不间断伊伐布雷定敏感性房性心动过速的临床和电生理相关性。

B. Banavalikar, J. Shenthar, D. Padmanabhan, S. P. Valappil, S. Singha, A. Kottayan, M. Ghadei, Muzaffar Ali
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引用次数: 17

摘要

背景:持续性局灶性房性心动过速(FAT)如果不治疗,可导致心室功能障碍和心力衰竭(心动过速诱发的心肌病)。脂肪的药物治疗往往是困难和无效的。伊伐布雷定治疗FAT的疗效尚未得到系统评价。方法研究对象为心脏结构正常且持续时间>24小时的不间断脂肪患者。未排除由脂肪引起的心室功能障碍患者。所有抗心律失常药物在开始使用伊伐布雷定之前至少停药5个半衰期。口服伊伐布雷定(成人,10毫克,两次,间隔12小时;儿科患者:0.28 mg/kg,分2次给药)在重症监护病房连续心电图监测下开始使用。阳性反应定义为心动过速终止,窦性心律恢复或心动过速抑制至<100次/分,在开始使用伊伐布雷定后12小时内无终止。结果28例患者平均年龄34.6±21.5岁;女性(60.7%)被纳入研究。最常见的症状是心悸(85.7%),其次是呼吸短促(25%)。心动过速时平均房率为170±21次/分,平均左室射血分数为54.7±14.3%。总体而言,18例(64.3%)患者在首次给药后6小时内出现反应。18名伊伐布雷定应答者中有13名随后进行了成功的导管消融。与其他心房部位产生的脂肪相比,起源于心房附件的脂肪是伊伐布雷定反应的预测因子(P=0.046)。结论西伐布雷定敏感性房性心动过速占非结构性心脏病患者持续性脂肪的64%。起源于心房附件的持续性脂肪比起源于其他心房部位的脂肪更容易对伊伐布雷定产生反应。我们的发现暗示了FAT发病机制中的有趣电流。
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Clinical and Electrophysiological Correlates of Incessant Ivabradine-Sensitive Atrial Tachycardia.
BACKGROUND Incessant focal atrial tachycardia (FAT), if untreated, can lead to ventricular dysfunction and heart failure (tachycardia-induced cardiomyopathy). Drug therapy of FAT is often difficult and ineffective. The efficacy of ivabradine has not been systematically evaluated in the treatment of FAT. METHODS The study group consisted of patients with incessant FAT (lasting >24 hours) and structurally normal hearts. Patients with ventricular dysfunction as a consequence of FAT were not excluded. All antiarrhythmic drugs were discontinued at least 5 half-lives before the initiation of ivabradine. Oral ivabradine (adults, 10 mg twice 12 hours apart; pediatric patients: 0.28 mg/kg in 2 divided doses) was initiated in the intensive care unit under continuous electrocardiographic monitoring. A positive response was defined as the termination of tachycardia with the restoration of sinus rhythm or suppression of the tachycardia to <100 beats per minute without termination within 12 hours of initiating ivabradine. RESULTS Twenty-eight patients (mean age, 34.6±21.5 years; women, 60.7%) were included in the study. The most common symptom was palpitation (85.7%) followed by shortness of breath (25%). The mean atrial rate during tachycardia was 170±21 beats per minute, and the mean left ventricular ejection fraction was 54.7±14.3%. Overall, 18 (64.3%) patients responded within 6 hours of the first dose of ivabradine. Thirteen of 18 ivabradine responders subsequently underwent successful catheter ablation. FAT originating in the atrial appendages was a predictor of ivabradine response compared with those arising from other atrial sites (P=0.046). CONCLUSIONS Ivabradine-sensitive atrial tachycardia constitutes 64% of incessant FAT in patients without structural heart disease. Incessant FAT originating in the atrial appendages is more likely to respond to ivabradine than that arising from other atrial sites. Our findings implicate the funny current in the pathogenesis of FAT.
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