Cardiovascular Effects of Spinal Cord Stimulation in Hypertensive Patients

Abstract

Background: Several animal and clinical studies have shown that thoracic spinal cord stimulation (SCS) may decrease mean arterial pressure (MAP). A previous study in normotensive participants demonstrated a small reduction in MAP during SCS at the T5-T6 spinal level. It has also been demonstrated that chronic SCS at the subthreshold stimulation level significantly improved angina attacks and 6 minute hall walk distance in drug refractory angina patients. Objectives: To determine if thoracic SCS at 2 different stimulation strengths would decrease blood pressure (BP) and heart rate (HR) during baseline conditions and during activation of the sympathetic system by the cold pressor test (CPT). Methods: Six hypertensive participants and 9 normotensive participants were evaluated. The SCS leads were implanted under sedation (midazolam and fentanyl) 3 days prior to the study. The SCS device was not implanted at the time of lead implantation; the exteriorized leads were connected to an external programmer at the time of the study. MAP was measured at the finger using beat-to-beat photoplethysmographic recordings at rest and during CPT with a Finometer (Model 1, Finapress Medical Systems, Amsterdam, The Netherlands). SCS at threshold (100%, SCS100) and subthreshold (80%, SCS80) intensities were randomly performed in the T5-T6 region of the spinal cord during normal conditions as well as during CPT. Each participant had 3 CPTs with the placebo (control, no SCS) CPT always performed first. CPT was performed by immersing the right hand into ice water for 90 seconds. Thirty seconds of beat-to-beat data prior to starting each CPT (baseline) was analyzed. During the 90 second CPT, the median values of the last 30 seconds of data were used for analysis. Heart rate variability (HRV) during baseline and SCS was computed using Kubios HRV Version 2.0 software (University of Kuopio, Kuopio, Finland). Since the median values of HR, MAP and their changes did not follow a normal distribution, groups were compared with a non-parametric Friedman’s or Wilcoxon’s signed rank test. The HRV data were normally distributed and a repeated measures analysis of variance (ANOVA) was used. Results: SCS did not significantly alter MAP or HR at baseline nor did it appear to blunt changes in MAP or HR in response to CPT. In the normotensive group, MAP was significantly elevated by a median value of 16 mmHg (P<0.001) during the placebo phase, and by 18 and 10.5 mmHg during the SCS80 and SCS100 phases, respectively. In the hypertensive group, an enhanced response to the CPT was observed. In these participants, the MAP was significantly elevated by a median value of 26.8 mmHg (P<0.001) during the placebo phase, and by 20 and 17 mmHg during the SCS80 and SCS100 phases, respectively. There was a non-significant trend for the CPT-induced increase in BP to be attenuated during SCS80. HRV tended to decrease in both the time and frequency domain in hypertensive participants, although this decrease was not statistically significant. Limitations: This was a pilot study including a limited number of participants Conclusions: Acute SCS at the T5-T6 region did not significantly alter MAP or HR compared to baseline (no SCS) in participants without sedation, supporting our previous findings in sedated patients. Hypertensive participants had a heightened response to transient cold stress, consistent with the literature. The observation of the tendency for a reduction in HRV in both the time and frequency domain in hypertensive participants is also consistent with the literature. In contrast to acute SCS, the hemodynamic effects of chronic SCS should be explored in the future. Key words: Spinal cord stimulation, hemodynamics, cold pressor test, heart rate variability, hypertension