Effects of spinal cord stimulation in angina pectoris induced by pacing and possible mechanisms of action.

Mannheimer, Clas; Eliasson, Tore; Andersson, Bert; Bergh, Claes‐Håkan; Augustinsson, Lars-Erik; Emanuelsson, Håkan; Waagstein, Finn

doi:10.1136/bmj.307.6902.477

Cited by 199 publications

(105 citation statements)

References 27 publications

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“…19 The proposed mechanisms behind the anti-ischaemic effect in coronary artery disease are contradictory. 20,21 Chauhan et al have demonstrated that TENS increased coronary blood flow at rest in patients with coronary artery disease and syndrome-X, 20 whereas other studies on TENS and spinal cord stimulation have shown a decrease in myocardial oxygen consumption. 21 The heart rate was unaffected throughout the study.…”

Section: Discussionmentioning

confidence: 99%

“…20,21 Chauhan et al have demonstrated that TENS increased coronary blood flow at rest in patients with coronary artery disease and syndrome-X, 20 whereas other studies on TENS and spinal cord stimulation have shown a decrease in myocardial oxygen consumption. 21 The heart rate was unaffected throughout the study. This finding is similar to those of other reports of haemodynamic changes during both low and high frequency TENS.…”

Section: Discussionmentioning

confidence: 99%

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The effect of transcutaneous electric nerve stimulation in patients with therapy-resistant hypertension

et al. 2000

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Objectives: Afferent nerve stimulation, such as acupuncture and transcutaneous electric nerve stimulation (TENS), has shown a blood pressure reduction in both animal and man. In the present open and non-controlled study we investigated the effect on 24-h ambulatory blood pressure of low frequency TENS in a group of hypertensive subjects who do not respond properly to pharmacological treatment. Method: Twelve patients were investigated. The patients were treated with TENS at two acupoints on both forearms for 30 min twice daily during 4 weeks. 24-hour ambulatory blood pressure monitoring was recorded 1 week before, at start, at the end and finally 1 week after the TENS treatment.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

The effect of transcutaneous electric nerve stimulation in patients with therapy-resistant hypertension

et al. 2000

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“…Furthermore, they observed a simultaneous decrease in heart rate and reduced systolic blood pressure, consistent with the antisympathetic effects of spinal cord stimulation. [92][93][94][95] In a similar model, intrathecal clonidine, which is known to cause centrally mediated bradycardia and hypotension because of its sympatholytic effects, when delivered via a catheter at T2-T4 spinal segments, also significantly reduced the occurrence of ventricular tachycardia and fibrillation during transient myocardial ischemia. 96 The report of sympathetic blockade in humans compared survival in a group of 49 patients with recurrent ventricular fibrillation (electrical storm) early after MI treated with standard advanced cardiac life support (ACLS) protocol vs sympathetic blockade.…”

Section: Selective Sympathetic Blockadementioning

confidence: 95%

The Role of the Autonomic Nervous System in Sudden Cardiac Death

Vaseghi

Shivkumar²

2008

Progress in Cardiovascular Diseases

336

233

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The cardiac autonomic nervous system consists of 2 branches-the sympathetic and the parasympathetic systems-that work in a delicately tuned, yet opposing fashion in the heart. This extrinsic control mechanism can dominate intrinsic regulatory mechanisms that modulate heart rate and cardiac output. These branches differ in their neurotransmitters (norepinephrine and acetylcholine) and exert stimulatory or inhibitory effects on target tissue via adrenergic and muscarinic receptors. Stimulation of the sympathetic branch exerts facilitatory effects on function, increasing heart rate and myocardial contractility, whereas the stimulation of the parasympathetic branch exerts inhibitory effects that decrease heart rate and contractility. The interplay between these two branches is complex and susceptible to control at several levels, from centrally mediated baroreceptors and chemoreceptors to local interneuronal interactions.Alterations in autonomic function occur in several interrelated cardiac conditions including sudden cardiac death, congestive heart failure, diabetic neuropathy, and myocardial ischemia. Although the full extent of these changes has not been elucidated, multiple autonomic remodeling mechanisms have been observed at both the neuronal fiber and myocardial cellular level that contribute to an arrhythmogenic substrate. We describe the anatomy of both systems in this review. However, the review will premdominantly focus on the sympathetic system, whose role in the modulation of cardiac arrhythmias is slightly better delineated. Cardiac Autonomic Innervation: NeuroanatomyBoth branches of the autonomic nervous system are composed of both afferent and efferent as well interneuronal fibers (Fig 1). Sympathetic innervation originates mainly in the right and left stellate ganglia. These fibers travel along the epicardial vascular structures of the heart and penetrate into the underlying myocardium similar to coronary vessels and end as sympathetic nerve terminals reaching the endocardium. Based on norepinephrine content studies, a gradient exists in sympathetic innervation from atria to the ventricles and from base to apex of the heart. Therefore, the atria are most densely innervated, but the ventricles are also supplied with a sympathetic network, most densely at the base. 1 Parasympathetic effects are carried by the right and left vagus nerves, originating in the medulla. The vagus nerve further divides into the superior and inferior cardiac nerves, finally merging with the postganglionic sympathetic neurons to form a plexus of nerves at the base of the heart, known as the cardiac plexus. In contrast to sympathetic neurons, after parasympathetic fibers cross the atrioventricular (AV) groove along the surface of the heart,

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“…Three of the trials (DeJongste, ESBY, Hautvast) assessed the frequency of angina attacks ( In the ESBY trial, the SCS patients had the device switched off during exercise testing, which would be expected to diminish its effectiveness (ESBY authors had previously reported on a case series of angina patients in which SCS when switched on could improve exercise training 103 ). The exercise test in the ESBY trial found that at 6 months CABG had a significantly greater increase in maximum workload capacity than SCS (p = 0.02).…”

Section: Angina -Functional Outcomesmentioning

confidence: 99%

Spinal cord stimulation for chronic pain of neuropathic or ischaemic origin: systematic review and economic evaluation

Simpson

Duenas²,

Holmes³

et al. 2009

Health Technol Assess

191

173

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Effects of spinal cord stimulation in angina pectoris induced by pacing and possible mechanisms of action.

Cited by 199 publications

References 27 publications

The effect of transcutaneous electric nerve stimulation in patients with therapy-resistant hypertension

The effect of transcutaneous electric nerve stimulation in patients with therapy-resistant hypertension

The Role of the Autonomic Nervous System in Sudden Cardiac Death

Spinal cord stimulation for chronic pain of neuropathic or ischaemic origin: systematic review and economic evaluation

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