Hellestrand K J, Nathan A W, Bexton R S, Spurrell R A, Camm A J
Am J Cardiol. 1983 Mar 1;51(5):770-6. doi: 10.1016/s0002-9149(83)80131-3.
Intravenous flecainide acetate was administered to 33 patients undergoing routine electrophysiologic study: 18 patients had a direct accessory atrioventricular (AV) pathway and 15 patients had functional longitudinal A-H dissociation (dual A-H pathways). Flecainide was given to 14 patients during sustained AV reentrant tachycardia and to 9 patients during sustained intra-AV nodal reentrant tachycardia. AV reentrant tachycardia was successfully terminated in 12 of 14 patients. Tachycardia termination was due to retrograde accessory pathway block in 11 patients and AV nodal block in 1. During flecainide administration, tachycardia cycle lengths increased (327 +/- 55 to 426 +/- 84 ms) principally because of retrograde conduction delay in the accessory pathway (127 +/- 34 to 197 +/- 67 ms). After flecainide administration, tachycardia reinitiation was not possible in 6 patients. In all 18 patients with accessory AV pathway conduction, flecainide significantly increased both anterograde and retrograde accessory pathway effective refractory periods, with anterograde accessory pathway block in 3 patients and retrograde accessory pathway block in 8. Intra-AV nodal reentrant tachycardia was successfully terminated in 8 of 9 patients. Tachycardia termination was due to retrograde "fast" A-H pathway block in 7 patients and anterograde "slow" A-H pathway block in 1 patient. During flecainide administration, tachycardia cycle lengths increased (326 +/- 50 to 433 +/- 64 ms) due to both anterograde, A-H and H-V (AV 242 +/- 97 to 343 +/- 75 ms), and retrograde, earliest ventricular to earliest atrial (51 +/- 14 to 70 +/- 23 ms) conduction delay. After flecainide administration, reinitiation of intra-AV nodal reentrant tachycardia was not possible in 4 patients. In all 15 patients with dual A-H pathways, flecainide selectively prolonged the retrograde effective refractory period of the fast A-H pathway, having little effect on anterograde fast A-H pathway refractoriness or on anterograde and retrograde slow A-H pathway refractoriness. Anterograde fast A-H pathway block occurred in 1 patient and retrograde fast A-H pathway block occurred in 6 patients. No serious adverse effects were encountered during the study. Flecainide acetate is an effective agent for the acute termination of both orthodromic AV and intra-AV nodal reentrant tachycardias. This antiarrhythmic action appears to be mediated through a predominant effect on either accessory AV pathway or retrograde fast A-H pathway refractoriness.
对33例接受常规电生理检查的患者静脉注射醋酸氟卡尼：18例患者有直接房室旁道，15例患者有功能性纵向A-H分离（双A-H径路）。14例持续性房室折返性心动过速患者和9例持续性房室结内折返性心动过速患者接受了氟卡尼治疗。14例患者中有12例房室折返性心动过速成功终止。心动过速终止的原因是11例患者发生逆向旁道阻滞，1例患者发生房室结阻滞。在注射氟卡尼期间，心动过速周期长度增加（从327±55毫秒增至426±84毫秒），主要是因为旁道逆向传导延迟（从127±34毫秒增至197±67毫秒）。注射氟卡尼后，6例患者无法再次诱发心动过速。在所有18例有房室旁道传导的患者中，氟卡尼显著增加了顺向和逆向旁道有效不应期，3例患者出现顺向旁道阻滞，8例患者出现逆向旁道阻滞。9例患者中有8例房室结内折返性心动过速成功终止。心动过速终止的原因是7例患者发生逆向“快”A-H径路阻滞，1例患者发生顺向“慢”A-H径路阻滞。在注射氟卡尼期间，心动过速周期长度增加（从326±50毫秒增至433±64毫秒），这是由于顺向A-H和H-V（房室从242±97毫秒增至343±75毫秒）以及逆向最早心室至最早心房（从51±14毫秒增至70±23毫秒）传导延迟所致。注射氟卡尼后，4例患者无法再次诱发房室结内折返性心动过速。在所有15例有双A-H径路的患者中，氟卡尼选择性地延长了快A-H径路的逆向有效不应期，对顺向快A-H径路不应期或顺向和逆向慢A-H径路不应期影响很小。1例患者出现顺向快A-H径路阻滞，6例患者出现逆向快A-H径路阻滞。研究期间未遇到严重不良反应。醋酸氟卡尼是急性终止正向房室折返性心动过速和房室结内折返性心动过速的有效药物。这种抗心律失常作用似乎主要是通过对房室旁道或逆向快A-H径路不应期的主要影响介导的。
