Background
The heart rate variability (HRV) is a non-invasive, objective and validated method for the assessment of autonomic nervous system. Although acute manifestations of COVID-19 were widely researched, long-term sequela of COVID-19 are still unknown. This study aimed to analyze autonomic function using HRV indices in the post-COVID period that may have a potential to enlighten symptoms of COVID long-haulers.
Methods
The 24-h ambulatory electrocardiography (ECG) recordings obtained >12 weeks after the diagnosis of COVID-19 were compared with age–gender-matched healthy controls. Patients who used drugs or had comorbidities that affect HRV and who were hospitalized with severe COVID-19 were excluded from the study.
Results
Time domain indices of HRV analysis (standard deviation of normal RR intervals in 24 h (SDNN 24 h) and root mean square of successive RR interval differences (RMSSD)) were significantly higher in post-COVID patients (
p
< 0.05 for all). Among frequency domain indices, high frequency and low frequency/high frequency ratio was significantly higher in post-COVID patients (
p
= 0.037 and
p
= 0.010, respectively). SDNN >60 ms [36 (60.0%) vs. 12 (36.4%),
p
= 0.028)] and RMSSD >40 ms [31 (51.7%) vs. 7 (21.2%),
p
= 0.003)] were more prevalent in post-COVID patients. Logistic regression models were created to evaluate parasympathetic overtone in terms of SDNN >60 ms and RMSSD >40 ms. After covariate adjustment, post-COVID patients were more likely to have SDNN >60 msn (OR: 2.4, 95% CI:1.2–12.8) and RMSSD >40 ms (OR: 2.5, 95% CI: 1.4–9.2).
Conclusion
This study revealed parasympathetic overtone and increased HRV in patients with history of COVID-19. This may explain the unresolved orthostatic symptoms occurring in post-COVID period which may be associated with autonomic imbalance.
Supplementary Information
The online version contains supplementary material available at 10.1007/s10840-022-01138-8.
SUMMARY INTRODUCTION Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a newly described virus responsible for the outbreak of the coronavirus disease 2019 (Covid-19), named by the World Health Organization (WHO) in February/2020. Patients with Covid-19 have an incidence of acute respiratory distress syndrome (ARDS) of 15.9-29% and sepsis is observed in all deceased patients. Moreover, disseminated intravascular coagulation (DIC) is one of the major underlying causes of death among these patients. In patients with DIC, there is a decrease in fibrinogen and an increase in D-dimer levels. Some studies have shown that fibrinogen and one of its end products, D-dimer, might have a predictive value for mortality in patients with non-Covid sepsis secondary to complications of DIC. Therefore, anticoagulation, considering its mortality benefits in cases of non-Covid sepsis, may also have an important role in the treatment of Covid-19. METHODS We reviewed the literature of all studies published by April 2020 on patients infected with Covid-19. Our review was limited to D-dimer and fibrinogen changes and anticoagulation recommendations. RESULTS Anticoagulation therapy can be started following the DIC diagnosis in Covid-19 patients despite the bleeding risks. In addition, the current evidence suggests a routine use of anticoagulation, particularly in patients with higher D-dimer levels (> 3.0 μg/mL). CONCLUSION Covid-19 is a systemic, hypercoagulable disease requiring more studies concerning treatment. Aanticoagulation is still an issue to be studied, but D-dimer rise and disease severity are the indicative factors to start treatment as soon as possible.
Thrombosis and distal embolization play crucial role in the etiology of no-reflow. CHA2DS2-VASc score is used to estimate the risk of thromboembolism in patients with atrial fibrillation. We tested the hypothesis that CHA2DS2-VASc can predict no-reflow among patients who underwent primary percutaneous coronary intervention (PCI). A total number of 2375 consecutive patients with ST-segment elevation myocardial infarction were assessed for the study. Patients were divided into 2 groups as no-reflow (n = 111) and control (n = 1670) groups according to post-PCI no-reflow status. CHA2DS2-VASc scores were calculated for all patients. CHA2DS2-VASc scores were significantly higher in the no-reflow group compared to the control group. After a multivariate regression analysis, CHA2DS2-VASc score remained as an independent predictor (odds ratio: 1.58, 95% confidence interval: 1.33-1,88, P < .001) of no-reflow. Receiver-operating characteristics analysis revealed the cutoff value of CHA2DS2-VASc score ≥2 as a predictor of no-reflow with a sensitivity of 66% and a specificity of 59%. Moreover, in-hospital mortality was also associated with significantly higher CHA2DS2-VASc scores. In conclusion, CHA2DS2-VASc score is associated with higher risk of no-reflow and in-hospital mortality rates in patients who underwent primary PCI.
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