Asymmetric Dimethylarginine as an Integrative Biomarker of Endothelial, Cardiometabolic and Hepatic Dysfunction in Stable Coronary Artery Disease

Q: What are the key findings of this study?

Highly elevated ADMA concentrations (>160 ng/mL) were associated with a markedly increased odds of overt endothelial dysfunction (OR 114.8) in patients with stable coronary artery disease.

Q: What is the clinical evidence from this study?

Study design: Cross-Sectional. Population: Stable Coronary Artery Disease (n=298). Intervention: Elevated Asymmetric Dimethylarginine (ADMA) >160 ng/mL vs. Normal ADMA concentrations (≤120 ng/mL). Primary outcome: Overt endothelial dysfunction (FMD < 7%) (OR 114.8, 95% CI 6.8-1935.0, p=<0.001).

Q: What does this research mean for the field?

In patients with stable coronary artery disease, ADMA concentrations >160 ng/mL are associated with markedly increased odds of overt endothelial dysfunction and closely track metabolic and hepatic impairment. Novelty: ClaimNovelty.INCREMENTAL. Consensus alignment: ConsensusAlignment.NEUTRAL.

Q: What question did this study set out to answer?

To evaluate the diagnostic utility of asymmetric dimethylarginine (ADMA) as an integrative biomarker for endothelial dysfunction, cardiometabolic burden, and metabolic dysfunction-associated steatotic liver disease in stable coronary artery disease.

L Zhussupbekova; Munisa Makhkamova; N. M. Nurillaeva; Dinara Nurkina; Farrukh Yuldashov; Doston Ubaydullayev

doi:10.3390/biomedicines14091927

August 27, 2026BiomedicinesOpen Access

Asymmetric Dimethylarginine as an Integrative Biomarker of Endothelial, Cardiometabolic and Hepatic Dysfunction in Stable Coronary Artery Disease

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Key result

High ADMA levels linked to marked endothelial dysfunction in stable CAD.

OR 114.8
95% CI 6.8-1935.0
P<0.001
n=298

Figures

Why the study?

CAD frequently coexists with cardiometabolic and hepatic dysfunction, but accessible biomarkers capturing this convergence remain limited.

Key Points

To evaluate the diagnostic utility of asymmetric dimethylarginine (ADMA) as an integrative biomarker for endothelial dysfunction, cardiometabolic burden, and metabolic dysfunction-associated steatotic liver disease in stable coronary artery disease.
Conducted a cross-sectional study enrolling 298 patients with stable coronary artery disease (functional class I–II) across two centers in Tashkent, Uzbekistan.
Quantified serum ADMA via ELISA, assessed endothelial function through flow-mediated dilation (FMD), and evaluated liver morphology with abdominal ultrasonography.
Analyzed associations between ADMA concentrations, cardiometabolic indices (TyG index, TG/HDL-C ratio), and clinical severity of coronary artery disease.
MASLD was present in 48.3% and metabolic syndrome in 62.4% of patients; those with MASLD experienced more weekly angina episodes (2.2 ± 1.4 vs. 1.5 ± 1.2, p = 0.004) and reduced exercise tolerance (68 ± 12 vs. 98 ± 15 W, p < 0.001).
ADMA correlated positively with BMI (rs = 0.42), waist circumference (rs = 0.39), TyG index (rs = 0.47), and TG/HDL-C ratio (rs = 0.44; all p < 0.001), with TyG index best predicting elevated ADMA (AUC 0.76, 95% CI 0.69–0.83).
ADMA levels >160 ng/mL were associated with markedly increased odds of overt endothelial dysfunction (OR 114.8, 95% CI 6.8–1935.0) and occurred in 93.1% of patients with MASLD versus 61.0% without (p < 0.001).

Study Design

Type

Cross-Sectional (n=298)

Blinding

Single-blind

Multicenter

Yes

Structured PICO

P

Population

298 adults aged 35-70 years with stable coronary artery disease (functional class I-II) evaluated in a cross-sectional study to assess ADMA as a biomarker of endothelial and cardiometabolic dysfunction.

