Spinal Cord Stimulation for Heart Failure and Arrhythmias

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Spinal Cord Stimulation for Heart Failure and Arrhythmias

Spinal Cord Stimulation: Background and Current Clinical Uses

Device, Leads, and Implantation Methodologies

Spinal cord stimulation (SCS) has been used worldwide in human populations for various conditions since the 1980s. Most modern systems are fully implantable and consist of a pulse generator (implanted in the abdominal, gluteal, or paraspinous region) connected to one or more spinal stimulating leads. The leads are implanted surgically or placed via percutaneous techniques into the dorsal epidural space, with the electrodes located at the spinal level appropriate for treatment of the indicated condition. A neurosurgeon or specially trained anesthesia or pain specialist will usually implant these systems. The initial implantable pulse generators had fixed-life, non-rechargeable batteries that lasted 1 to 4 years, thus requiring a generator change when the battery was depleted. Some newer generators have rechargeable battery systems that greatly extend the lifespan of the systems and alleviate the need for frequent generator changes. The spinal leads have four to eight electrodes spaced at regular intervals to allow for stimulation of narrow versus wide local fields. For most applications, the lead electrode location is a critical determinant of long-term clinical efficacy. The stimulus parameters are most often tailored to the specific treatment condition, but generally have outputs in the range of 0.5 to 5 V stimulus amplitude and 0.1 to 0.3 ms pulse duration, delivered at 30 to 100 Hz. At the higher range of stimulus parameters, skeletal muscle capture can become an issue, whereas the lower range of outputs might not have the intended neuromodulatory effect. Stimulation is generally applied intermittently (i.e., for discrete on-off periods) to avoid nerve tachyphylaxis. However, it is not uncommon for SCS to be delivered continuously with modern systems, depending on the clinical application. Most systems allow for limited patient titration of SCS settings via an external controller. SCS is generally well tolerated with few complications, but rarely, complications seen in implanted cardiac devices are seen in these systems (e.g., device or lead failure, lead migration, infection).

Treatment of Chronic Pain Syndromes

Spinal cord stimulation was first used clinically to treat complex pain syndromes refractory to medical therapy. It is approved by the U.S. Food and Drug Administration and is used widely for the treatment of complex regional pain syndromes in the cervical and lumbar distributions and the extremities. A recent metaanalysis found that SCS is a cost-effective and acceptable therapy in patients who have persistent neuropathic pain despite adequate conventional medical therapy.1 Randomized studies have found that SCS provides additional benefits over conventional medical therapy for treatment of chronic pain.2 The mechanism by which it treats chronic pain is widely thought to be due to interruption of the ascending pain signals within the spinal cord, although efficacy is also linked to placement of the electrodes in a position that produces mild paresthesia in the dermatomal location of the chronic pain. This finding suggests that the mechanism of pain suppression is highly complex and involves efferent and afferent limbs of the nervous system.

Treatment of Cardiac Angina

Spinal cord stimulation was first used in the late 1980s for the treatment of chronic angina refractory to medical or revascularization therapy. It is an approved therapy for this condition in many European countries. Many case reports and two randomized studies have reported that SCS is more efficacious than medical therapy alone in this population that is difficult to treat.3 The placement of the SCS electrode is usually at spinal segments C8 to T1 and slightly left of midline. In this location, SCS output settings are generally set to produce a slight paresthesia over the left precordium, which somehow blunts the chronic angina symptoms.4 The mechanism by which SCS produces analgesia and antiischemia effects is not clear, but some evidence suggests it is a vagal-dependent process.5 Others have theorized that it produces direct effects on the coronary vasculature by promoting vasodilatation.3,6

Spinal Cord Stimulation: Cardiac Effects from Preclinical Studies in Animal Models

Heart failure (HF) is associated with excessive mortality, often via associated ventricular tachyarrhythmias (VTs). Derangements in autonomic nervous system (ANS) signaling are noted in HF, and many modern HF and VT therapies target the ANS. Neuromodulatory therapy with SCS targeting the ANS has been shown to provide clinical benefits in experimental heart failure models.

Modulation of Cardiac Autonomic Nerve Activity

In anesthetized canines, Foreman et al.7 demonstrated that provocative coronary artery occlusion was associated with increased intracardiac nerve firing. Interestingly, this nerve activity was suppressed by active SCS at spinal segment T1, with no change in other cardiac parameters such as heart rate or blood pressure.7 They concluded that this finding could provide insight into the beneficial effect of SCS in patients with chronic angina pectoris. In another study in a rabbit cardiac ischemia model, preemptive SCS delivered at spinal segment C8-T2 (delivered before and during coronary artery occlusion) reduced subsequent cardiac infarct size. In this study, SCS initiated after the onset of coronary artery occlusion had no effect on subsequent infarct size. The reduction in infarct size by preemptive SCS was blocked by treatment with α- or β-adrenergic receptor blockers, leading the authors to conclude that this cardioprotective effect was mediated by adrenergic neurons of the ANS.8

Effects on Cardiac Electrophysiology and Electrical Conduction

Olgin et al.9 examined the effects of SCS on cardiac electrophysiology in anesthetized normal canines. In this work, acute epidural spinal cord stimulation at segment T1 significantly increased spontaneous sinus cycle length and the AH interval. Vagal nerve transection, but not ansae subclaviae transection, eliminated the effects of SCS on sinus rate and AH interval. The authors concluded that SCS enhanced parasympathetic activity via a vagus nerve–dependent mechanism.9 In a canine model of established postinfarction heart failure, subsequent coronary artery balloon occlusion produced ventricular arrhythmias.10

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