Abstract

Introduction: Spinal cord stimulation (SCS) is effective neuromodulation therapy for pain, but little is known about the effectiveness of SCS for arrhythmia prevention in chronic myocardial infarction (MI). Hypothesis: Chronic SCS reduces MI-induced cardiac sympathoexcitation and reduces ventricular arrhythmias. Methods: Yorkshire pigs were randomized to chronic left circumflex coronary artery MI alone (n=11) or MI + chronic SCS (n=9). Epidural SCS lead was placed percutaneously T1-T4 of the spinal cord and reactive SCS was performed at 10 kHz, 0.03ms, and 2.5mA after MI. Holter ECG was recorded for heart rate variability (HRV) analysis, performed throughout 4-5 weeks post-MI. To create acute stress in chronic MI, epicardial extraventricular programmed stimulus (S1/S2 pacing), and acute left anterior descending coronary artery (LAD) ischemia(1h)+reperfusion(2h) (I/R) injury were conducted during terminal experiment. SCS was continued throughout terminal experiment. Cardiac electrophysiological data (activation recovery interval (ARI) and dispersion of repolarization (DOR)), as well as ventricular arrhythmia quantification were measured by placing a 56-electrode mesh sock over the heart . Data is shown as mean±SEM. Results: 1 week after MI, 30min HRV showed a higher high-frequency band and lower very-low and low-frequency band with SCS (%HF: MI 25±4 vs SCS 51±4, p=0.0028. %VLF: 50±4 vs 30±3, p=0.0015. %LF: 22±2 vs 14±2, p=0.047). In the terminal experiment, SCS reduced the maximum slope (Smax) of the electrical restitution curve described by S1/S2 pacing (Smax: MI 0.6±0.03 vs SCS 0.4±0.05, p=0.023). After acute LAD ischemia, SCS reduced global %ARI change (MI -19±3% vs SCS -11±1%, p=0.019), specifically in the ischemic region (MI -31±4% vs SCS -16±3%, p=0.008), and global %DOR (MI 1513±288% vs SCS 595±144%, p=0.011). Chronic SCS also reduced ventricular tachycardia and ventricular fibrillation during acute I/R (MI 15±3 vs SCS 5±0.8, p=0.014). Conclusions: Reactive SCS therapy mitigates cardiac autonomic imbalance in chronic MI and protects from new acute ischemia induced cardiac sympathoexcitation and ventricular arrhythmias.

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