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氟卡尼对刺激诱导性室性心动过速的电生理效应

[Electrophysiological effects of flecainide on stimulus-inducible ventricular tachycardia].

作者信息

Breithardt G, Borggrefe M, Yeh H L, Seipel L

出版信息

Z Kardiol. 1982 Apr;71(4):278-83.

PMID:7090468
Abstract

13 patients (54 +/- 11.8 years) with either spontaneously occurring ventricular tachycardia (N = 12) or recurrent syncope (n = 1) probably due to ventricular tachycardia were studied electrophysiologically. In all patients, ventricular tachycardia could be initiated by programmed right ventricular stimulation during the control study. Ventricular tachycardia was sustained in eleven patients and non-sustained in the remaining two. After several days of oral administration of flecainide (400 to 500 mg per day) sustained ventricular tachycardia could still be initiated in seven cases that had to be interrupted by overdrive stimulation in five cases, and by cardioversion in the remaining two. In six cases, short, self-terminating episodes of ventricular tachycardia were induced. In four patients, induction of ventricular tachycardia was unchanged or made easier, whereas in seven cases ventricular tachycardia was more difficult to induce (i.e. later during the step-like stimulation program). The mean rate of induced ventricular tachycardia decreased from 215 +/- 59.4/min (+/- S.D.) to 169 +/- 44.1/min during flecainide (p less than 0.025). The interval between the tachycardia-initiating beat and the first beat of tachycardia increased from 323 +/- 61.1 ms to 438 +/-148.3 ms (P less than 0.02). The effective refractory period of the right ventricle was prolonged from 240 +/- 20.5 ms t 279 +/- 37.3 ms (P less than 0.005). The plasma concentration of flecainide at the time of stimulation was 995 +/- 238 ng/ml. Thus, flecainide exerts a marked effect on the rate of induced ventricular tachycardia, whereas the mode of induction did not change considerably. The prophylactic effect of long-term therapy with flecainide in patients with recurrent ventricular tachycardia needs further studies.

摘要

对13例患者(年龄54±11.8岁)进行了电生理研究,其中12例为自发性室性心动过速,1例反复晕厥(可能由室性心动过速所致)。在对照研究中,所有患者均可通过程控右心室刺激诱发室性心动过速。11例患者的室性心动过速呈持续性,其余2例为非持续性。口服氟卡尼(每天400至500毫克)数天后,7例仍可诱发持续性室性心动过速,其中5例需通过超速刺激终止,其余2例通过心脏复律终止。6例诱发出短暂的、自行终止的室性心动过速发作。4例患者诱发室性心动过速的情况未变或更容易诱发,而7例患者诱发室性心动过速则更困难(即在阶梯式刺激程序中更晚诱发出)。氟卡尼治疗期间,诱发的室性心动过速平均心率从215±59.4次/分钟(±标准差)降至169±44.1次/分钟(P<0.025)。心动过速起始搏动与心动过速第一搏动之间的间期从323±61.1毫秒增至438±148.3毫秒(P<0.02)。右心室有效不应期从240±20.5毫秒延长至279±37.3毫秒(P<0.005)。刺激时氟卡尼的血浆浓度为995±238纳克/毫升。因此,氟卡尼对诱发的室性心动过速心率有显著影响,而诱发方式没有明显改变。氟卡尼长期治疗对复发性室性心动过速患者的预防作用有待进一步研究。

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