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Use of adenosine as a diagnostic tool for dual atrioventricular nodal pathways: Response of control patients to incremental doses of adenosine

机译:腺苷作为双房室结通路的诊断工具的应用:对照患者对腺苷剂量增加的反应

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摘要

Background: Adenosine at low doses preferentially blocks fast over slow pathway conduction in patients with dual atrioventricular (AV) nodal physiology and typical AV nodal reentrant tachycardia (AVNRT). During atrial pacing, this effect is manifested as an abrupt increase in the AH interval with low doses of adenosine. This demonstration of dual AV nodal physiology may be useful as a diagnostic tool during electro‐physiologic studies in patients with supraventricular tachycardia who are not easily inducible, as clear demonstration of dual AV nodal pathways may indicate that AVNRT is a likely diagnosis and that further attempts at arrhythmia induction should be tailored in that direction. However, to be a useful test, adenosine should not cause an abrupt increase in AH interval in patients without dual AV nodal physiology. Hypothesis: This study was designed to investigate the prevalence of dual AV nodal pathways with administration of adenosine in patients with no history suggestive of AVNRT. Methods: Thirty‐seven patients who had no prior history of AVNRT and were undergoing electrophysiologic study for standard indications were enrolled. Baseline Wenckebach cycle length (WCL) and AV nodal effective refractory periods were measured at atrial pacing cycle lengths of 400 and 600 ms. The atrium was then paced at WCL + 50 ms, and WCL + 100 ms, while incrementally larger doses of intravenous adenosine were administered until AV nodal block occurred. Results: The mean (± standard deviation) doses of adenosine required to cause AV nodal block while pacing at WCL + 50 ms and WCL + 100 ms were 7.1 ±3.9 and 7.4±4.5 mg, respectively. In 1 of 37 patients (2.7%, 95% confidence interval 0–8%), an abrupt prolongation of the AH interval was seen with the administration of adenosine during atrial pacing as well as during the atrial refractory period determination. In all other patients, no dual AV nodal physiology was demonstrated during the refractory period determination, and there were only gradual changes in the AH interval with atrial pacing during administration of adenosine. Conclusion: Among patients with no history suggestive of AV nodal reentrant tachycardia, only 2.7% have clinically silent dual AV nodal pathways using this method. Incremental adenosine infusion during electrophysiologic study can be used as a highly specific diagnostic tool for patients with dual AV nodal pathways.
机译:背景:对于患有双房室(AV)淋巴结生理性和典型的AV淋巴结折返性心动过速(AVNRT)的患者,低剂量的腺苷优先阻断慢速通道传导。在心房起搏期间,这种作用表现为低剂量腺苷使AH间隔突然增加。双重AV节点生理学的这种表现可能在不易诱发的室上性心动过速患者的电生理研究中可用作诊断工具,因为双重AV节点通路的明确表现可能表明AVNRT是一种可能的诊断方法,并且需要进一步尝试心律失常的诱导应朝那个方向进行。但是,作为一项有用的测试,对于没有双重AV节点生理的患者,腺苷不应引起AH间隔的突然增加。假设:本研究旨在研究无AVNRT病史的患者中,使用腺苷给予双重AV淋巴结通路的患病率。方法:招募了37例无AVNRT既往史并接受电生理检查以适应标准指征的患者。在心房起搏周期长度为400和600 ms时测量基线Wenckebach周期长度(WCL)和AV结有效不应期。然后将心房调整为WCL + 50 ms和WCL + 100 ms,同时逐渐增加剂量的静脉内腺苷直至AV结块发生。结果:在WCL + 50 ms和WCL + 100 ms起搏时,引起AV结节阻滞所需的腺苷平均剂量(±标准差)分别为7.1±3.9和7.4±4.5 mg。在37例患者中,有1例(2.7%,95%置信区间0–8%)在心房起搏以及心房不应期测定中,腺苷的使用会导致AH间隔突然延长。在所有其他患者中,在不应期确定过程中均未发现双重AV淋巴结生理现象,在腺苷给药期间,随着心房起搏,AH间隔仅逐渐改变。结论:在无病史提示AV结折返性心动过速的患者中,只有2.7%的患者使用此方法具有临床上沉默的双重AV结节。在电生理研究过程中,递增腺苷输注可作为双重AV淋巴结通路患者的高度特异性诊断工具。

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