Spinal cord stimulation for chronic intractable angina pectoris: A unifiedtheory on its mechanism

The use of spinal cord stimulation (SCS) for chronic intractable anginal pa in was first described in 1987. Numerous studies have demonstrated its effi cacy in improving exercise tolerance, decreasing frequency of anginal episo des, and prolonging time to electrocardiographic signs of ischemia. This re view will examine the potential mechanisms of this antianginal effect and p ropose a unified hypothesis explaining it. The effect of SCS involves a mut ual interaction of decreased pain, decreased sympathetic tone, and a likely redistribution of myocardial blood flow to ischemic regions. Spinal cord s timulation reduces the transmission of nociceptive impulse via the spinotha lamic tract due to an enhanced release of gamma aminobutyric acid (GABA) fr om dorsal hom interneurons. Improvement of myocardial blood flow at the mic rovascular level has been demonstrated by positron emission tomography (PET ). A decreased sympathetic tone has been shown by norepinephrine kinetics, tests of sympathetic reflexes, and the use of ganglionic blockers. We hypot hesize that SCS exerts its beneficial effects by decreasing pain and decrea sing sympathetic tone, the result of which is decreased myocardial oxygen c onsumption along with an improved myocardial microcirculatory blood flow.