Cardiac Baroreflex Sensitivity and Heart Rate Variability Following COVID‐19 in Young Adults
Authors: Garza Nicole A. , Nandadeva Damsara , Stephens Brandi Y. , Grotle Ann‐Katrin , Skow Rachel J. , Young Benjamin E. , Fadel Paul J. 
Published: May 2022

BackgroundThe COVID‐19 pandemic has evolved into an unprecedented public health crisis, with over 255 million cases and over 5 million deaths worldwide. Emerging evidence indicates that many previously healthy young adults diagnosed with COVID‐19 experience persistent symptoms beyond the acute phase of the illness, a phenomenon coined “long‐COVID”. Several clinical reports suggest that long‐COVID may negatively impact the autonomic nervous system, leading to blood pressure (BP) dysregulation. However, the effects of COVID‐19 on indices of cardiac autonomic modulation (heart rate variability; HRV) and cardiac baroreflex sensitivity (cBRS) beyond the acute phase of the illness remain unclear. Likewise, the influence of COVID‐19 symptomology on these indices is also not well understood. Therefore, the purpose of this study was to determine the impact of COVID‐19 and persistent symptomology on cBRS and HRV in otherwise healthy young adults beyond the acute phase of illness. We hypothesized that young adults who have had COVID‐19 would exhibit attenuated cBRS and HRV compared to healthy controls and these impairments would be greatest in COVID‐19 subjects with persistent symptoms.MethodsWe studied 24 healthy adults (age = 22 ± 1 years; mean ± standard error) with a lab‐confirmed diagnosis of COVID‐19 (COVID; 11 ± 1 weeks from diagnosis) and twelve adults (age = 23 ± 1 years) who never had COVID‐19 (control). COVID subjects reported being either asymptomatic (n = 13) or symptomatic (n = 11) at the time of testing. Heart rate (ECG) and arterial BP (finger photoplethysmography) were continuously recorded during a ten‐minute resting baseline. The Sequence Method was used to estimate spontaneous cBRS for up gains (increase systolic BP: increase R‐R interval), down gains (decrease systolic BP: decrease R‐R interval), and for overall gains. HRV was determined using normalized high frequency power (HF; normalized units), the ratio between low frequency power and high frequency power (LF/HF; frequency‐domain) and root mean square of successive differences between normal heartbeats (RMSSD; time‐domain).ResultsWe found that cBRS and HRV were not different between control and COVID subjects (P > 0.05 for all comparisons). Further, there were no significant differences in overall gains between controls (24 ± 3 ms/mmHg), asymptomatic COVID (24 ± 3 ms/mmHg), and symptomatic COVID (26 ± 3 ms/mmHg, P = 0.934) groups. Similarly, no group differences were found in up or down gains (both P > 0.05). Likewise, for HRV, no differences were observed in the HF power (control: 56 ± 6 n.u., asymptomatic: 60 ± 5 n.u., symptomatic: 63 ± 3 n.u., P = 0.580), LF/HF ratio (control: 1.19 ± 0.38, asymptomatic: 0.73 ± 0.14, symptomatic: 0.58 ± 0.09, P = 0.195) or RMSSD (control: 82 ± 16 ms, asymptomatic: 77 ± 14 ms, symptomatic: 86 ± 14 ms, P = 0.909) between groups.ConclusionThese preliminary data suggest that beyond the acute phase of COVID‐19, cBRS and HRV are preserved in healthy young adults, regardless of persistent symptomology.