Spinal Cord Stimulation and 30‐Minute Heart Rate Variability in Refractory Angina Patients

Anselmino, Matteo; Ravera, Laura; Luca, Anna De; Capriolo, Michele; Bordese, Roberto; Trevi, Gian Paolo; Grimaldi, Roberto

doi:10.1111/j.1540-8159.2009.02174.x

Cited by 21 publications

(15 citation statements)

References 30 publications

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“…In patients with refractory angina, a similar decrease in sympathovagal balance was also reported with SCS, assessed by the same method of spectral analysis of the heart rate variability. 35 The effects of SCS on sympathetic activity have also been reported in a number of other studies using different assessment methods: (i) in a rat model of mononeuropathy, SCS was reported to suppress pathological hyperexcitability of a wide dynamic of range spinal neurons after peripheral nerve lesions 36 ; (ii) in a number of animal studies led by Linderoth, the peripheral vasodilatory effects of SCS were linked to the inhibition of efferent sympathetic activity as noted in the current. [37][38][39][40] Improvement of GI motility resulting from the inhibition of the sympathetic activity has been reported in numerous previous studies.…”

Section: Discussionsupporting

confidence: 65%

“…The decrease in sympathetic activity and sympathovagal balance with SCS observed in this study suggests the involvement of the extrinsic autonomic pathway as we initially hypothesized. In patients with refractory angina, a similar decrease in sympathovagal balance was also reported with SCS, assessed by the same method of spectral analysis of the heart rate variability . The effects of SCS on sympathetic activity have also been reported in a number of other studies using different assessment methods: (i) in a rat model of mononeuropathy, SCS was reported to suppress pathological hyperexcitability of a wide dynamic of range spinal neurons after peripheral nerve lesions; (ii) in a number of animal studies led by Linderoth, the peripheral vasodilatory effects of SCS were linked to the inhibition of efferent sympathetic activity as noted in the current .…”

Section: Discussionmentioning

confidence: 59%

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Therapeutic potential of spinal cord stimulation for gastrointestinal motility disorders: a preliminary rodent study

Guan

Sun

Foreman

et al. 2013

Neurogastroenterology Motil

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Section: Discussionsupporting

confidence: 65%

Section: Discussionmentioning

confidence: 59%

Therapeutic potential of spinal cord stimulation for gastrointestinal motility disorders: a preliminary rodent study

Guan

Sun

Foreman

et al. 2013

Neurogastroenterology Motil

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“…Similar autonomic mechanisms were also reported in previous studies in different clinical settings. Assessed by the same method of spectral analysis of HRV, SCS was found to decrease the sympathovagal ratio in patients with refractory angina and in diabetic rats . Assessed by total body norepinephrine, SCS was also noted to decrease overall sympathetic activity in patients with anginal pectoris .…”

Section: Discussionmentioning

confidence: 86%

Prokinetic effects of spinal cord stimulation and its autonomic mechanisms in dogs

Zhang¹,

Feng²,

Tu³

et al. 2019

Neurogastroenterology Motil

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Gastric dysmotility is a major pathophysiology factor in gastroparesis, functional dyspepsia (FD), and postoperative ileus (POI); it includes gastric myoelectric activity (slow wave) dysrhythmia and gastric contractile hypomotility. The prevalence of functional dyspepsia is 10%-40% in Western countries and 5%-30% in Asia. 1 The prevalence of postoperative ileus is between 10% and 30% for Abstract Background: Spinal cord stimulation (SCS) is widely used to treat chronic pain by inhibiting sympathetic activity; however, it is unknown whether it exerts a prokinetic effect on gastric motility. Our aim was to explore effects and possible mechanisms of SCS on glucagon-induced gastric dysmotility and dysrhythmia.Methods: Seven female dogs with electrodes chronically placed on the dorsal column of the spinal cord between T10 and T12 segments were studied in 2 randomized sessions (glucagon + sham-SCS, glucagon + SCS). SCS at T10 using a set of optimized stimulation parameters was performed for 30 minute immediately after glucagon injection. The antral manometry, electrogastrogram, and electrocardiogram were recorded to assess gastric contractions, gastric slow waves (GSW), and autonomic functions, respectively. Key Results: (a) Compared to baseline, glucagon decreased antral motility index (MI) (6315 ± 565 vs 3243 ± 775, P < 0.001), reduced the percentage of normal GSW (89 ± 3% vs 58 ± 3%, P < 0.01), and increased sympathetic activity (0.25 ± 0 0.06 vs 0.60 ± 0.07, P < 0.01). (b) The sympathetic activity was negatively correlated with antral MI (r = −0.558; P < 0.01) and the percentage of gastric normal slow wave (r = −0.616; P < 0.01). (c) SCS prevented the glucagon-induced impairment in antral hypomotility (MI: 5770 ± 927 vs 5521 ± 1238, P > 0.05) and GSW abnormalities (% of normal waves: 84 ± 4% vs 79 ± 6%, P > 0.05) and sympathetic activity (0.27 ± 0.03 vs 0.33 ± 0.07, P > 0.05). Conclusion: Spinal cord stimulation dramatically improves glucagon-induced impairment in gastric contractions and slow waves by inhibiting sympathetic activity. K E Y W O R D S autonomic function, gastric motility, gastric slow waves, neuromodulation, spinal cord stimulation

