Shinlapawittayatorn Krekwit, Sungnoon Rattapong, Chattipakorn Siriporn, Chattipakorn Nipon
Cardiac Electrophysiology Unit, Department of Physiology, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand.
J Cardiovasc Electrophysiol. 2006 Mar;17(3):292-5. doi: 10.1111/j.1540-8167.2006.00348.x.
Although fatal arrhythmia and sudden death have been reported in patients taking sildenafil citrate, its effect on defibrillation efficacy has not been investigated. The aim of this study was to test the hypothesis that sildenafil citrate increases the shock strength required to successfully defibrillate during ventricular fibrillation (VF).
A total of 26 pigs (20-25 kg) were randomly assigned into three groups. In each group, the defibrillation threshold (DFT) was determined at the beginning of the study using a three-reversal up/down protocol. Each shock (RV-SVC, biphasic) was delivered after 10 seconds of VF. Group 1 (n = 10) received 50 mg and group 2 (n = 10) received 100 mg of sildenafil citrate intravenously at a rate of 2 mL/minute for 50 minutes. Group 3 (n = 6) received 100 mL of saline intravenously at the same rate as in group 1. The DFT was determined again after the drug (drug-DFT) and saline (saline-DFT) administration. For 100-mg sildenafil citrate infusion, the DFT (483 +/- 39 V, 18 +/- 3 J) was significantly (P < 0.003 and P < 0.01, respectively) higher than the control-DFT (407 +/- 123 V, 13 +/- 7 J). This sildenafil citrate infusion increased the DFT approximately 19% by voltage, and approximately 38% by total energy. After 50-mg sildenafil citrate infusion, the DFT (454 +/- 28 V, 15 +/- 2 J) was not different than the control DFT (449 +/- 28 V, 15 +/- 2 J). Saline infusion (391 +/- 18 V, 12 +/- 1 J) did not alter the control DFT (399 +/- 22 V, 12 +/- 1 J).
The 100-mg sildenafil citrate infusion, representing a supra-therapeutic plasma level, significantly increased the DFT. This finding indicates that VF occurring during supra-therapeutic sildenafil citrate treatment would require a stronger shock to successfully defibrillate.
尽管已有服用枸橼酸西地那非的患者发生致命性心律失常和猝死的报道，但其对除颤效果的影响尚未得到研究。本研究的目的是验证枸橼酸西地那非会增加心室颤动（VF）期间成功除颤所需的电击强度这一假设。
总共26头猪（20 - 25千克）被随机分为三组。在研究开始时，每组使用三反转上下法测定除颤阈值（DFT）。每次电击（右心室 - 上腔静脉，双相）在VF持续10秒后施加。第1组（n = 10）以2毫升/分钟的速率静脉注射50毫克枸橼酸西地那非，持续50分钟。第2组（n = 10）以相同速率静脉注射100毫克枸橼酸西地那非，持续50分钟。第3组（n = 6）以与第1组相同的速率静脉注射100毫升生理盐水。在给予药物（药物 - DFT）和生理盐水（生理盐水 - DFT）后再次测定DFT。对于100毫克枸橼酸西地那非输注，DFT（483±39伏，18±3焦）显著高于对照DFT（407±123伏，13±7焦）（分别为P < 0.003和P < 0.01）。这种枸橼酸西地那非输注使DFT在电压方面增加了约19%，在总能量方面增加了约38%。输注50毫克枸橼酸西地那非后，DFT（454±28伏，15±2焦）与对照DFT（449±28伏，15±2焦）无差异。输注生理盐水（391±18伏，12±1焦）未改变对照DFT（399±22伏，12±1焦）。
输注100毫克枸橼酸西地那非，代表超治疗血浆水平，显著增加了DFT。这一发现表明，在枸橼酸西地那非超治疗剂量治疗期间发生的VF需要更强的电击才能成功除颤。
