To investigate the mechanisms linking cardiovascular symptoms in long COVID (PASC) to endothelial and cardiac dysfunction, specifically focusing on the role of the ADMA–DDAH–NOx pathway.
Key Findings:
PASC+ exhibited the highest inflammatory and thrombotic markers, with D-dimer > 3-fold higher than controls and hs-CRP nearly threefold higher.
PASC+ had lower NOx and significantly higher ADMA compared to controls and PASC−, indicating insufficient DDAH upregulation.
Endothelial function was significantly impaired in PASC+, evidenced by lower brachial and microvascular flow-mediated dilation (FMD).
PASC+ individuals showed worse longitudinal cardiac mechanics and higher levels of hs-troponin and NT-proBNP, with lower ejection fraction.
Interpretation:
The findings suggest that an imbalance in the ADMA–DDAH–NOx pathway contributes to endothelial dysfunction and cardiac involvement in PASC, highlighting a potential target for therapeutic intervention.
Limitations:
The study is cross-sectional, limiting causal inferences.
Sample size may not fully represent the broader population of long COVID patients.
Conclusion:
The dysregulation of the ADMA–DDAH–NOx axis is associated with cardiovascular symptoms in long COVID, indicating a need for further investigation into this pathway for risk stratification and treatment.
