University of California-Los Angeles (UCLA) Cardiac Arrhythmia Center, David Geffen School of Medicine, Los Angeles, California; UCLA Neurocardiology Research Center of Excellence, Los Angeles, California; Molecular, Cellular & Integrative Physiology Program, UCLA, Los Angeles, California.
University of California-Los Angeles (UCLA) Cardiac Arrhythmia Center, David Geffen School of Medicine, Los Angeles, California; UCLA Neurocardiology Research Center of Excellence, Los Angeles, California.
Heart Rhythm. 2017 Nov;14(11):1665-1672. doi: 10.1016/j.hrthm.2017.06.025. Epub 2017 Jun 16.
Autonomic dysfunction contributes to induction of ventricular tachyarrhythmia (VT).
To determine the efficacy of charge-balanced direct current (CBDC), applied to the T1-T2 segment of the paravertebral sympathetic chain, on VT inducibility post-myocardial infarction (MI).
In a porcine model, CBDC was applied in acute animals (n = 7) to optimize stimulation parameters for sympathetic blockade and in chronic MI animals (n = 7) to evaluate the potential for VTs. Chronic MI was induced by microsphere embolization of the left anterior descending coronary artery. At termination, in anesthetized animals and following thoracotomy, an epicardial sock array was placed over both ventricles and a quadripolar carousel electrode positioned underlying the right T1-T2 paravertebral chain. In acute animals, the efficacy of CBDC carousel (CBDCC) block was assessed by evaluating cardiac function during T2 paravertebral ganglion stimulation with and without CBDCC. In chronic MI animals, VT inducibility was assessed by extrasystolic (S1-S2) stimulations at baseline and under >66% CBDCC blockade of T2-evoked sympathoexcitation.
CBDCC demonstrated a current-dependent and reversible block without impacting basal cardiac function. VT was induced at baseline in all chronic MI animals. One animal died after baseline induction. Of the 6 remaining animals, only 1 was reinducible with simultaneous CBDCC application (P < .002 from baseline). The ventricular effective refractory period (VERP) was prolonged with CBDCC (323 ± 26 ms) compared to baseline (271 ± 32 ms) (P < .05).
Axonal block of the T1-T2 paravertebral chain with CBDCC reduced VT in a chronic MI model. CBDCC prolonged VERP, without altering baseline cardiac function, resulting in improved electrical stability.
自主神经功能障碍可导致室性心动过速(VT)的发生。
确定平衡电荷直流电(CBDC)应用于椎旁交感神经链 T1-T2 节段对心肌梗死后 VT 可诱导性的疗效。
在猪模型中,将 CBDC 应用于急性动物(n=7)以优化交感神经阻滞的刺激参数,并在慢性 MI 动物(n=7)中评估 VT 的潜在可能性。通过左前降支冠状动脉微球栓塞诱导慢性 MI。在实验结束时,在麻醉动物和开胸后,将心外膜套索数组放置在两个心室上,并将四极 carousel 电极置于右 T1-T2 椎旁链下方。在急性动物中,通过评估 T2 椎旁神经节刺激时 CBDC carousel(CBDCC)阻滞前后的心脏功能来评估 CBDCC 阻滞的效果。在慢性 MI 动物中,通过基础状态和 T2 诱发的交感兴奋的 >66% CBDCC 阻滞下的期外刺激来评估 VT 可诱导性。
CBDCC 表现出电流依赖性和可逆性阻滞,而不影响基础心脏功能。所有慢性 MI 动物在基础状态下均诱导出 VT。一只动物在基础诱导后死亡。在 6 只剩余动物中,只有 1 只在同时应用 CBDCC 时可重新诱导(与基础状态相比,P <.002)。与基础状态相比,CBDCC 延长了心室有效不应期(VERP)(323±26 ms 比 271±32 ms)(P <.05)。
在慢性 MI 模型中,CBDC 对 T1-T2 椎旁链的轴突阻滞减少了 VT。CBDCC 延长了 VERP,而不改变基础心脏功能,从而提高了电稳定性。