The use of spinal cord stimulation (SCS) for chronic intractable anginal pain was first described in 1987. Numerous studies have demonstrated its efficacy in improving exercise tolerance, decreasing frequency of anginal episodes, and prolonging time to electrocardiographic signs of ischemia. This review will examine the potential mechanisms of this antianginal effect and propose a unified hypothesis explaining it. The effect of SCS involves a mutual interaction of decreased pain, decreased sympathetic tone, and a likely redistribution of myocardial blood flow to ischemic regions. Spinal cord stimulation reduces the transmission of nociceptive impulse via the spinothalamic tract due to an enhanced release of gamma aminobutyric acid (GABA) from dorsal horn interneurons. Improvement of myocardial blood flow at the microvascular 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 hypothesize that SCS exerts its beneficial effects by decreasing pain and decreasing sympathetic tone, the result of which is decreased myocardial oxygen consumption along with an improved myocardial microcirculatory blood flow.