Hatzinikolaou H, Rodriguez L M, Smeets J L, Timmermans C, Vrouchos G, Grecas G, Wellens H J
Department of Cardiology, G Papanikolaou General Hospital, Exohi, Thessaloniki, Greece.
Heart. 1998 Feb;79(2):165-8. doi: 10.1136/hrt.79.2.165.
To examine the effect of isoprenaline on slow and fast pathway properties and tachycardia initiation.
Consecutive patients, prospective study.
Referral centre for cardiology, academic hospital.
24 patients suffering from common type atrioventricular nodal reentrant tachycardia (AVNRT).
Programmed electrical stimulation and radiofrequency catheter ablation of the slow pathway.
AVNRT was induced before and after the administration of isoprenaline in nine patients (group 1), before isoprenaline only in five (group 2), and after isoprenaline only in 10 (group 3). The anterograde effective refractory period of the fast pathway was prolonged significantly during isoprenaline administration in group 1 (405 (31) v 335 (34) ms, p < 0.001) and shortened in group 2 (308 (57) v 324 (52) ms, p = 0.005). There was also significant shortening in group 3 (346 (85) v 395 (76) ms, p < 0.001). Isoprenaline administration did not result in a significant change of the anterograde effective refractory period of the slow pathway in groups 1 and 3, but eliminated slow pathway conduction in group 2. Isoprenaline significantly shortened the minimal and maximal atrial to His bundle conduction interval recording in response to each extrastimulus of the slow pathway (210 (24) v 267 (25) ms, p < 0.001 and 275 (25) v 328 (25) ms, p < 0.001, respectively) in group 1 and significantly prolonged these intervals (331 (34) v 274 (34) ms and 407 (33) v 351 (33) ms, respectively) in group 3. In all groups only minimal changes in the refractory period of the atrium occurred after isoprenaline administration. The effect of isoprenaline was also measured on the ventricular effective refractory period and on the minimal and maximal length of the ventriculoatrial (V2-A2) interval during ventricular pacing. Isoprenaline did not result in a significant change of the ventricular effective refractory period in groups 1 and 2 nor of the shortest and longest V2-A2 interval. In group 3, however, the ventricular effective refractory period and the shortest and longest V2-A2 interval shortened significantly after isoprenaline administration.
In group 1 isoprenaline did not affect inducibility of AVNRT because it prolonged the fast pathway refractory period without affecting slow pathway conduction. In group 2 isoprenaline shortened the fast pathway refractory period and appeared to abolish slow pathway conduction. Consequently, isoprenaline prevented induction of AVNRT. In group 3 isoprenaline facilitated induction of AVNRT. This effect seemed primarily to be the result of shortening of retrograde refractoriness of the fast pathway with prolongation of slow pathway anterograde conduction and refractory period.
研究异丙肾上腺素对快慢径路特性及心动过速诱发的影响。
连续患者的前瞻性研究。
学术医院的心脏病转诊中心。
24例常见型房室结折返性心动过速（AVNRT）患者。
程控电刺激及慢径路射频导管消融。
9例患者（第1组）在给予异丙肾上腺素前后诱发了AVNRT，5例（第2组）仅在给予异丙肾上腺素前诱发，10例（第3组）仅在给予异丙肾上腺素后诱发。第1组在给予异丙肾上腺素期间快径路的前传有效不应期显著延长（40５（31）对335（34）毫秒，p<0.001），第2组缩短（308（57）对324（52）毫秒，p = 0.005）。第3组也有显著缩短（346（85）对395（76）毫秒，p<0.001）。第1组和第3组给予异丙肾上腺素后慢径路的前传有效不应期无显著变化，但第2组消除了慢径路传导。异丙肾上腺素显著缩短了第1组慢径路对每个额外刺激的最小和最大心房至希氏束传导间期（分别为210（24）对267（25）毫秒，p<0.001和275（25）对328（25）毫秒，p<0.001），第3组则显著延长了这些间期（分别为331（34）对274（34）毫秒和407（33）对351（33）毫秒）。所有组在给予异丙肾上腺素后心房不应期仅有微小变化。还测量了异丙肾上腺素对心室有效不应期以及心室起搏时室房（V2-A2）间期最小和最大长度的影响。第1组和第2组给予异丙肾上腺素后心室有效不应期无显著变化，V2-A2间期最短和最长值也无变化。然而，第3组在给予异丙肾上腺素后心室有效不应期以及最短和最长V2-A2间期显著缩短。
第i组中异丙肾上腺素不影响AVNRT的诱发，因为它延长了快径路不应期而不影响慢径路传导。第2组中异丙肾上腺素缩短了快径路不应期并似乎消除了慢径路传导。因此，异丙肾上腺素阻止了AVNRT的诱发。第3组中异丙肾上腺素促进了AVNRT的诱发。这种效应似乎主要是快径路逆向不应期缩短以及慢径路前传传导和不应期延长的结果。
