Glatter K A, Cheng J, Dorostkar P, Modin G, Talwar S, Al-Nimri M, Lee R J, Saxon L A, Lesh M D, Scheinman M M
Cardiovascular Research Institute and Section of Cardiac Electrophysiology, University of California-San Francisco, CA, USA.
Circulation. 1999 Mar 2;99(8):1034-40. doi: 10.1161/01.cir.99.8.1034.
We correlated the electrophysiologic (EP) effects of adenosine with tachycardia mechanisms in patients with supraventricular tachycardias (SVT).
Adenosine was administered to 229 patients with SVTs during EP study: atrioventricular (AV) reentry (AVRT; n=59), typical atrioventricular node reentry (AVNRT; n=82), atypical AVNRT (n=13), permanent junctional reciprocating tachycardia (PJRT; n=12), atrial tachycardia (AT; n=53), and inappropriate sinus tachycardia (IST; n=10). There was no difference in incidence of tachycardia termination at the AV node in AVRT (85%) versus AVNRT (86%) after adenosine, but patients with AVRT showed increases in the ventriculoatrial (VA) intervals (13%) compared with typical AVNRT (0%), P<0.005. Changes in atrial, AV, or VA intervals after adenosine did not predict the mode of termination of long R-P tachycardias. For patients with AT, there was no correlation with location of the atrial focus and adenosine response. AV block after adenosine was only observed in AT patients (27%) or IST (30%). Patients with IST showed atrial cycle length increases after adenosine (P<0.05) with little change in activation sequence. The incidence of atrial fibrillation after adenosine was higher for those with AVRT (15%) compared with typical AVNRT (0%) P<0.001, or atypical AVNRT (0%) but similar to those with AT (11%) and PJRT (17%).
The EP response to adenosine proved of limited value to identify the location of AT or SVT mechanisms. Features favoring AT were the presence of AV block or marked shortening of atrial cycle length before tachycardia suppression. Atrial fibrillation was more common after adenosine in patients with AVRT, PJRT, or AT. Patients with IST showed increases in cycle length with little change in atrial activation sequence after adenosine.
我们将腺苷的电生理（EP）效应与室上性心动过速（SVT）患者的心动过速机制进行了关联。
在EP研究期间，对229例SVT患者给予腺苷：房室折返性心动过速（AVRT；n = 59）、典型房室结折返性心动过速（AVNRT；n = 82）、非典型AVNRT（n = 13）、永久性交界性反复性心动过速（PJRT；n = 12）、房性心动过速（AT；n = 53）和不适当窦性心动过速（IST；n = 10）。腺苷给药后，AVRT（85%）与AVNRT（86%）在房室结处心动过速终止的发生率无差异，但与典型AVNRT（0%）相比，AVRT患者的室房（VA）间期增加（13%），P<0.005。腺苷给药后心房、房室或VA间期的变化不能预测长R-P心动过速的终止方式。对于AT患者，心房激动灶的位置与腺苷反应无相关性。腺苷后房室传导阻滞仅在AT患者（27%）或IST患者（30%）中观察到。IST患者腺苷后心房周期长度增加（P<0.05），激动顺序变化不大。与典型AVNRT（0%）相比，AVRT患者腺苷后房颤发生率更高（15%），P<0.001，或与非典型AVNRT（约0%）相比，但与AT患者（11%）和PJRT患者（17%）相似。
腺苷的EP反应在识别AT或SVT机制的位置方面价值有限。有利于AT的特征是存在房室传导阻滞或心动过速抑制前心房周期长度明显缩短。AVRT、PJRT或AT患者腺苷后房颤更常见。IST患者腺苷后周期长度增加，心房激动顺序变化不大。
