these patients, accessory pathway conduction was temporarily abolished by ice mapping in the right anterolateral AV groove. In the remaining 9 patients the accessory pathway was permanently ablated in the right anterolateral AV groove. Three patients underwent operative dissection of the AV node as a concomitant procedure to prevent AV node reentrant tachycardia. All patients in this study with an electrophysiologic presentation suggesting a nodoventricular pathway were found to have a right AV pathway with decremental properties mimicking a nodoventricular pathway. Epicardial activation during anterograde preexcitation suggested ventricular insertion at the base of the heart as for typical AV pathways or insertion in the right bundle branch system.

Cryoablation of Medically Refractory Nodoventricular Tachycardia

Paroxysmal wide QRS tachycardia, based on a nodoventricular accessory connection, is an uncommon arrhythmia. In this report, the endocardial and epicardial mapping and cryoablation of a nodoventricular fiber, documented to participate in medically refractory tachycardia in an 11-year-old boy, are described. Epicardial cryothermia, applied at the earliest site of right ventricular activation, resulted in the abrupt termination of tachycardia. Endocardial cryothermia was subsequently applied in the perinodal region, the presumed site of origin of the nodoventricular fiber. No tachyarrhythmias were inducible postoperatively, and no antiarrhythmic treatment has been required during 18 months of follow-up. Based on precise anatomic localization of the nodoventricular connection, a definitive cure of associated tachyarrhythmias may be possible utilizing cryothermia, without the requirement for extensive intraoperative dissection.

Participation of a concealed nodoventricular fiber in the genesis of paroxysmal tachycardias

An unusual form of tachycardia circuit is described. The circuit incorporates a concealed nodoventricular fiber that conducts in a retrograde path, connects the atrioventricular node and the right ventricle, and also includes the distal portion of the atrioventricular node, the His-Purkinje system, and the ventricle. The study patient was first seen with paroxysmal tachycardias of normal QRS duration, complete right bundle branch block, and complete left bundle branch block. Electrophysiologic studies disclosed poor anterograde atrioventricular nodal conduction with a block proximal to His deflection that occurred at an atrial paced cycle length of 600 msec with no ventriculoatrial conduction. The tachycardias were inducible with two ventricular extrastimuli, had a His deflection that preceded each QRS complex and an HV interval identical to that during sinus rhythm, and revealed ventriculoatrial dissociation. Tachycardia with QRS patterns of right bundle branch block had a cycle 30 to 35 msec longer than tachycardias with either normal QRS duration or complete left bundle branch block. Tachycardias could be entrained by appropriate right ventricular pacing at rates slightly faster than the rate of tachycardia. Tachycardias could be terminated abruptly by an intravenous bolus of either adenosine triphosphate or verapamil.

Electrophysiologic differences between nodoventricular (Mahaim) fiber and atrioventricular accessory fiber with decremental properties

Electrophysiologic differences between nodoventricular (Mahaim) fiber and atrioventricular accessory fiber with decremental properties

A case of nodoventricular fiber with narrow and wide QRS tachycardia with atrioventricular dissociation

A case of nodoventricular fiber with narrow and wide QRS tachycardia with atrioventricular dissociation

Surgical therapy for supraventricular tachycardia, a potentially curable disorder

One hundred fifty-six patients underwent investigation and operation for supraventricular tachycardia: 145 had attempts at curative operations and 11 had His bundle section. Operative mortality was 0.68% and there were no late deaths among patients having curative operations. One patient died suddenly 1 year after His bundle section. All patients underwent electrophysiologic study before discharge and 6 months postoperatively. A satisfactory result, without supraventricular tachycardia and without medication, was achieved in 96.5% of all patients. Ninety-three percent have no supraventricular tachycardia and no demonstrable reentrant pathway at electrophysiologic study. All free wall accessory atrioventricular connections were divided and 97.7% of the patients were cured. Ninety percent of patients with posterior septal accessory atrioventricular connections had a satisfactory result, with cure demonstrated at late electrophysiologic study in 84%. Fifteen patients with atrioventricular junctional reentrant tachycardia were all cured, with preservation of normal atrioventricular conduction. Eight (88%) of nine patients with right atrial tachycardia were cured, and two patients with nodoventricular fibers and one patient with incessant atrioventricular junctional tachycardia had satisfactory results. Supraventricular tachycardia is now a potentially curable disorder when managed by low risk surgical procedures that offer a high cure rate.

