Grogin H R, Lee R J, Kwasman M, Epstein L M, Schamp D J, Lesh M D, Scheinman M M
Cardiovascular Research Institute, University of California San Francisco.
Circulation. 1994 Jul;90(1):272-81. doi: 10.1161/01.cir.90.1.272.
Several mechanisms have been proposed to explain the pathogenesis of tachycardia in patients with Mahaim tracts. The tachycardia may involve antegrade conduction over an atriofascicular pathway with decremental properties or a nodofascicular pathway.
We report six patients with recurrent episodes of preexcited tachycardia with findings consistent with "Mahaim tract" conduction. All patients exhibited decremental antegrade preexcited conduction with atrial pacing and a preexcited tachycardia with initial activation of the proximal right bundle branch. In four patients (group 1), atrial premature complexes (APCs) induced at the tricuspid annulus just after the inscription of the septal atrial electrogram and during left bundle branch block preexcited tachycardia advanced the next preexcited ventricular complex. In these patients, discrete Mahaim potentials were inscribed over the right anterolateral or lateral tricuspid annulus. Two patients (group 2) had evidence of dual atrioventricular nodal conduction. APCs during left bundle branch block tachycardia just after inscription of the septal atrial electrogram failed to advance the next ventricular complex with similar preexcited morphology, and no Mahaim potentials could be recorded from the tricuspid annulus. In group 1 patients, application of radiofrequency energy to sites recording the Mahaim potentials resulted in tachycardia cure. For patients in group 2, selective slow atrioventricular nodal pathway ablation in the midseptal region resulted in complete ablation of both the slow atrioventricular nodal pathway and Mahaim conduction in two patients.
Mahaim tachycardia can be due to atriofascicular pathways, which may be ablated over the right tricuspid annulus, or to septal pathways, which may arise from the slow atrioventricular nodal pathway in patients with dual atrioventricular nodal physiology. In the latter circumstance, successful ablation is achieved by placing the lesion in the midseptal region.
已提出多种机制来解释Mahaim纤维束患者心动过速的发病机制。这种心动过速可能涉及具有递减特性的房室束旁道或结室束的前向传导。
我们报告了6例反复发生预激性心动过速的患者，其表现与“Mahaim纤维束”传导一致。所有患者在心房起搏时均表现出递减性前向预激传导，且预激性心动过速起始于右束支近端的激动。4例患者（第1组），在间隔心房电图记录后即刻于三尖瓣环诱发的房性早搏复合体（APCs），以及在左束支阻滞预激性心动过速期间，可使下一个预激性心室复合体提前。在这些患者中，在右前外侧或外侧三尖瓣环记录到离散的Mahaim电位。2例患者（第2组）有双房室结传导的证据。在间隔心房电图记录后即刻于左束支阻滞心动过速期间的APCs未能使下一个形态相似的预激心室复合体提前，且在三尖瓣环未记录到Mahaim电位。在第1组患者中，对记录到Mahaim电位的部位施加射频能量可治愈心动过速。对于第2组患者，在中隔区域选择性消融慢房室结径路可使2例患者的慢房室结径路和Mahaim传导均完全消融。
Mahaim心动过速可能源于房室束旁道，可在右三尖瓣环进行消融，也可能源于间隔旁道，在具有双房室结生理功能的患者中，间隔旁道可能起源于慢房室结径路。在后一种情况下，通过在中隔区域放置消融灶可成功消融。
