Abstract 19912: Direct Current Block of the Paravertebral Chain Stabilizes Ventricular Electrical Function Post-Myocardial Infarction
Background: Surgical sympathetic decentralization has evolved to effectively treat refractory ventricular arrhythmias but has irreversible off target side effects. Bioelectric therapies applied to the sympathetic nervous system may provide an effective and reversible method to prevent ventricular arrhythmias.
Objective: To assess the efficacy of charge balanced direct current (CBDC), applied to the T1-T2 region of the paravertebral chain, to impact the ventricular arrhythmia potential post-myocardial infarction (MI).
Methods: In a porcine model (n=7), MI was induced beyond the first diagonal in the left anterior descending coronary artery by microsphere injection. Terminal procedures were performed (8-16 weeks) thereafter. Following a mid-sternal thoracotomy, a 56-epicardial-electrode sock was placed over both ventricles and a quadripolar carousel electrode positioned underlying the right T1-T2 paravertebral chain. The efficacy of CBDC carousel (CBDCC) block was assessed by stimulating the right T3 paravertebral ganglion with and without CBDCC. VT inducibility to a S1-S2 pacing protocol was then assessed at baseline (BL) and repeated under >50% CBDCC blockade of functional sympathetic efferent projections to the heart.
Results: VT was induced at baseline in all animals (n=7). One animal died after baseline induction. Of the 6 remaining animals, only one was re-inducible for VT with simultaneous CBDCC application (p< 0.002 from baseline). The S2 effective refractory period (ERP) was also prolonged with DCC (323±26ms) compared to baseline (271±32ms) (p<0.05). ARI was not altered compared to baseline as a result of CBDCC.
Conclusions: Axonal modulation of the T1-T2 paravertebral chain with CBDCC significantly reduced ventricular arrhythmias in a chronic MI model by 83%. CBDCC altered ventricular ERP, without altering baseline ARI, resulting in improved electrical stability.
- Arrhythmias, treatment of
- Myocardial infarction
- Autonomic nervous system
- Autonomic Control
Author Disclosures: U. Buckley: None. R.W. Chui: None. P.S. Rajendran: None. T. Vrabec: None. K. Shivkumar: Research Grant; Significant; GlaxoSmithKline. J.L. Ardell: Research Grant; Significant; GlaxoSmithKline.
- © 2016 by American Heart Association, Inc.