Clinical Report: Cardiovascular Symptoms in Long COVID Linked to Endothelial Dysfunction
Overview
This study identifies an imbalance in the ADMA–DDAH–NOx pathway associated with cardiovascular symptoms in long COVID. Participants with persistent symptoms exhibited significant endothelial dysfunction and cardiac involvement compared to controls.
Background
Post-acute sequelae of COVID-19 (PASC) is a significant public health issue, affecting 10%-20% of individuals post-infection. Cardiovascular manifestations are common and can indicate underlying endothelial and cardiac dysfunction, necessitating further investigation into their mechanisms for effective management.
Data Highlights
Group
D-dimer
hs-CRP
ADMA
NOx
Ejection Fraction
PASC+
High (>3-fold vs Controls)
High (~3-fold vs Controls)
Higher
Lower
Lower
PASC−
Normal
Normal
Normal
Normal
Normal
Controls
Normal
Normal
Normal
Normal
Normal
Key Findings
PASC+ individuals had significantly higher inflammatory markers compared to controls.
ADMA levels were substantially elevated in the PASC+ group, indicating impaired endothelial function.
Endothelial function, measured by flow-mediated dilation, was significantly lower in PASC+ participants.
PASC+ participants exhibited worse cardiac mechanics and higher levels of hs-troponin and NT-proBNP.
Ejection fraction was lower in PASC+ compared to both controls and PASC− groups.
Clinical Implications
The findings suggest that monitoring the ADMA–DDAH–NOx pathway may be beneficial for risk stratification in patients with long COVID. Clinicians should consider targeted interventions to address endothelial dysfunction in this population.
Conclusion
This study highlights the importance of the ADMA–DDAH–NOx axis in understanding cardiovascular symptoms in long COVID, suggesting potential avenues for therapeutic intervention.
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