Mizusawa Yuka, Sakurada Harumizu, Nishizaki Mitsuhiro, Hiraoka Masayasu
Department of Cardiology, Tokyo Metropolitan Hiroo Hospital, Shibuya-ku, Japan.
J Cardiovasc Pharmacol. 2006 Mar;47(3):359-64. doi: 10.1097/01.fjc.0000206437.27854.65.
Quinidine is suggested as an effective agent to suppress ventricular fibrillation (VF) in the Brugada syndrome by inhibiting transient outward K(+) current (Ito) leading to the reduction and abbreviation of the disparity of repolarization in the right ventricular outflow region and ST segment elevation in the right precordial leads of electrocardiogram. We sought to assess the efficacy of low-dose (300-600 mg) quinidine sulfate on the prevention of ventricular fibrillation induction by programmed electrical stimulation (PES) and spontaneous ventricular fibrillation episodes during the subsequent follow-up period. Electrophysiologic study was performed in 14 patients with the Brugada syndrome (14 men, mean age 50 +/- 11 years, range 32-75) before and during the treatment with low-dose quinidine and evaluated the efficacy of the drug therapy. Ventricular fibrillation was induced in all the patients by programmed electrical stimulation at baseline. After oral quinidine administration (300 mg or 600 mg/d), programmed electrical stimulation was repeated. Ventricular fibrillation induction was prevented in 6 of 14 patients (44%). Serum quinidine concentration was higher in the patients with suppressed VF induction than those without (1.88 +/- 0.44 versus 1.31 +/- 0.43 microg/ml, respectively). After programmed electrical stimulation, 9 of 14 patients (64%), in whom four had implantable cardioverter defibrillator implantation, continued to receive quinidine. During a mean follow-up period of 31 months on quinidine, no side effects except one with diarrhea were observed (12.5%). There were no ventricular fibrillation recurrences in 3 of the 9 patients, who had frequent implantable cardioverter defibrillator discharges due to ventricular fibrillation attacks before treatment with quinidine. Low-dose quinidine has a potential as an adjunctive therapy for patients of the Brugada syndrome with frequent implantable cardioverter defibrillator discharges.
奎尼丁被认为是一种通过抑制瞬时外向钾电流(Ito)来抑制Brugada综合征患者室颤(VF)的有效药物,这会导致右心室流出区域复极离散度降低以及心电图右胸前导联ST段抬高幅度减小。我们试图评估低剂量(300 - 600 mg)硫酸奎尼丁预防程序电刺激(PES)诱发室颤以及后续随访期间自发性室颤发作的疗效。对14例Brugada综合征患者(14例男性,平均年龄50±11岁,范围32 - 75岁)在低剂量奎尼丁治疗前和治疗期间进行了电生理研究,并评估了药物治疗的疗效。所有患者在基线时均通过程序电刺激诱发出室颤。口服奎尼丁(300 mg或600 mg/d)后,再次进行程序电刺激。14例患者中有6例(44%)的室颤诱发被预防。室颤诱发被抑制的患者血清奎尼丁浓度高于未被抑制的患者(分别为1.88±0.44与1.31±0.43 μg/ml)。程序电刺激后,14例患者中有9例(64%)继续接受奎尼丁治疗,其中4例已植入植入式心律转复除颤器。在平均31个月的奎尼丁随访期间,除1例出现腹泻(12.5%)外未观察到其他副作用。9例在使用奎尼丁治疗前因室颤发作频繁接受植入式心律转复除颤器电击的患者中,有3例未再发生室颤。低剂量奎尼丁对于频繁接受植入式心律转复除颤器电击的Brugada综合征患者有作为辅助治疗的潜力。