Impaired Vagal Activity in Long-COVID-19 Patients, 2022, Acanfora et al

Discussion in 'Long Covid research' started by Andy, May 30, 2022.

  1. Andy

    Andy Committee Member

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    Hampshire, UK
    Abstract

    Long-COVID-19 refers to the signs and symptoms that continue or develop after the “acute COVID-19” phase. These patients have an increased risk of multiorgan dysfunction, readmission, and mortality. In Long-COVID-19 patients, it is possible to detect a persistent increase in D-Dimer, NT-ProBNP, and autonomic nervous system dysfunction.

    To verify the dysautonomia hypothesis in Long-COVID-19 patients, we studied heart rate variability using 12-lead 24-h ECG monitoring in 30 Long-COVID-19 patients and 20 No-COVID patients. Power spectral analysis of heart rate variability was lower in Long-COVID-19 patients both for total power (7.46 ± 0.5 vs. 8.08 ± 0.6; p < 0.0001; Cohens-d = 1.12) and for the VLF (6.84 ± 0.8 vs. 7.66 ± 0.6; p < 0.0001; Cohens-d = 1.16) and HF (4.65 ± 0.9 vs. 5.33 ± 0.9; p = 0.015; Cohens-d = 0.76) components. The LF/HF ratio was significantly higher in Long-COVID-19 patients (1.46 ± 0.27 vs. 1.23 ± 0.13; p = 0.001; Cohens-d = 1.09). On multivariable analysis, Long-COVID-19 is significantly correlated with D-dimer (standardized β-coefficient = 0.259), NT-ProBNP (standardized β-coefficient = 0.281), HF component of spectral analysis (standardized β-coefficient = 0.696), and LF/HF ratio (standardized β-coefficient = 0.820).

    Dysautonomia may explain the persistent symptoms in Long COVID-19 patients. The persistence of a procoagulative state and an elevated myocardial strain could explain vagal impairment in these patients. In Long-COVID-19 patients, impaired vagal activity, persistent increases of NT-ProBNP, and a prothrombotic state require careful monitoring and appropriate intervention.

    Open access, https://www.mdpi.com/1999-4915/14/5/1035/htm
     
    Lisa108 and Peter Trewhitt like this.
  2. rvallee

    rvallee Senior Member (Voting Rights)

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    Location:
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    POTS is probably the issue that I see the most recovery from on LC forums. It's hard to understand how it hasn't been possible yet to study it in detail given how you can basically follow it from trigger to resolution in a matter of weeks in some cases and there are objective measurements that can be done.

    Significant dysautonomia can still remain after, but in many cases it also completely goes away. If anything is a target of easy study it's this. Bummer that none of the important work was done before as this issue was never taken seriously. I don't understand the complete lack of learning lessons from this. Endlessly frustrating. We're seriously going to see progress made at the pace of funerals.
     

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