title: Thoracic spinal cord stimulation improves cardiac contractile function and myocardial oxygen consumption in a porcine model of ischemic heart failure.
abstract: BACKGROUND
  Prior experimental studies show that thoracic spinal cord stimulation (SCS) improves left ventricular (LV) ejection fraction (LVEF). The mechanism of this improvement in the LV contractile function after SCS and its effects on the myocardial oxygen consumption remains unknown.
  
  
  RESULTS
  We performed thoracic SCS (T1-T2 level) followed by 4 weeks of rapid ventricular pacing in 9 adult pigs with ischemic heart failure (HF) induced by myocardial infarction (MI). At 24 hours off-pacing, detailed echocardiogram and invasive hemodynamic assessment were performed to determine LV contractile function and myocardial oxygen consumption. Serum norepinephrine level was measured before and after SCS. SCS was performed on 2 occasions for 15 minutes, 30 minutes apart (recovery) with 50 Hz frequency (pulse width 0.2 millisecond, 90% of motor threshold at 2 Hz output). Echocardiogram revealed significant decrease in LVEF (33.8 ± 1.8% vs 66.5 ± 1.7%, P < 0.01) after induction of MI and HF. Compared with MI and HF, acute SCS significantly increased LVEF and +dP/dt (all P < 0.05). Withdrawal of SCS during recovery decreased +dP/dt, but not LVEF that increased again with repeated SCS. Myocardial oxygen consumption also significantly decreased during SCS compared with MI and HF (P = 0.006) without any change in serum norepinephrine level (P = 0.9). Speckle tracking imaging showed significant improvement in global and regional circumferential strains over the infarcted mid and apical regions, decreased in time to peak circumferential strain over the lateral and posterior wall after SCS, and the degree of intraventricular dyssynchrony during SCS compared with MI and HF (P < 0.05).
  
  
  CONCLUSIONS
  In a porcine model of ischemic HF, acute SCS improved global and regional LV contractile function and intraventricular dyssynchrony, and decreased myocardial oxygen consumption without elevation of norepinephrine level.
authors.affiliation: Cardiology Division, Department of Medicine, Queen Mary Hospital, University of Hong Kong, Hong Kong, China.
authors.forename: Yuan
authors.initials: Y
authors.lastname: Liu
authors.forename: Wen-Sheng
authors.initials: WS
authors.lastname: Yue
authors.forename: Song-Yan
authors.initials: SY
authors.lastname: Liao
authors.forename: Yuelin
authors.initials: Y
authors.lastname: Zhang
authors.forename: Ka-Wing
authors.initials: KW
authors.lastname: Au
authors.forename: Chika
authors.initials: C
authors.lastname: Shuto
authors.forename: Cary
authors.initials: C
authors.lastname: Hata
authors.forename: Euljoon
authors.initials: E
authors.lastname: Park
authors.forename: Peter
authors.initials: P
authors.lastname: Chen
authors.forename: Chung-Wah
authors.initials: CW
authors.lastname: Siu
authors.forename: Hung-Fat
authors.initials: HF
authors.lastname: Tse
mesh_terms: D000818:Animals; D015415:Biomarkers / Q000097:blood; D006328:Cardiac Catheterization; D004195:Disease Models, Animal; D015150:Echocardiography, Doppler; D004599:Electric Stimulation Therapy / Q000379:methods*; D005260:Female; D006333:Heart Failure / Q000175:diagnosis / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology / Q000628:therapy*; D009200:Myocardial Contraction; D017202:Myocardial Ischemia / Q000150:complications* / Q000378:metabolism / Q000503:physiopathology; D009206:Myocardium / Q000378:metabolism*; D009638:Norepinephrine / Q000097:blood; D010101:Oxygen Consumption; D020127:Recovery of Function; D013116:Spinal Cord; D013318:Stroke Volume; D013552:Swine; D013904:Thoracic Vertebrae; D013997:Time Factors; D018487:Ventricular Dysfunction, Left / Q000175:diagnosis / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology / Q000628:therapy*; D016277:Ventricular Function, Left
chemical_list: D015415:Biomarkers; D009638:Norepinephrine