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
Contactless analysis of heart rate variability during cold pressor test using radar interferometry and bidirectional LSTM networks