O

Outcome

Diagnostic value of ADMA as a biomarker of endothelial dysfunction (assessed by flow-mediated dilation), cardiometabolic burden, and metabolic dysfunction-associated steatotic liver disease (MASLD)surrogate

Main Result

Odds Ratio: 114.8 (95% CI 6.8–1935)

p-value: p=<0.001

In patients with stable CAD, elevated ADMA levels strongly correlate with endothelial, metabolic, and hepatic dysfunction, highlighting its potential as an integrative biomarker for cardiometabolic risk.

Limitations

Cross-sectional design precludes establishing causality.
Wide confidence intervals for odds ratios due to small cell counts in reference strata.
Lack of adjustment for baseline pharmacological treatments.
Single-region recruitment limits generalizability.
Lack of external validation for ADMA thresholds.
Models not adjusted for age, sex, smoking status, or renal function.
Control group not matched to CAD cohort and comparative statistical analyses not presented
No formal a priori sample-size or statistical power calculation was performed
Potential confounding by baseline pharmacological treatments (statins, antiplatelets, antihypertensives) which were not adjusted for in multivariable models
ADMA diagnostic cut-offs have not been externally validated

Implication

May support ADMA for risk stratification in stable CAD; hypothesis-generating and should not change practice without prospective validation.

Abstract

Background: Coronary artery disease (CAD) frequently coexists with cardiometabolic and hepatic dysfunction, yet accessible biomarkers capturing this convergence remain limited. Asymmetric dimethylarginine (ADMA), an endogenous nitric oxide synthase inhibitor, has been proposed as an integrative marker of endothelial and metabolic impairment. This study aimed to evaluate the diagnostic value of ADMA as a unified biomarker of endothelial dysfunction (ED), cardiometabolic burden, and metabolic dysfunction-associated steatotic liver disease (MASLD) in patients with stable CAD. Methods: In this cross-sectional study, 298 patients with stable CAD (functional class I–II) were enrolled at two centers in Tashkent, Uzbekistan. Serum ADMA was measured by ELISA; endothelial function was assessed by flow-mediated dilation (FMD). Associations between ADMA, metabolic indices, MASLD, and CAD severity were analyzed. Results: MASLD was present in 48.3% of CAD patients and metabolic syndrome (MetS) in 62.4%. Patients with MASLD had more severe angina, reduced exercise tolerance, and greater ischemic burden than those without. ADMA correlated positively with BMI, waist circumference, TyG index, and TG/HDL-C ratio (all p < 0.001), with the TyG index showing the strongest predictive value for elevated ADMA (AUC 0.76). A dose–response relationship linked rising ADMA to worsening FMD; concentrations >160 ng/mL conferred markedly increased odds of overt ED (OR 114.8, 95% CI 6.8–1935.0) and were disproportionately prevalent in patients with MASLD (93.1% vs. 61.0%, p < 0.001). Conclusions: ADMA is markedly elevated in stable CAD and closely tracks endothelial, metabolic, and hepatic dysfunction. These cross-sectional associations position ADMA as a promising, hypothesis-generating integrative biomarker; prospective longitudinal studies are needed before its use for risk stratification in primary and cardiovascular care can be recommended.

Discussion

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Cite This Study

Zhussupbekova et al. (2026) conducted a cross-sectional in Stable Coronary Artery Disease (n=298). Elevated Asymmetric Dimethylarginine (ADMA) >160 ng/mL vs. Normal ADMA concentrations (≤120 ng/mL) was evaluated on Overt endothelial dysfunction (FMD < 7%) (OR 114.8, 95% CI 6.8-1935.0, p=<0.001). Highly elevated ADMA concentrations (>160 ng/mL) were associated with a markedly increased odds of overt endothelial dysfunction (OR 114.8) in patients with stable coronary artery disease.

synapsesocial.com/papers/6a92995f8e5d7d1fc0c113b1 https://doi.org/10.3390/biomedicines14091927

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Asymmetric Dimethylarginine as an Integrative Biomarker of Endothelial, Cardiometabolic and Hepatic Dysfunction in Stable Coronary Artery Disease

Figures

Key Points

Study Design

Structured PICO

Main Result

Limitations

Implication

Abstract

Discussion

Cite This Study

Asymmetric Dimethylarginine as an Integrative Biomarker of Endothelial, Cardiometabolic and Hepatic Dysfunction in Stable Coronary Artery Disease

Figures

Key Points

Study Design

Structured PICO

Main Result

Limitations

Implication

Abstract

Discussion

Cite This Study

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