Frontiers in cardiovascular medicineMay 7, 2026

Blood vessel and heart problems in long COVID with heart symptoms linked to imbalance in a key blood vessel signaling pathway

Long Covid Weekly Brief ↗PubMed ↗DOI ↗OA ↗

Updated Jun 28, 2026

Abstract

Essence

Long COVID patients with persistent cardiovascular symptoms showed ADMA-DDAH-NOx pathway imbalance alongside worse endothelial and cardiac measures.

Evidence

This cross-sectional phenotyping study compared 49 RECOVER participants across never-infected controls, recovered COVID-19 without persistent symptoms, and PASC with cardiovascular symptoms, finding in the symptomatic PASC group higher ADMA, lower NOx, impaired brachial and microvascular flow-mediated dilation, worse cardiac longitudinal mechanics, higher hs-troponin and NT-proBNP, and lower ejection fraction.

Caveat

The study was small and observational, so it shows an association in a symptomatic subgroup rather than proving that the pathway imbalance causes long COVID cardiovascular dysfunction.

Simplified

BACKGROUND: Post-acute sequelae of COVID-19 (PASC) commonly feature lingering symptoms of persistent cardiovascular pathology, yet the mechanisms remain incompletely defined. The ADMA-DDAH-NOaxis is a central regulator of endothelial function: ADMA inhibits endothelial NOx synthase, while DDAH clears most circulating ADMA. Although ADMA is linked to acute COVID-19 severity, its regulation in PASC remains largely unknown. x

METHODS: We performed integrated vascular and cardiac phenotyping in 49 RECOVER participants: never-infected controls ( = 10), recovered COVID-19 without persistent symptoms (PASC-, = 20), and PASC with persistent cardiovascular-related symptoms lasting ≥12 weeks post-infection (PASC+, = 19). We measured ADMA, DDAH, NO, inflammatory/coagulation markers, endothelial function [brachial and microvascular flow-mediated dilation (FMD)], and cardiac structure and function using comprehensive echocardiography with speckle-tracking strain. n n n

RESULTS: PASC+ exhibited the highest inflammatory and thrombotic markers, with D-dimer being > 3-fold higher than controls, and hs-CRP nearly threefold higher. PASC+ demonstrated lower NOx and substantially higher ADMA than the other two groups, accompanied by only modest DDAH upregulation, suggesting insufficient counter-regulation. Endothelial function was significantly impaired in the PASC+ group compared to the control and PASC- groups, as evidenced by lower brachial and microvascular FMD. PASC+ individuals exhibited worse longitudinal mechanics and higher levels of hs-troponin and NT-proBNP. Ejection fraction was lower in PASC+ compared with Controls and PASC-.

CONCLUSIONS: These findings identify an imbalance in the ADMA-DDAH-NOaxis that is associated with endothelial dysfunction and cardiac involvement in cardiovascular-symptom PASC, supporting a potentially targetable pathway for risk stratification and therapeutic investigation. x

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Long CovidIssue #36

Long COVID linked to 2x higher heart disease risk in Stockholm study of 9,000 patients

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Blood vessel and heart problems in long COVID with heart symptoms linked to imbalance in a key blood vessel signaling pathway

Abstract

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