Accessory Nodoventricular (Mahaim) Fibers: A Clinical Review

Pacing and Clinical ElectrophysiologyVolume 9, Issue 6 p. 868-884 Accessory Nodoventricular (Mahaim) Fibers: A Clinical Review KENNETH A. ELLENBOGEN, Corresponding Author KENNETH A. ELLENBOGEN Division of Cardiology, Department of Medicine, Duke University Medical Center, Durham, North CarolinaAddress for reprints: Kenneth A. Ellenbogen, M.D., Cardiology Section (111 J). McGuire V.A. Medical Center, 1201 Broad Rock Blvd., Richmond, Virginia 23249.Search for more papers by this authorNORMAN M. RAMIREZ, NORMAN M. RAMIREZ Division of Cardiology, Department of Medicine, Duke University Medical Center, Durham, North CarolinaSearch for more papers by this authorDOUGLAS L. PACKER, DOUGLAS L. PACKER Division of Cardiology, Department of Medicine, Duke University Medical Center, Durham, North CarolinaSearch for more papers by this authorWILLIAM G. O'CALLAGHAN, WILLIAM G. O'CALLAGHAN Division of Cardiology, Department of Medicine, Duke University Medical Center, Durham, North CarolinaSearch for more papers by this authorG. STEPHEN GREEK, G. STEPHEN GREEK Division of Cardiology, Department of Medicine, Duke University Medical Center, Durham, North CarolinaSearch for more papers by this authorANTHONY L. SINTETOS, ANTHONY L. SINTETOS Division of Cardiology, Department of Medicine, Duke University Medical Center, Durham, North CarolinaSearch for more papers by this authorMARCEL R. GILBERT, MARCEL R. GILBERT Division of Cardiology, Department of Medicine, Duke University Medical Center, Durham, North CarolinaSearch for more papers by this authorLAWRENCE D. GERMAN, LAWRENCE D. GERMAN Division of Cardiology, Department of Medicine, Duke University Medical Center, Durham, North CarolinaSearch for more papers by this author KENNETH A. ELLENBOGEN, Corresponding Author KENNETH A. ELLENBOGEN Division of Cardiology, Department of Medicine, Duke University Medical Center, Durham, North CarolinaAddress for reprints: Kenneth A. Ellenbogen, M.D., Cardiology Section (111 J). McGuire V.A. Medical Center, 1201 Broad Rock Blvd., Richmond, Virginia 23249.Search for more papers by this authorNORMAN M. RAMIREZ, NORMAN M. RAMIREZ Division of Cardiology, Department of Medicine, Duke University Medical Center, Durham, North CarolinaSearch for more papers by this authorDOUGLAS L. PACKER, DOUGLAS L. PACKER Division of Cardiology, Department of Medicine, Duke University Medical Center, Durham, North CarolinaSearch for more papers by this authorWILLIAM G. O'CALLAGHAN, WILLIAM G. O'CALLAGHAN Division of Cardiology, Department of Medicine, Duke University Medical Center, Durham, North CarolinaSearch for more papers by this authorG. STEPHEN GREEK, G. STEPHEN GREEK Division of Cardiology, Department of Medicine, Duke University Medical Center, Durham, North CarolinaSearch for more papers by this authorANTHONY L. SINTETOS, ANTHONY L. SINTETOS Division of Cardiology, Department of Medicine, Duke University Medical Center, Durham, North CarolinaSearch for more papers by this authorMARCEL R. GILBERT, MARCEL R. GILBERT Division of Cardiology, Department of Medicine, Duke University Medical Center, Durham, North CarolinaSearch for more papers by this authorLAWRENCE D. GERMAN, LAWRENCE D. GERMAN Division of Cardiology, Department of Medicine, Duke University Medical Center, Durham, North CarolinaSearch for more papers by this author First published: November 1986 https://doi.org/10.1111/j.1540-8159.1986.tb06636.xCitations: 40AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Citing Literature Volume9, Issue6November 1986Pages 868-884 RelatedInformation

