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The first spinal cord stimulator was implanted for intractable angina in 1987. Following this innovation there followed extensive scrutiny of neurostimulation in patients suffering from coronary artery disease, with several observational trials demonstrating the ability of spinal cord stimulation (SCS) to diminish angina, reduce the frequency of hospital admissions, and improve quality of life.
SCS moderates the symptoms of angina by inhibition of pain perception through the release of spinal inhibitory neurotransmitters at the level of the dorsal horn, and also potentially by liberation of cardiac β endorphins. In addition it has been established that neurostimulation also achieves its benefit in part by reduction in cardiac ischaemia.1 The proposed mechanism for this observation is altered cardiac autonomic balance.
Heart rate variability (HRV) has been used to verify this proposed influence on cardiac autonomic tone. The two trials published to date, however, have failed to demonstrate any such effect.23 Both studies used long term Holter (24 and 48 hour) ECG recording intervals in which baseline conditions were not controlled and spinal cord stimulators were activated only for a minority of the post-implant recording periods. The aim of this study was to use short term HRV recordings to assess directly the influence of SCS on HRV in a controlled experimental setting.
Sixteen consecutive patients with chronic …
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