Thoracic spinal cord stimulation reduces the risk of ischemic ventricular arrhythmias in a postinfarction heart failure canine model

Ziad F. Issa, Xiaohong Zhou, Michael R. Ujhelyi, Josh Rosenberger, Deepak Bhakta, William Groh, John Miller, Douglas P. Zipes

Research output: Contribution to journalArticle

114 Citations (Scopus)

Abstract

Background - Thoracic spinal cord stimulation (SCS) is a promising therapy in treating refractory angina. This study was designed to investigate SCS with regard to the risk of arrhythmias during myocardial ischemia and its cardiac electrophysiological effects. Methods and Results - We studied 22 dogs with healed anterior myocardial infarction (MI) and superimposed heart failure (HF) induced by rapid ventricular pacing. SCS was applied at the dorsal T,-T2 segments of the spinal cord (at 50 Hz, 0.2 ms) for 15 minutes. Transient (2-minute) myocardial ischemia was induced on 2 separate occasions (no SCS and SCS) to provoke ventricular arrhythmias (ventricular tachycardia/ventricular fibrillation; VT/VF). Ischemic episodes were separated by 90 minutes, and dogs were randomly assigned to receive SCS or no SCS before the first or second ischemic episode. SCS reduced the occurrence of VT/VF from 59% to 23% when SCS was applied during transient myocardial ischemia (odds ratio, 0.36; 95% confidence interval, 0.1626 to 0.5646; P=0.0009). SCS also decreased sinus rate by 7.5±14 bpm (P=0.048), increased the PR interval by 11.1±14.7 ms (P=0.009), and reduced systolic blood pressure by 9.8±13.6 mm Hg (P=0.02). Conclusions - Thoracic SCS appears to protect against ischemic VT/VF in a canine model of healed MI and HF. SCS reduced sinus rate and systolic blood pressure, changes consistent with the previously known antisympathetic effect of SCS, which may have contributed to the antiarrhythmic benefits.

Original languageEnglish
Pages (from-to)3217-3220
Number of pages4
JournalCirculation
Volume111
Issue number24
DOIs
StatePublished - Jun 21 2005

Fingerprint

Spinal Cord Stimulation
Canidae
Cardiac Arrhythmias
Thorax
Heart Failure
Blood Pressure
Myocardial Ischemia
Myocardial Infarction
Dogs
Ventricular Fibrillation
Ventricular Tachycardia

Keywords

  • Arrhythmia
  • Electric stimulation
  • Ischemia
  • Nervous system, autonomic
  • Spinal cord

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine

Cite this

Thoracic spinal cord stimulation reduces the risk of ischemic ventricular arrhythmias in a postinfarction heart failure canine model. / Issa, Ziad F.; Zhou, Xiaohong; Ujhelyi, Michael R.; Rosenberger, Josh; Bhakta, Deepak; Groh, William; Miller, John; Zipes, Douglas P.

In: Circulation, Vol. 111, No. 24, 21.06.2005, p. 3217-3220.

Research output: Contribution to journalArticle

Issa, Ziad F. ; Zhou, Xiaohong ; Ujhelyi, Michael R. ; Rosenberger, Josh ; Bhakta, Deepak ; Groh, William ; Miller, John ; Zipes, Douglas P. / Thoracic spinal cord stimulation reduces the risk of ischemic ventricular arrhythmias in a postinfarction heart failure canine model. In: Circulation. 2005 ; Vol. 111, No. 24. pp. 3217-3220.
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AU - Zhou, Xiaohong

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AU - Rosenberger, Josh

AU - Bhakta, Deepak

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AU - Miller, John

AU - Zipes, Douglas P.

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N2 - Background - Thoracic spinal cord stimulation (SCS) is a promising therapy in treating refractory angina. This study was designed to investigate SCS with regard to the risk of arrhythmias during myocardial ischemia and its cardiac electrophysiological effects. Methods and Results - We studied 22 dogs with healed anterior myocardial infarction (MI) and superimposed heart failure (HF) induced by rapid ventricular pacing. SCS was applied at the dorsal T,-T2 segments of the spinal cord (at 50 Hz, 0.2 ms) for 15 minutes. Transient (2-minute) myocardial ischemia was induced on 2 separate occasions (no SCS and SCS) to provoke ventricular arrhythmias (ventricular tachycardia/ventricular fibrillation; VT/VF). Ischemic episodes were separated by 90 minutes, and dogs were randomly assigned to receive SCS or no SCS before the first or second ischemic episode. SCS reduced the occurrence of VT/VF from 59% to 23% when SCS was applied during transient myocardial ischemia (odds ratio, 0.36; 95% confidence interval, 0.1626 to 0.5646; P=0.0009). SCS also decreased sinus rate by 7.5±14 bpm (P=0.048), increased the PR interval by 11.1±14.7 ms (P=0.009), and reduced systolic blood pressure by 9.8±13.6 mm Hg (P=0.02). Conclusions - Thoracic SCS appears to protect against ischemic VT/VF in a canine model of healed MI and HF. SCS reduced sinus rate and systolic blood pressure, changes consistent with the previously known antisympathetic effect of SCS, which may have contributed to the antiarrhythmic benefits.

AB - Background - Thoracic spinal cord stimulation (SCS) is a promising therapy in treating refractory angina. This study was designed to investigate SCS with regard to the risk of arrhythmias during myocardial ischemia and its cardiac electrophysiological effects. Methods and Results - We studied 22 dogs with healed anterior myocardial infarction (MI) and superimposed heart failure (HF) induced by rapid ventricular pacing. SCS was applied at the dorsal T,-T2 segments of the spinal cord (at 50 Hz, 0.2 ms) for 15 minutes. Transient (2-minute) myocardial ischemia was induced on 2 separate occasions (no SCS and SCS) to provoke ventricular arrhythmias (ventricular tachycardia/ventricular fibrillation; VT/VF). Ischemic episodes were separated by 90 minutes, and dogs were randomly assigned to receive SCS or no SCS before the first or second ischemic episode. SCS reduced the occurrence of VT/VF from 59% to 23% when SCS was applied during transient myocardial ischemia (odds ratio, 0.36; 95% confidence interval, 0.1626 to 0.5646; P=0.0009). SCS also decreased sinus rate by 7.5±14 bpm (P=0.048), increased the PR interval by 11.1±14.7 ms (P=0.009), and reduced systolic blood pressure by 9.8±13.6 mm Hg (P=0.02). Conclusions - Thoracic SCS appears to protect against ischemic VT/VF in a canine model of healed MI and HF. SCS reduced sinus rate and systolic blood pressure, changes consistent with the previously known antisympathetic effect of SCS, which may have contributed to the antiarrhythmic benefits.

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