Wide QRS Supraventricular Tachycardia Due to Coexisting Mahaim and Kent Pathways

In two patients with Wolff-Parkinson-White syndrome, we observed the unusual coexistence of functional Mahaim and accessory atrioventricular pathways. In the first patient, three types of reciprocating tachycardia were demonstrable: (1) anterograde conduction over the atrioventricular (AV) node with right bundle branch block (RBBB) and retrograde conduction via a right-sided atrioventricular accessory pathway; (2) anterograde conduction through the AV node with RBBB and retrograde conduction via two (right-sided and septal) anomalous pathways; and (3) anterograde conduction through nodoventricular fibers and retrograde conduction over a right-sided accessory pathway. In the second patient the reentry circuit was comprised of AV node fasciculoventricular fiber in an anterograde direction and a right-sided accessory pathway in a retrograde direction. We believe this to be the first report of triple accessory pathways, consisting of two atrioventricular and one nodoventricular connection, demonstrated by intracardiac electrophysiologic study.

Catheter atrioventricular junction ablation for recurrent supraventricular tachycardia with nodoventricular fibers

Patients with nodoventricular (Mahaim) fibers are predisposed to the development of a variety of arrhythmias, which are usually amenable to pharmacologic management. 1 Closed-chest catheter atrioventricular (AV) junction albation, which has been shown to be an effective treatment for supraventricular tachycardia, 2,3 has recently been applied in a patient with tachycardia involving a Mahaim fiber. 5 We report observations in 2 cases in which tachycardia was effectively controlled using this technique, including 3-year follow-up of nodoventricular fiber conduction in 1 patient and absence of retrograde conduction in both patients. The inability of the nodoventricular fibers to conduct retrogradely has not been previously described.

Clinical spectrum of ventricular tachycardia with left bundle branch morphology

Twenty-nine patients with apparent ventricular tachycardia (VT) of left bundle branch block (LBBB) morphology were evaluated. Tachycardia was associated with an organic basis in 24 of 29 patients: 7 had Mahaim fibers of the nodoventricular type, 7 had arrhythmogenic right ventricular dysplasia, 5 had coronary heart disease, 3 had biventricular cardiomyopathy, and 2 had associated congenital heart disease. In many patients the underlying cardiac disease was not readily apparent. In the patients with a Mahaim fiber, the electrocardiogram taken during sinus rhythm was frequently normal. A reentry tachycardia with anterograde conduction over the nodoventricular fiber could mimic VT as diagnosed by the usual criteria; nodoventricular fibers were, therefore, often unsuspected before electrophysiologic evaluation. In patients with arrhythmogenic right ventricular dysplasia, cineangiography demonstrated abnormalities of the right ventricle, but only minor or no abnormalities of the left ventricle. Clinical and electrocardiographic features were not distinctive. Of the 29 patients, 22 had serious symptoms accompanying the tachyarrhythmia or had required cardioversion. Patients were followed up for an average of 20 months: 4 patients died. Thus, VT exhibiting an LBBB morphology is not uncommon and is frequently associated with organic heart disease, serious symptoms, and significant mortality. Right ventricular angiography and electrophysiologic study may clarify the diagnosis in these patients.

Treatment of drug resistant A-V reciprocating tachycardias with multiprogrammable dual demand A-V sequential (DVI,MN) pacemakers.

Programmable dual A-V sequential demand (DVI,MN) pacemakers were implanted in eight patients with recurrent or incessant, drug-refractory, A-V reciprocating tachycardias. This was done after intracardiac studies had identified a variety of electrogenetic mechanisms which include tachycardias involving Kent bundles, (manifest or concealed Wolff-Parkinson-White syndrome), nodoventricular (Mahaim) fibers, enhanced A-V node pathways (Lown-Ganong-Levine syndrome), and dual intranodal pathways. The antitachycardia features of the pacemaker were evaluated during the electrophysiological studies. No immediate postoperative complications occurred after implantation. Furthermore, during the follow-up periods (4 to 20 months), clinical assessment, ambulatory (Holter) monitoring and invasive (as well as noninvasive) evaluations have confirmed continuous effectiveness in recognizing and automatically terminating the tachycardias. Late pacemaker system malfunction has not occurred. The frequency of the tachycardias and the dosage of concomitantly-administered antiarrhythmic medications were significantly reduced. Furthermore, preliminary studies performed in our laboratory suggest that DVI,MN pacemakers may also be useful in certain types of intra-atrial reentry tachycardias coexisting with sinus node dysfunction.