Spinal Cord Stimulation for Long-term Treatment of Severe Angina Pectoris

What Does the Evidence Say?

Mats Börjesson; Paulin Andréll; Clas Mannheimer


Future Cardiol. 2011;7(6):825-833. 

In This Article

SCS in Severe Angina Pectoris: Mechanisms

Spinal cord stimulation has been used for treating severe and refractory angina pectoris since the 1980s. Initially, critics of the method were concerned that a pure pain relieving effect may be dangerous for the patient with symptomatic ischemic heart disease. However, subsequent studies demonstrated that SCS alleviates anginal symptoms without masking the symptoms of acute myocardial infarction.[20,21] Importantly, SCS seems to decrease the underlying myocardial ischemia, by several possible mechanisms.

The initial hypotheses concerning the mechanisms behind the favorable effects of SCS in angina pectoris focused on a possible increase in the blood flow to ischemic regions, particularly as SCS had been found to increase the circulation in peripheral vascular beds.[22] However, so far, there is no stable experimental support for this redistributing effect of SCS ('the Robin Hood effect') on coronary flow.[23]

Spinal cord stimulation has an anti-ischemic effect in humans, which has been demonstrated in a number of short-term studies from different centers, using different techniques for objectively showing signs of reduced myocardial ischemia, including lactate measurements and PET studies.[24–26] The anti-ischemic effect seems to be due to decreased myocardial oxygen consumption rather than due to an effect on myocardial blood flow.[26,27] Evidence supporting the anti-ischemic effect is also provided by infarction studies in animals,[28,29] where application of SCS produced a reduction in infarction size after controlled occlusion of a large coronary vessel.

Spinal cord stimulation may give rise to reduced oxygen consumption via a number of putative mechanisms. It has been shown in animal experimental studies that β-endorphin, via antagonistic effects on local opioid receptors (µ-receptors) in the myocardium, reduces oxygen consumption. Stimulation induced release of β-endorphin in the myocardium has been suggested as one possible mechanism to the decrease in myocardial oxygen consumption.[30] In addition, SCS seems to reduce sympathetic activity.[31,32]

More recent animal studies also show that SCS gives rise to catecholamine release in the myocardium, which may contribute to the development of protective changes, similar to those occurring in 'ischemic preconditioning'; however, in this case, without any signs of ischemia. SCS appears to have the potential to induce other types of changes that may be observed in connection with ischemic preconditioning, such as activation of protein kinase C.[29] The mechanism of action of SCS in myocardial ischemia is not yet fully elucidated, several mechanisms might contribute to the beneficial effect of SCS, including effects on myocardial blood flow as well as neurohormonal mechanisms, as described above.

Furthermore, SCS seems to exert beneficial effects on arrhythmias and ventricular function in animal models of heart failure. The underlying mechanism of action has been suggested to be modulation of autonomic tone – sympatholytic, vagomimetric or both. However, the mechanism(s) of action is most likely complex and involves changes in nervous, cardiac and endocrine tissues.[33]


Comments on Medscape are moderated and should be professional in tone and on topic. You must declare any conflicts of interest related to your comments and responses. Please see our Commenting Guide for further information. We reserve the right to remove posts at our sole discretion.