Kim Y H, Leitch J W, Klein G J, Yee R, Leather R A
Department of Medicine, University of Western Ontario, London.
Can J Cardiol. 1992 Sep;8(7):716-20.
To determine if pharmacological interventions aimed at altering autonomic tone would allow induction of orthodromic atrioventricular reentrant tachycardia in asymptomatic patients with the Wolff-Parkinson-White electrocardiographic pattern.
Prospective interventional protocol in consecutive eligible patients.
University hospital.
Eighteen asymptomatic patients (13 male and five female) with the Wolff-Parkinson-White electrocardiographic pattern without inducible tachycardia in the drug-free state.
Electrophysiological assessment was performed at baseline, after intravenous administration of atropine (0.03 mg/kg) and during isoproterenol infusion (0.5 to 2 micrograms/min).
Orthodromic reciprocating tachycardia was not inducible at baseline because of absent retrograde accessory pathway conduction in seven patients. In five patients, orthodromic atrial echo beats could be induced (which blocked retrogradely in the accessory pathway in three patients and anterogradely in the atrioventricular node in two). In the remaining six patients, neither orthodromic echo beats nor reciprocating tachycardia could be induced despite intact retrograde accessory pathway conduction. Following atropine administration (mean dose 1.9 +/- 0.3 mg), anterograde and retrograde accessory pathway effective refractory periods decreased from 360 +/- 172 to 284 +/- 62 ms and from 340 +/- 38 to 296 +/- 32 ms, respectively (both P < 0.05 versus control). Orthodromic reciprocating tachycardia was induced in two patients (nonsustained in one). During isoproterenol infusion (mean dose 1.0 +/- 0.3 micrograms/min), anterograde and retrograde accessory pathway effective refractory periods decreased further to 243 +/- 23 and 248 +/- 22 ms, respectively (both P < 0.05 versus after atropine); two further patients had inducible orthodromic reciprocating tachycardia (nonsustained in one). No patient with absent retrograde accessory pathway conduction developed retrograde accessory pathway conduction or reciprocating tachycardia with isoproterenol and/or atropine.
Isoproterenol and/or atropine allowed tachycardia induction in four of 18 asymptomatic patients with the Wolff-Parkinson-White electrocardiographic pattern. In the majority of these patients, tachycardia is not inducible because of deficient retrograde accessory pathway conduction which does not improve with autonomic facilitation.
确定旨在改变自主神经张力的药物干预措施是否能使无症状的预激综合征心电图模式患者诱发顺向型房室折返性心动过速。
对连续符合条件的患者采用前瞻性干预方案。
大学医院。
18例无症状的预激综合征心电图模式患者(13例男性,5例女性),在未用药状态下不能诱发心动过速。
在基线、静脉注射阿托品(0.03mg/kg)后以及静脉输注异丙肾上腺素(0.5至2微克/分钟)期间进行电生理评估。
7例患者因逆向房室旁道传导缺失,在基线时不能诱发顺向型折返性心动过速。5例患者可诱发顺向型房性回波搏动(3例患者在房室旁道逆向阻滞,2例患者在房室结前向阻滞)。其余6例患者尽管逆向房室旁道传导完整,但既不能诱发顺向型回波搏动,也不能诱发折返性心动过速。静脉注射阿托品(平均剂量1.9±0.3mg)后,房室旁道前向和逆向有效不应期分别从360±172毫秒降至284±62毫秒,从340±38毫秒降至296±32毫秒(与对照组相比,P均<0.05)。2例患者诱发了顺向型折返性心动过速(1例为非持续性)。在静脉输注异丙肾上腺素期间(平均剂量1.0±0.3微克/分钟),房室旁道前向和逆向有效不应期进一步降至243±23毫秒和248±22毫秒(与注射阿托品后相比,P均<0.05);又有2例患者可诱发顺向型折返性心动过速(1例为非持续性)。没有逆向房室旁道传导缺失的患者在使用异丙肾上腺素和/或阿托品后出现逆向房室旁道传导或折返性心动过速。
异丙肾上腺素和/或阿托品可使18例无症状预激综合征心电图模式患者中的4例诱发心动过速。在这些患者中,大多数因逆向房室旁道传导不足而不能诱发心动过速,自主神经兴奋并不能改善这种情况。