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“…In all 3 patients, there was an observation of significant reduction of TWA magnitude associated with SCS therapy 15 . Similarly, improvements in heart rate variability (HRV) have been associated with SCS angina therapy, particularly in reducing HRV measures of sympathetic activity (low/high frequency ratio) 16 . Another study, using a porcine animal model of ischemia and reperfusion, showed that SCS favorably impacts myocardial ischemic burden, infarct size, and arrhythmia risk 17 …”

Section: Editorial Commentmentioning

confidence: 94%

“…15 Similarly, improvements in heart rate variability (HRV) have been associated with SCS angina therapy, particularly in reducing HRV measures of sympathetic activity (low/high frequency ratio). 16 Another study, using a porcine animal model of ischemia and reperfusion, showed that SCS favorably impacts myocardial ischemic burden, infarct size, and arrhythmia risk. 17 Liu et al add several novel observations to those previously reported.…”

Section: Editorial Commentmentioning

confidence: 99%

Spinal Cord Stimulation: A Triple Threat Therapy?

Cao¹,

Saxon²

2011

Cardiovasc electrophysiol

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In the Journal, Liu et al. provide compelling evidence that acute spinal cord stimulation (SCS) improves myocardial energetics, ventricular function, and efficiency in a porcine model of postinfarct heart failure (HF). 1 The presumptive mechanism for this improvement (not explored in this study) is attributed to both reduced sympathetic stimulation, and enhanced parasympathetic activity, which is thought to be vagally mediated. 2,3 These salutary effects have been reported to occur even in the presence of neurohormonal blockade with beta-receptor blocker and angiotension inhibitor therapies. 3 Compensatory changes in the autonomic nervous system activity are known to impact adversely the clinical course of HF and to cause a host of adverse structural changes that further worsen cardiac function. Advances in pharmacologic therapy for HF over the past 20 years have been achieved by attenuating these changes with drugs like betareceptor blockers, angiotensin converting enzyme inhibitors, angiotensin receptor blockers, and aldosterone antagonists. These therapies greatly improve functional status, cause neurohormonal and structural reverse remodeling, reduce hospitalization, and increase survival. 4 There are compelling parallels between the pharmacologic neurohormonal agents and stimulatory neurohormonal therapy achieved with SCS. 5 A confluence of animal and human data indicate that sympathetic activation can predispose to ventricular arrhythmias and that parasympathetic activation is protective. 6,7 Similarly, particularly in HF, treatments that block excitatory neural traffic to the heart and achieve enhanced parasympathetic effects like beta-blocker receptor therapy and angiotension inhibitor therapy can increase the threshold to arrhythmia development and sudden death through direct and indirect effects. [8][9][10][11] Issa et al. demonstrated in a canine model of postinfarction HF that SCS reduces the incidence of transient ischemia related ventricular arrhythmias while simultaneously decreasing sinus rate, increasing the PR interval, and reducing systolic blood pressure. 12 Lopshire et al. evaluated the incidence of ventricular tachyarrhythmias with chronic SCS in canines after left anterior descending artery embolization and ICD implantation. The animals were assigned to control medical therapy (carvedilol), or SCS. After 10 weeks, the greatest recovery in

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Spinal Cord Stimulation and 30‐Minute Heart Rate Variability in Refractory Angina Patients

Abstract: (PACE 2009; 32:37-42) spinal cord stimulation, heart rate variability, refractory angina

Cited by 21 publications

References 30 publications

Therapeutic potential of spinal cord stimulation for gastrointestinal motility disorders: a preliminary rodent study

Therapeutic potential of spinal cord stimulation for gastrointestinal motility disorders: a preliminary rodent study

Prokinetic effects of spinal cord stimulation and its autonomic mechanisms in dogs

Spinal Cord Stimulation: A Triple Threat Therapy?

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