(607.3) Cardiac Baroreflex Sensitivity and Heart Rate Variability Following COVID-19 in Young Adults

Poster Board Number: E528

Nicole Garza (University of Texas at Arlington), Damsara Nandadeva (University of Texas at Arlington), Brandi Stephens (University of Texas at Arlington), Ann-Katrin Grotle (University of Texas at Arlington), Rachel Skow (University of Texas at Arlington), Benjamin Young (University of Texas at Arlington), Paul Fadel (University of Texas at Arlington)

Background: The 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.

Methods: We 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).

Results: We found that cBRS and HRV were not different between control and COVID subjects (P gt; 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 gt; 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.

Conclusion: These preliminary data suggest that beyond the acute phase of COVID-19, cBRS and HRV are preserved in healthy young adults, regardless of persistent symptomology. 

Support or Funding Information

This work was supported by American Heart Association Grant # 827597/Damsara Nandadeva/2021 and Nicole Garza was supported by NIH NIDDK Award Number R25DK078381.