COVID-19 and Its Impact on Heart Rate Variability: A Recent Study
Several studies have suggested that COVID-19 can influence heart rate variability (HRV), with the severity of infection playing a crucial role in determining its impact. However, it remains uncertain whether the duration since infection also affects HRV parameters.
A recent study published in Scientific Reports examined how mild COVID-19 influences HRV.
Study Overview
This cross-sectional study was conducted at Universidade Ceuma and Universidade Federal de São Carlos in Brazil. Researchers proposed that individuals who had previously contracted SARS-CoV-2—the virus responsible for COVID-19—might experience decreased HRV and increased sympathetic nervous system activity in the early stages of infection.
The study included adults aged 18 and older who had tested positive for COVID-19 via RT-PCR between November 2020 and September 2023. Only individuals with mild symptoms, such as cough, sore throat, fever, muscle pain, fatigue, and loss of taste or smell, were considered. Those who had suffered moderate to severe COVID-19, had cardiovascular or chronic pulmonary diseases, were pregnant, or had a history of illicit drug use were excluded from the study.
Participants were categorized into four groups:
-
Group 1 (G1): Individuals assessed within six weeks post-infection.
-
Group 2 (G2): Participants evaluated two to six months after recovery.
-
Group 3 (G3): Individuals examined seven to twelve months after infection.
-
Control Group (CG): Pre-pandemic participants with no history of COVID-19 or major health conditions.
Key Findings
The study analyzed data from 130 individuals, with 31 in CG, 34 in G1, 30 in G2, and 35 in G3. All groups were comparable in terms of age, body mass, height, and cognitive function. Physical activity levels, assessed through Baecke’s questionnaire, showed no significant differences across groups.
Certain health conditions were more prevalent in specific groups. Hypertension and obesity were more common in G1 (35% and 41%, respectively), while G2 had a higher prevalence of dyslipidemia (27%). Additionally, G1 had a greater proportion of unvaccinated individuals and reported more symptoms such as fatigue, headache, anxiety, and cough.
Linear HRV analysis showed that G1 and G2 had lower HRV values than CG, suggesting autonomic imbalance, reduced parasympathetic activity, and increased sympathetic dominance. Non-linear HRV analysis indicated greater regularity in heart rate patterns, further supporting the idea of autonomic disruption.
Regression models highlighted that age and time since infection significantly affected HRV parameters, particularly RMSSD (root mean square of successive differences) and SD1 (short-term HRV measure).
G1 and G2 showed reduced parasympathetic activity compared to CG, signifying heightened stress and sympathetic dominance. In contrast, G3 exhibited improved HRV markers, including increased RMSSD and high-frequency (HF) power, indicating partial autonomic recovery.
Although all groups had lower parasympathetic activity (reduced HF) than CG, G1 displayed the most significant drop in absolute HF power. Moreover, low-frequency (LF) power—a marker of sympathetic dominance—was elevated in G1 and G2 but reduced in G3, suggesting potential recovery over time.
Age was found to be a key determinant of standard deviation of normal-to-normal (SDNN) intervals, while BMI, hypertension, and dyslipidemia had no significant impact. Stress emerged as a crucial factor negatively affecting HRV.
Ultimately, the study concluded that both age and time since diagnosis influence HRV recovery, indicating that COVID-19 has a temporary effect on the autonomic nervous system.
