Baroreflex sensitivity is impaired in survivors of mild COV-19 at 3–6 months of clinical recovery; association with carotid artery stiffness, 2023

[Mij]

Abstract
The association between the stiffening of barosensitive regions of central arteries and the derangements in baroreflex functions remains unexplored in COVID-19 survivors.

Fifty-seven survivors of mild COVID-19 (defined as presence of upper respiratory tract symptoms and/or fever without shortness of breath or hypoxia; SpO2 > 93%), with an age range of 22–66 years (27 females) participated at 3–6 months of recovering from the acute phase of RT-PCR positive COVID-19. Healthy volunteers whose baroreflex sensitivity (BRS) and arterial stiffness data were acquired prior to the onset of the pandemic constituted the control group. BRS was found to be significantly lower in the COVID survivor group for the systolic blood pressure-based sequences (BRSSBP) [9.78 (7.16–17.74) ms/mmHg vs 16.5 (11.25–23.78) ms/mmHg; p = 0.0253].

The COVID survivor group showed significantly higher carotid β stiffness index [7.16 (5.75–8.18) vs 5.64 (4.34–6.96); (p = 0.0004)], and pulse wave velocity β (PWVβ) [5.67 (4.96–6.32) m/s vs 5.12 (4.37–5.41) m/s; p = 0.0002]. BRS quantified by both the sequence and spectral methods showed an inverse correlation with PWVβ in the male survivors. Impairment of BRS in the male survivors of mild COVID-19 at 3–6 months of clinical recovery shows association with carotid artery stiffness.

https://physoc.onlinelibrary.wiley.com/doi/10.14814/phy2.15845

 

[SNT Gatchaman]

In this study the subjects were evaluated supine —

Continuous noninvasive recording of ECG and blood pressure was done simultaneously for 5 min to compute BRS using spontaneous sequence and spectral methods. Participants rested for 15 min in supine position before the signals were acquired.

But see also Baroreceptor Reflex and Integrative Stress Responses in Chronic Fatigue Syndrome (2010, Psychosomatic Medicine) —

Objective: Altered cardiovascular responses to mental and postural stressors have been reported in chronic fatigue syndrome (CFS). This study examined whether those findings may involve changes in baroreceptor reflex functioning.

Methods: Chronotropic baroreceptor reflex (by sequential analysis) and cardiovascular stress responses were recorded during postural (5-minute of active standing) and cognitive (speech task) stress testing in patients with CFS grouped into cases with severe (N = 21) or less severe (N = 22) illness, and in 29 matched control subjects.

Results: Patients with CFS had a greater decline in baroreceptor reflex sensitivity (BRS) during standing, although only those with severe CFS were significantly different from the controls. Systolic blood pressure declined during standing in the control group but was maintained in the CFS patients. In contrast, the patients with less severe CFS had blunted increases in blood pressure during the speech task, which could not, however, be explained by inadequate inhibition of the baroreceptor reflex, with all groups showing an appropriate reduction in BRS during the task.

Conclusions: These results indicate that in CFS, deficiencies in orthostatic regulation, but not in centrally mediated stress responses, may involve the baroreceptor reflex. This study also suggests that classifying patients with CFS on illness severity may discriminate between patients with abnormalities in peripheral vs. central mechanisms of cardiovascular stress responses.

This study indicates that CFS alters baroreceptor reflex functioning. This included increased baroreflex sensitivity in the supine position and a greater reduction in sensitivity on standing. The effect of illness was accentuated in the patients with severe CFS and was associated with a deviation from the normal pattern of SBP response to standing. There were no discernible effects of illness on the baroreflex modulation by stressors, however.

A greater decline in BRS and maintained SBP during standing in the severe CFS group was therefore suggestive of an abnormal orthostatic hemodynamic function compensated by increased sympathetic vasomotor activity.

Sodium loading in patients with orthostatic syncope, while expanding their blood volume and increasing orthostatic tolerance, also reduced BRS. Presumably, the effect of treatment was to improve blood flow, suggesting that cardiovagal baroreflex augmentation may develop as an adaptation to low cardiac output, for which there is some evidence in patients with severe CFS.