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长RP'心动过速中递减性逆向传导径路的电生理特性差异

Differential electrophysiologic properties of decremental retrograde pathways in long RP' tachycardia.

作者信息

Lerman B B, Greenberg M, Overholt E D, Swerdlow C D, Smith R T, Sellers T D, DiMarco J P

出版信息

Circulation. 1987 Jul;76(1):21-31. doi: 10.1161/01.cir.76.1.21.

Abstract

Long RP' supraventricular tachycardias (SVT) often demonstrate both slow and decremental conduction properties in the retrograde pathway of the reentrant circuit. The electrophysiologic properties of these pathways are poorly understood. We studied 10 patients with long RP' SVT (RP'/RR, 0.52 to 0.71); five had the unusual form of atrioventricular nodal reentry (fast-slow) and five patients had accessory AV pathways with slow, decremental retrograde conduction properties. During SVT, the effects of intravenous adenosine (37.5 to 150 micrograms/kg), which increases potassium current (iK) in supraventricular tissue and hyperpolarizes membrane potential toward Ek (-90 mV), and the response to slow-inward channel blockade with verapamil (0.10 to 0.20 mg/kg iv) were evaluated. Adenosine and verapamil has similar effects in the presence of fast-slow AV nodal reentry since both agents terminated SVT by producing block in the retrograde slow AV nodal pathway. In contrast, adenosine and verapamil had differential effects on retrograde conduction in decremental accessory pathways. Adenosine terminated all episodes of SVT in the retrograde decremental pathway, whereas verapamil had a direct effect on this tissue in only two of five patients. Decremental retrograde accessory pathways can therefore demonstrate at least two types of electrophysiologic responses. Pathways that respond only to adenosine-induced hyperpolarizing K+ current likely comprise depressed fast-Na+ channel tissue, i.e., partially depolarized (greater than -60 to -70 mV) atrial tissue. In contrast, decremental accessory pathways that respond to both modulation of the slow-inward calcium current and K+ conductance have pharmacologic properties similar to those of the AV node and may represent more completely depolarized atrial fibers with resting membrane potentials of -60 mV or less.

摘要

长RP'室上性心动过速(SVT)在折返环路的逆向传导途径中常表现出缓慢和递减传导特性。这些传导途径的电生理特性尚不清楚。我们研究了10例长RP' SVT患者(RP'/RR为0.52至0.71);其中5例患有不寻常形式的房室结折返(快-慢型),5例患者有房室旁道,具有缓慢、递减的逆向传导特性。在SVT发作期间,评估了静脉注射腺苷(37.5至150微克/千克)的作用,腺苷可增加室上组织中的钾电流(iK)并使膜电位超极化至Ek(-90 mV),以及评估了维拉帕米(0.10至0.20毫克/千克静脉注射)对慢内向通道阻滞的反应。在快-慢型房室结折返存在时,腺苷和维拉帕米有相似的作用,因为两种药物均通过阻滞逆向慢房室结途径来终止SVT。相比之下,腺苷和维拉帕米对递减性旁道的逆向传导有不同作用。腺苷可终止递减性逆向传导途径中的所有SVT发作,而维拉帕米仅对5例患者中的2例该组织有直接作用。因此,递减性逆向旁道可表现出至少两种类型的电生理反应。仅对腺苷诱导的超极化钾电流有反应的传导途径可能包含功能受抑制的快钠通道组织,即部分去极化(大于-60至-70 mV)的心房组织。相比之下,对慢内向钙电流和钾电导的调节均有反应的递减性旁道具有与房室结相似的药理特性,可能代表静息膜电位为-60 mV或更低的更完全去极化的心房纤维。

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