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Updated: Apr 20, 2026
Studying the Coding Profiles of Somatic Stimulation on Cardiac-locked Neuronal Responses in the Rat Spinal Dorsal Horn
Published on: May 23, 2025
Effect of spinal cord stimulation on myocardial perfusion reserve in patients with refractory angina pectoris
Antti Saraste1, Heikki Ukkonen2, Antti Varis3
1Turku PET Centre, Turku University Hospital and University of Turku, Kiinamyllynkatu 4-8, Turku FI-20520, Finland Heart Center, Turku University Hospital and University of Turku, Turku, Finland antsaras@utu.fi.
Aims:
Epidural spinal cord stimulation (SCS) provides symptom relief in refractory angina pectoris, but its mechanism of action remains incompletely understood. We studied effects of short-term SCS therapy on myocardial ischaemia tolerance, myocardial perfusion reserve (MPR), and endothelium-mediated vasodilatation induced by cold pressor test (CPT) in patients with refractory angina pectoris.
Methods And Results:
We prospectively recruited 18 patients with refractory angina pectoris and studied them after implantation of SCS device at baseline before starting the therapy and after 3 weeks of continuous SCS therapy. Myocardial ischaemia was evaluated by dobutamine stress echocardiography. Global and regional myocardial blood flow (MBF) were measured using positron emission tomography and (15)O-water at rest, during adenosine stress, and in response to CPT. Systemic haemodynamics were comparable before and after 3 weeks of SCS at rest, during adenosine stress and during CPT. Appearance of angina pectoris induced by dobutamine stress was delayed after SCS therapy. Global MPR increased (P = 0.02) from 1.7 ± 0.6 at baseline to 2.0 ± 0.6 after 3-week SCS therapy. This was associated with a significant reduction in global MBF at rest and increase in MBF induced by adenosine in the ischaemic regions. Global MBF response to CPT was improved after SCS (0.27 ± 0.20 vs. 0.40 ± 0.15, P = 0.03).
Conclusion:
Short-term SCS therapy improved myocardial ischaemia tolerance, absolute MPR, and endothelium-mediated vasomotor function in refractory angina pectoris, indicating that this therapy can alleviate myocardial perfusion abnormalities in advanced CAD.
