Highlights
- •Prevalence of cardiac dysautonomia in multiple sclerosis varies between studies.
- •Diminished sympathetic function was found in multiple sclerosis.
- •Baroreceptor reflex was decreased in multiple sclerosis compared to controls.
- •Baroreceptor sensitivity can quantify cardiac dysautonomia in multiple sclerosis.
Abstract
Background
Prevalence of cardiovascular autonomic dysfunction (CAD) in multiple sclerosis (MS)
varies between studies. Cardiac autonomic function is usually assessed by cardiovascular
reflex tests. We hypothesized that MS is associated with CAD, quantifiable by non-invasive
means including quantification of baroreceptor sensitivity (BRS) and heart rate variability.
Methods
In this study a comprehensive suite of cardiovascular autonomic tests based only on
the spontaneous changes of heart rate and blood pressure was applied to 23 MS patients
and age and gender-matched controls. From 5-min continuous non-invasive recording
of the electrocardiogram and blood pressure, heart-rate, blood pressure, and autonomic
function variables were calculated. Analysis included heart rate variability in the
time domain, heart rate and blood pressure variability in the frequency domain, and
baroreceptor sensitivity in both the time and frequency domain.
Results
BRS measured by the frequency technique in high frequency band was found to be significantly
lower in MS (16 ± 9 ms/mmHg) compared to controls (29 ± 17 ms/mmHg) (p < 0.05). Also
mean of BRS modulus in MS averaged 15 ± 8 ms/mmHg which is significantly lower compared
to controls (25 ± 15 ms/mmHg) (p < 0.05). Systolic blood pressure variability in the
high frequency band (0.15–0.5 Hz) was found to be significantly higher in the MS compared
to controls (5.8 ± 16.7 mmHg2 vs. 1.3 ± 0.8 mmHg2) (p < 0.05).
Conclusions
The results, using techniques novel to MS investigation, showed diminished baroreceptor
reflex and impaired sympathetic function using frequency domain systolic blood pressure
variability analysis.
Keywords
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Article info
Publication history
Published online: March 26, 2018
Accepted:
March 23,
2018
Received in revised form:
March 8,
2018
Received:
January 3,
2018
Identification
Copyright
© 2018 Elsevier B.V. All rights reserved.
