Plotnikov Alexei N, Bucchi Annalisa, Shlapakova Iryna, Danilo Peter, Brink Peter R, Robinson Richard B, Cohen Ira S, Rosen Michael R
Center for Molecular Therapeutics, Columbia University, New York, New York 10032, USA.
Heart Rhythm. 2008 Feb;5(2):282-8. doi: 10.1016/j.hrthm.2007.09.028. Epub 2007 Oct 3.
A potential concern about biological pacemakers is their possible malfunction, which might create ventricular tachycardias (VTs).
The purpose of this study was to test our hypothesis that should VTs complicate implantation of HCN-channel-based biological pacemakers, they would be suppressed by inhibitors of the pacemaker current, I(f).
We created a chimeric channel (HCN212) containing the N- and C-termini of mouse HCN2 and the transmembrane region of mouse HCN1 and implanted it in HEK293 cells. Forty-eight hours later, in whole-cell patch clamp recordings, mean steady state block induced by 3 microM ivabradine (IVB) showed HCN1 = HCN212 > HCN2 currents. The HCN212 adenoviral construct was then implanted into the canine left bundle branch in 11 dogs. Complete AV block was created via radiofrequency ablation, and a ventricular demand electronic pacemaker was implanted (VVI 45 bpm). Electrocardiogram, 24-hour Holter monitoring, and pacemaker log record check were performed for 11 days.
All dogs developed rapid VT (>120 bpm, maximum rate = 285 +/- 37 bpm) at 0.9 +/- 0.3 days after implantation that persisted through 5 +/- 1 days. IVB, 1 mg/kg over 5 minutes, was administered during rapid VT, and three dogs received a second dose 24 hours later. While VT terminated with IBV in all instances within 3.4 +/- 0.6 minutes, no effect of IVB on sinus rate was noted.
We conclude that (1) I(f)-associated tachyarrhythmias-if they occur with HCN-based biological pacemakers-can be controlled with I(f)-inhibiting drugs such as IVB; (2) in vitro, IVB appears to have a greater steady state inhibiting effect on HCN1 and HCN212 isoforms than on HCN4; and (3) VT originating from the HCN212 injection site is suppressed more readily than sinus rhythm. This suggests a selectivity of IVB at the concentration attained for ectopic over HCN4-based pacemaker function. This might confer a therapeutic benefit.
生物起搏器一个潜在的问题是其可能出现故障,这可能会引发室性心动过速(VTs)。
本研究的目的是检验我们的假设,即如果VTs使基于超极化激活环核苷酸门控通道(HCN通道)的生物起搏器植入变得复杂,那么它们会被起搏电流I(f)的抑制剂所抑制。
我们构建了一个嵌合通道(HCN212),其包含小鼠HCN2的N端和C端以及小鼠HCN1的跨膜区域,并将其植入人胚肾293(HEK293)细胞中。48小时后,在全细胞膜片钳记录中,3 microM伊伐布雷定(IVB)诱导的平均稳态阻滞显示HCN1 = HCN212 > HCN2电流。然后将HCN212腺病毒构建体植入11只犬的左束支。通过射频消融造成完全性房室传导阻滞,并植入心室按需型电子起搏器(VVI 45次/分钟)。进行11天的心电图、24小时动态心电图监测以及起搏器日志记录检查。
所有犬在植入后0.9±0.3天出现快速VT(>120次/分钟,最大心率 = 285±37次/分钟),并持续5±1天。在快速VT期间给予IVB,1毫克/千克,持续5分钟,3只犬在24小时后接受了第二剂。虽然在所有情况下VT均在3.4±0.6分钟内被IBV终止,但未观察到IVB对窦性心率有影响。
我们得出结论:(1)如果基于HCN的生物起搏器出现与I(f)相关的快速性心律失常,可以用I(f)抑制药物如IVB进行控制;(2)在体外,IVB对HCN1和HCN212亚型的稳态抑制作用似乎比对HCN4的作用更大;(3)起源于HCN212注射部位的VT比窦性心律更容易被抑制。这表明在达到的浓度下,IVB对异位起搏功能比对基于HCN4的起搏功能具有选择性。这可能带来治疗益处。