Mahaim Fibre Tachycardia: Recognition and Management

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

Dez anos da Revista Multiface e o Incentivo à Pesquisa na Graduação

A Revista Multiface Online é um periódico organizado por alunos de graduação da UFMG e que publica exclusivamente trabalhos produzidos por graduandos, nas áreas de Economia, Administração e Relações Econômicas Internacionais. Contando com 10 anos de existência e sendo uma revista disponibilizada no formato digital, a Multiface tem recebido trabalhos de alunos das mais diversas universidades do país. Nesse sentido, este trabalho tem como objetivo apresentar o periódico e as características particulares que o tornam um espaço de incentivo à pesquisa na graduação. Entre estes está o processo de avaliação, que busca sempre produzir pareceres construtivos, a fim de contribuir para a formação de novos pesquisadores desde a graduação. Além disso, a existência de uma revista editorada por alunos de graduação também possibilita a formação de membros de comitês editoriais desde a graduação

Chronic Activation of γ2 AMPK Induces Obesity and Reduces β Cell Function.

Despite significant advances in our understanding of the biology determining systemic energy homeostasis, the treatment of obesity remains a medical challenge. Activation of AMP-activated protein kinase (AMPK) has been proposed as an attractive strategy for the treatment of obesity and its complications. AMPK is a conserved, ubiquitously expressed, heterotrimeric serine/threonine kinase whose short-term activation has multiple beneficial metabolic effects. Whether these translate into long-term benefits for obesity and its complications is unknown. Here, we observe that mice with chronic AMPK activation, resulting from mutation of the AMPK γ2 subunit, exhibit ghrelin signaling-dependent hyperphagia, obesity, and impaired pancreatic islet insulin secretion. Humans bearing the homologous mutation manifest a congruent phenotype. Our studies highlight that long-term AMPK activation throughout all tissues can have adverse metabolic consequences, with implications for pharmacological strategies seeking to chronically activate AMPK systemically to treat metabolic disease

Critical Assessment of the Concepts and Misconceptions of the Cardiac Conduction System over the Last 100 Years: The Personal Quest of Robert H. Anderson

Anatomical concepts regarding the conduction system of the heart have been a matter of debate since pioneering work done at the beginning of the 20th century. Robert H. Anderson was actively involved in this field for half a century. We aimed to investigate how his own concepts evolved over time. We have assessed anatomical concepts relating to the cardiac conduction system appearing since the key contributions made in the initial decade of the 20th century, analyzing them from the perspective of Robert H. Anderson, particularly focusing on the anatomical aspects of structures such as accessory atrioventricular pathways, including the so-called Mahaim-type fibers, connections between the atrioventricular node and the atrial myocardium, and so-called “specialized” internodal atrial tracts. To accomplish this task, we have taken as our starting point the initial concepts published in the first decade of the century, along with those subsequently reported up to 1976, and assessing them in the light of our most recently published works. The concepts put forward by Robert Anderson with regard to atrioventricular nodal bypass tracts, atrioventricular nodal inputs, decrementally conducting accessory pathways, and “tracts” for internodal atrial conduction, have remained consistent along the time frame of half a century

Confounding factors leading to misdiagnosing ventricular tachycardia as supraventricular in the emergency room

Studies conducted during the last 50 years have proposed electrocardiographic criteria and algorithms to determine if a wide QRS tachycardia is ventricular or supraventricular in origin. Sustained ventricular tachycardia is an uncommon reason for consultation in the emergency room. The latter and the complexity of available electrocardiographic diagnostic criteria and algorithms result in frequent misdiagnoses. Good hemodynamic tolerance of tachycardia in the supine position does not exclude its ventricular origin. Although rare, ventricular tachycardia in patients with and without structural heart disease may show a QRS duration <120 ms. Interruption of tachycardia by coughing, carotid sinus massage, Valsalva maneuver, or following the infusion of adenosine or verapamil should not discard the ventricular origin of the arrhythmia. In patients with regular, uniform, sustained broad QRS tachycardia, the presence of structural heart disease or A-V dissociation strongly suggest its ventricular origin. Occasionally, ventricular tachycardia can present with AV dissociation without this being evident on the 12-lead ECG. Cardiac auscultation, examination of the jugular venous pulse, and arterial pulse palpation provide additional clues for identifying A-V dissociation during tachycardia. This paper does not review the electrocardiographic criteria for categorizing tachycardia as ventricular but rather why emergency physicians misdiagnose these patients