Mahaim Fibre Tachycardia: Recognition and Management\n

\n\n Dr. Gallagher et al1 wrote 22 years ago that "the role of Mahaim fibers in the genesis of cardiac arrhythmias in man has been controversial since they were first described " in the late 30's by Dr. Ivan Mahaim2. The very early reports were strictly anatomical studies2,3,4,5,6. This histopathologic quest did not end yet. Mahaim fibers were supposed to be accessory connections taking off from the His bundle and fascicles (FV-fasciculoventricular) to the right ventricle or from the atrioventricular node (NV-nodoventricular fibers) to the right ventricle. Anderson et al7 proposed 2 varieties of NV fibers, one that arises from the transitional zone and the other which inserted from the deep, compact nodal portion of the AV junction. In his pioneering work HJJ Wellens paved the road for clinical electrophysiological investigation. He was the first to study a patient with accessory pathway with decremental properties and long conduction times assuming its relationship with the fibers described long ago by "Mahaim", as reported in his doctoral thesis8 in 1971. The term nodofascicular (NF) was applied when the retrograde His bundle potential preceded the ventricular deflection, while nodoventricular pathway would be appropriate when the retrograde His bundle deflection followed the ventricular potential. It took some years to electrophysiologists realize the conceptual mismatch among the "Mahaim" physiology and structure described by Mahaim et al. An important observation was done in 1978 by Becker et al5 who found an accessory node associated with a bundle of specialized fibers measuring 1 cm and coursing through the right ventricle, mimicking a second AV conduction system located on the lateral tricuspid annulus. However, that did not change the mainstream concept of NV fibers. During the early 80's many centers started to refer patients with drug refractory tachycardias to surgical treatment. According to the current concepts at that time targeting the A-V node would be the logic strategy for curative treatment of patients with NV/NF fibers. Some courageous electrophysiologists used a new technique consisting of high-energy catheter ablation of the A-V node to treat a patient with "Mahaim" fiber, which yielded complete AV block and persistent preexcitation9. The turning point came in 1988 at the University Hospital of Western Ontario, Canada, when Klein, Guiraudon et al10 had decided to extensively freeze the A-V node and upper His bundle region of a 29 year old man and they soon realized that preexcitation did not go away. It became clear for them that his accessory pathway was not linked whatsoever to the A-V node. The next patient was luckier, and had kept intact his A-V node, while his "Mahaim fibers" were successfully severed after ice mapping produced a consistent zone of reversible block in the accessory pathway at the right lateral aspect of the tricuspid annulus. Klein's manuscript was received on August 24, 1987, and published the next year on JACC. Two months later (October 20, 1987) Circulation received a manuscript from Tchou P et al11 entitled "Atriofascicular connection or a nodoventricular fiber? Electrophysiologic elucidation of the pathway and associated reentrant circuit". From a single case report we were taught how simple it is to make sure that such pathways arise from the atrium. In recent years catheter ablation techniques have shed more light on the subject. Discrete "Mahaim" potentials that are considered surrogates of pseudo-Mahaim tissue depolarization, are used as an effective target for ablation12,13. A number of pharmacologic14 and histologic data5,6,15,16, electrophysiologic maneuvers and observations during radiofrequency catheter ablation like heat induced "Mahaim" automaticity19,20 are regarded as evidences of either an ectopic A-V node or remnants of the specialized A-V ring tissue. The NV/NF fibers are now considered a rare item but there are some convincing reports21 of narrow and regular QRS tachycardias with ventriculoatrial dissociation. The last variety which is known as fasciculoventricular pathway22 seems to play no role in clinical tachycardias but as long as it is very often associated with bypass tracts they should be correctly recognized and not targeted for ablation, avoiding unnecessary damage to the A-V node-His bundle conduction system.

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