Tebbenjohanns J, Pfeiffer D, Schumacher B, Korte T, Jung W, Lüderitz B
Medizinische Universitätsklinik und Poliklinik Bonn.
Z Kardiol. 1996;85 Suppl 6:191-9.
Adenosine has potent cardiac electrophysiologic effects including a negative chronotropic action on the sinus node and a predominant negative dromotropic action on the AV node. The latter property has mainly led to the use of adenosine as antiarrhythmic agent for the acute management of paroxysmal supraventricular tachycardia (PSVT) mediated by a reentrant mechanism involving the AV node. The effects of adenosine are dose-dependent and of very short duration since the half-life is less than 10s. The efficacy rates for termination of AV reentrant tachycardias were found to be 35% with 3 mg, 60-70% with 6 mg, 80% with 9 mg, and 90-95% with 12 mg adenosine. The AV nodal depressant effects of adenosine have also been used for determining the mechanism of wide QRS tachycardias for differentiating supraventricular tachyarrhythmias with aberrant conduction from ventricular tachycardia. Adenosine either terminates or slows almost all types of supraventricular tachyarrhythmias or it leads to unmasking of the underlying mechanism such as atrial flutter with aberrant conduction. One form of ventricular tachycardia, the idiopathic type originating from the right ventricular outflow tract can usually be terminated with adenosine due to its cAMP-mediated mechanism. Adenosine is helpful to detect or to increase preexcitation which is important for planning a catheter ablation procedure since the preexcitation pattern allows to localize the accessory pathway. Since the action of adenosine usually does not alter the accessory pathway conduction it is also useful for control ablation efficacy noninvasively in terms of antegrade conduction and during ventricular pacing for the retrograde conduction. Further evaluation and research is necessary for better understanding of adenosine action on the human atrial electrophysiology since it provokes atrial fibrillation in some patients, and of adenosine action on the different pathways in AV nodal reentrant tachycardias and some accessory pathways with decremental (AV nodal-like) conduction properties.
腺苷具有强大的心脏电生理效应,包括对窦房结的负性变时作用以及对房室结的主要负性变传导作用。后者这一特性主要促使腺苷被用作抗心律失常药物,用于急性处理由涉及房室结的折返机制介导的阵发性室上性心动过速(PSVT)。腺苷的作用具有剂量依赖性且持续时间极短,因为其半衰期小于10秒。研究发现,终止房室折返性心动过速的有效率在使用3毫克腺苷时为35%,6毫克时为60 - 70%,9毫克时为80%,12毫克时为90 - 95%。腺苷对房室结的抑制作用也已被用于确定宽QRS波心动过速的机制,以区分伴有差异性传导的室上性快速心律失常与室性心动过速。腺苷几乎能终止或减慢所有类型的室上性快速心律失常,或者导致潜在机制的暴露,如伴有差异性传导的心房扑动。一种室性心动过速,即起源于右心室流出道的特发性类型,通常可因腺苷的cAMP介导机制而被终止。腺苷有助于检测或增加预激,这对于规划导管消融手术很重要,因为预激模式有助于定位附加旁路。由于腺苷的作用通常不会改变附加旁路的传导,所以它在正向传导方面以及在心室起搏进行逆向传导时,对于无创控制消融效果也很有用。鉴于腺苷在一些患者中会诱发房颤,以及其对房室结折返性心动过速中不同路径和一些具有递减(类似房室结)传导特性的附加旁路的作用,有必要进行进一步的评估和研究,以更好地理解腺苷对人体心房电生理的作用。