Iwai Sei, Markowitz Steven M, Stein Kenneth M, Mittal Suneet, Slotwiner David J, Das Mithilesh K, Cohen Jennifer D, Hao Steven C, Lerman Bruce B
Department of Medicine, Division of Cardiology, Cornell University Medical Center, New York, NY 10021, USA.
Circulation. 2002 Nov 26;106(22):2793-9. doi: 10.1161/01.cir.0000040587.73251.48.
We previously proposed that adenosine has mechanism-specific effects on atrial tachycardia (AT), such that adenosine terminates AT attributable to triggered activity, transiently suppresses automatic rhythms, and has no effect on macroreentrant AT. This, however, remains controversial, because other studies have reported that adenosine terminates reentrant AT. To clarify this issue, we used 3D electroanatomic mapping to delineate the tachycardia circuit and thereby determine whether the response to adenosine differentiates focal from macroreentrant AT.
We examined the effect of adenosine on 43 ATs in 42 consecutive patients (59+/-15 years of age; 26 female) who received adenosine during tachycardia and whose mechanism of AT was characterized by pharmacological perturbation, entrainment, 3D electroanatomic mapping, and results of radiofrequency ablation. Eight tachycardias were macroreentrant (noncavotricuspid isthmus-dependent), and 35 ATs were focal (either triggered or automatic). Adenosine administered during AT (at doses sufficient to result in AV block) terminated or transiently suppressed focal AT in 33 of 35 cases, whereas 8 of 8 macroreentrant ATs were adenosine insensitive (P<0.001). Twenty-eight of 35 focal ATs were located along the crista terminalis or tricuspid annulus.
The response of AT to adenosine can immediately differentiate atrial tachycardia arising from a focal source from that attributable to macroreentry. This finding can be exploited to facilitate developing a focused, strategic ablative approach at the onset of a procedure.
我们之前提出，腺苷对房性心动过速（AT）具有机制特异性作用，即腺苷可终止由触发活动引起的AT，短暂抑制自律性心律，而对大折返性AT无影响。然而，这一观点仍存在争议，因为其他研究报告称腺苷可终止折返性AT。为阐明这一问题，我们使用三维电解剖标测来描绘心动过速环路，从而确定对腺苷的反应是否能区分局灶性与大折返性AT。
我们研究了腺苷对42例连续患者中43次AT的影响（年龄59±15岁；女性26例），这些患者在心动过速期间接受了腺苷治疗，其AT机制通过药理学干扰、拖带、三维电解剖标测及射频消融结果进行了特征性分析。8次心动过速为大折返性（非腔静脉三尖瓣峡部依赖性），35次AT为局灶性（触发或自律性）。在AT期间给予腺苷（剂量足以导致房室传导阻滞），35例局灶性AT中有33例被终止或短暂抑制，而8例大折返性AT中有8例对腺苷不敏感（P<0.001）。35例局灶性AT中有28例位于终末嵴或三尖瓣环。
AT对腺苷的反应可立即区分源于局灶性起源的房性心动过速与大折返性房性心动过速。这一发现可用于在手术开始时促进制定有针对性的、策略性的消融方法。
