Spinal cord stimulation effects on myocardial ischemia, infarct size, ventricular arrhythmia, and noninvasive electrophysiology in a porcine ischemia-reperfusion model.
BACKGROUND
Susceptibility to ventricular arrhythmias and sudden cardiac death can be reduced by modulation of autonomic tone. Spinal cord stimulation (SCS) presumably affects autonomic tone and reduces myocardial ischemia.


OBJECTIVE
The purpose of this study was to investigate whether SCS could reduce myocardial ischemia, infarct size, and ventricular arrhythmias as well as repolarization alterations in a porcine ischemia-reperfusion model.


METHODS
Anesthetized common Landrace pigs were randomized to SCS (n = 10) or sham treatment (n = 10) before, during, and after 45 minutes of coronary occlusion. Area at risk, infarct size, and spontaneous ventricular arrhythmias were analyzed. Continuous three-dimensional vectorcardiograms was recorded and analyzed with respect to ECG intervals, ST-segment, and T-vector and T-vector-loop morphology.


RESULTS
SCS was associated with significantly (P <.04) fewer episodes of nonsustained ventricular tachycardia (NSVT) and sustained ventricular tachycardia (SVT), particularly during mid-left anterior descending artery (LAD) occlusion (SCS vs non-SCS; NSVT, mid- and proximal LAD: 0 vs 22 and 45 vs 72; SVT, mid- and proximal LAD: 3 vs 15 and 5 vs 5). No difference in ventricular fibrillation episodes was observed. The SCS group had significantly less ST elevation (P <.03) but similar area at risk, infarct size, and ratio of infarct size/area at risk. Ischemia induced increases of T(amplitude) and T(area) suggesting increased repolarization gradients, which were significantly reduced by SCS (P <.01 for both).


CONCLUSIONS
SCS appears to have an antiarrhythmic effect on spontaneous NSVT and SVT during ischemia-reperfusion in association with a reduction of repolarization alterations. Vectorcardiography signs of myocardial ischemia were reduced by SCS, but this intervention was not accompanied by any effect on infarct size.
Department of Molecular and Clinical Medicine/Cardiology, Sahlgrenska Academy, University of Gothenburg, Sweden. Jacob.Odenstedt@vgregion.se
Jacob
J
Odenstedt
Bengt
B
Linderoth
Lennart
L
Bergfeldt
Olof
O
Ekre
Lars
L
Grip
Clas
C
Mannheimer
Paulin
P
Andréll
D000818:Animals; D004195:Disease Models, Animal; D004599:Electric Stimulation Therapy / Q000379:methods*; D004562:Electrocardiography; D004567:Electrodes, Implanted; D005260:Female; D009203:Myocardial Infarction / Q000209:etiology / Q000503:physiopathology / Q000517:prevention & control; D017202:Myocardial Ischemia / Q000209:etiology / Q000503:physiopathology / Q000517:prevention & control*; D015428:Myocardial Reperfusion Injury / Q000150:complications* / Q000503:physiopathology / Q000628:therapy; D013116:Spinal Cord; D013552:Swine; D017180:Tachycardia, Ventricular / Q000209:etiology / Q000503:physiopathology / Q000517:prevention & control*; D016896:Treatment Outcome