Ischemic pain is the only nociceptive pain that is proven to respond to SCS. As opposed to mechanisms involved in neuropathic pain attenuation, beneficial effect of SCS on ischemic pain involves attenuation of tissue ischemia as a result of increasing and/or redistributing blood flow to ischemic area or by decreasing tissue oxygen demand to the ischemic area. SCS has been shown to improve microcirculation in an animal model [27]. These effects appear to be mediated by two mechanisms: (1) suppression of efferent sympathetic activity (via nicotinic ganglionic receptors and mainly alpha-1 adrenoreceptors in the periphery) and (2) antidromic mechanisms involving the dorsal roots that stimulate the release of calcitonin gene-related peptide (CGRP) [15]. The balance of these mechanisms depends on a variety of factors including the tone of the sympathetic nervous system, patient factors (diet, genetic differences, etc.), and intensity of SCS [29]. Figure 45.1 illustrates the mechanisms and neurotransmitters known or hypothesized to be involved in the effects of SCS in PAOD. A thorough review of the putative mechanisms behind the effects of SCS on peripheral vascular disease is found in Wu et al. [29].

Angina usually occurs during episodes of vasospasm or occlusion of the coronary vessels that results in an imbalance between the supply and the demand of oxygen in the heart due to decreased blood flow to the heart. Patients with angina pectoris are often managed effectively through pharmacological treatment with beta-receptor blocking agents, long-acting nitrates, and calcium antagonists, by revascularization procedures such as coronary bypass surgery (CABG) or by percutaneous transluminal coronary angioplasty (PTCA); however, a segment of patients suffering from chronic angina pectoris does not respond to conventional treatments [30]. Many patients suffering from severe disabling angina (New York Heart Association (NYHA) classes III–IV) suffer from concurrent comorbidities, making them unsuitable for major invasive procedure. Other patients suffer from widespread obliteration or distal lesions that do not permit successful surgical interventions. Regardless of the etiology, these patients suffer from what is termed treatment refractory angina and have a low quality of life, limited physical capacity, and frequent hospital admissions representing a large costs for society [31]. Patients suffering from treatment refractory angina led clinicians to develop alternative strategies such as neuromodulation to provide pain relief. In European estimates, refractory angina is a common condition with a prevalence of 100,000 patients [32]. SCS has been used to treat such therapy-resistant angina pectoris since the mid-1980s [33, 34]. The first ten cases of SCS directed specifically at the treatment of angina were reported in 1987 by Murphy and Giles [34].

Patient selection involves specific criteria that maximize the likelihood of clinical success and eliminates patients that are not likely to benefit in an effort to prevent these patients from undergoing an unnecessary procedure in lieu of their multiple comorbidities. The following inclusion and exclusion criteria are adapted from [26].