The mechanism of auricular paroxysmal tachycardia

Abstract

URICULAR paroxysmal tachycardia was long ago described and recognized as a clinical entity, but the fundamental mechanism or mechanisms responsible for this disorder have not yet been finally ascertained.', 2 Unlike auricular flutter and auricular fibrillation, it cannot be readily induced in experimental animals, and cannot, therefore, be easily studied by this met,hod. Speculations as to its nature must, therefore, be based on pertinent observations on man. We propose to discuss from this standpoint the following features of this disturbance : (1) the form of the anricular deflect.ions; (2) the effects of exertion, vagal stimulation, digitalis, quinidine, and other drugs upon the auricular rate and the duration of the paroxysms; (3) similarities, differences, and relations between it and auricular flutter and fibrillation; (4) the spontaneous occurrence of auriculoventricular block in a small number of cases and the difficulty or impossibility of producing it in most of the others; and (5) the occurrence of alternation in the auricular cycle length. We wish particularly to examine the su ggestion3 that auricular paroxysmal tachycardia is caused by circus rhythm involving one of the specialized auricular nodes. When Mines4 described circus rhythm he suggested that it might be responsible for some cases of paroxysmal. tachycardia in man. Iliescu and Sebastian? were among the first to su ggest that auricular paroxysmal tachycardia is due to circus contraction. Their reasoning was based chiefly on the a,ction of quinidine in this disorder. Lewis2 pointed out that the tot.al amount of auricular muscle is not sufficiently large to accommodate a circus mechanism at known rates of conduction in aurieular

A rare case of sinoatrial nodal reentrant tachycardia (SANRT) with underlying intermittent wolf parkinson white (WPW) syndrome

“…In 1943, Barker and co-workers described reentry tachycardias reporting "a circus rhythm could be accommodated in auricular muscle and in one of the specialized nodes at known rates of conduction and with cycle lengths such as occur in paroxysmal tachycardia" [5]. Heterogeneity of different types of Reentrant tachycardias was not appreciated at that time for few subsequent years due to lack of invasive electrophysiology until in 1968, when Han, Malozzi and Moe finally demonstrated the existence of sinoatrial echoes [6].…”

Atriyoventriküler nodal reenteran taşikardi: Patofizyolojiden tedaviye

“…Bu aritminin altında yatan "reentry" (yeniden giriş) mekanizması ilk olarak 1900'lü yılların başında ortaya atılmış ve bir çok araştırmacı bunun üzerinde çalışmıştır [4,5]. 1940 sonrasında reentry mekanizmasının atriyoventrilüer (AV) nodda yerleştiği tespit edildi [6]. İlerleyen yıllarda yapılan hayvan çalışmaları sayesinde AV nodda ikili yolak olduğu ortaya konuldu [7,8].…”

Contribuição da análise eletrofisiológica e anatômica do circuito atípico da taquicardia atrioventricular nodal

“…In the great majority of cases, it produces uncomfortable symptoms that may require medical intervention, whether in a situation of a sustained episode or for secondary prevention in order to avoid new episodes 4 .…”

“…Previous studies [2][3][4][5] have demonstrated that patients with NAVT classically have two anatomically and electrophysiologically distinct conduction pathways. Presently, there is electrophysiological proof that the dual nodal pathway is commonly composed of a circuit that encompasses a slow conduction pathway with a short refractory period (the "alpha" route in old nomenclature) and another route with fast conduction and a long refractory period (the "beta" route in old nomenclature) that determine the substrate for the reentry mechanism 5 .…”