What is the clinical evidence from this study?

Study design: Cross-Sectional. Population: Metabolic dysfunction-associated steatotic liver disease (MASLD) (n=425). Intervention: Metabolic dysfunction-associated steatotic liver disease (MASLD) vs. No MASLD. Primary outcome: Overall coronary atherosclerotic plaque presence (OR 2.22, 95% CI 1.04-4.73, p=0.038).

What does this research mean for the field?

Metabolic dysfunction–associated steatotic liver disease is independently associated with an increased presence of coronary atherosclerotic plaque, with higher liver stiffness linked to obstructive stenosis and calcified plaque. Novelty: ClaimNovelty.INCREMENTAL. Consensus alignment: ConsensusAlignment.NEUTRAL.

What question did this study set out to answer?

To evaluate the relationship between stages of hepatic steatosis and fibrosis and specific coronary artery disease phenotypes using paired elastography and computed tomography angiography.

September 17, 2026Hepatology InternationalOpen Access

Coronary atherosclerosis across stages of metabolic dysfunction–associated steatotic liver disease: a VCTE–CCTA study

Q: What are the key findings of this study?

Metabolic dysfunction-associated steatotic liver disease was independently associated with more than twofold higher odds of overall coronary atherosclerotic plaque presence (OR 2.22).

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Key result

MASLD is linked to ~122% higher odds of coronary atherosclerotic plaque presence.

OR 2.22
95% CI 1.04-4.73
P=0.038
n=425

Why the study?

Does MASLD increase the presence of coronary atherosclerotic plaque in adults with cardiometabolic conditions?

Key Points

To evaluate the relationship between stages of hepatic steatosis and fibrosis and specific coronary artery disease phenotypes using paired elastography and computed tomography angiography.
Included 425 adults who underwent paired vibration-controlled transient elastography (VCTE) and coronary computed tomography angiography (CCTA) within a three-month interval.
Defined metabolic dysfunction–associated steatotic liver disease (MASLD) as controlled attenuation parameter (CAP) ≥248 dB/m and significant fibrosis as liver stiffness measurement (LSM) ≥8 kPa.
Classified coronary outcomes using Coronary Artery Disease Reporting and Data System guidelines and modeled associations using multivariable logistic regression adjusted for cardiometabolic covariates.
Individuals with MASLD had a significantly higher prevalence of overall coronary plaque than those without MASLD (81.6% vs 60.7%, p<0.001), remaining independently associated after full adjustment (OR 2.22, 95% CI 1.04–4.73; p=0.038).
Prevalence of obstructive stenosis did not significantly differ between participants with and without MASLD (28.4% vs 22.8%, p=0.186), and MASLD did not increase odds of calcified plaque or CAD severity.
Each 1 kPa increase in liver stiffness was associated with higher odds of obstructive stenosis (OR 1.14, 95% CI 1.00–1.30) and calcified plaque (OR 1.18, 95% CI 1.04–1.34).

Study Design

Type

Cross-Sectional (n=425)

Multicenter

Structured PICO

Does MASLD increase the presence of coronary atherosclerotic plaque in adults with cardiometabolic conditions?

Population

425 adults aged 18 to 80 years with cardiometabolic risk factors who underwent both vibration-controlled transient elastography and coronary computed tomography angiography.

Exposure

Metabolic dysfunction-associated steatotic liver disease (MASLD) defined as controlled attenuation parameter (CAP) ≥248 dB/m and at least one cardiometabolic risk factor

Comparator

Non-MASLD (individuals with cardiometabolic risk factors but without CAP-defined hepatic steatosis)

Outcome

Presence of overall coronary atherosclerotic plaque (any visible coronary atherosclerotic lesion in any coronary segment)surrogate

Main Result

Odds Ratio: 2.22 (95% CI 1.04–4.73)

Absolute Event Rate: 81.6% vs 60.7%

p-value: p=0.038

MASLD is independently associated with a more than twofold higher odds of coronary atherosclerotic plaque presence, suggesting a link between hepatic steatosis and early atherogenesis.

Limitations

Cross-sectional design precludes causal inference and determination of temporal relationships.
Lack of mechanistic biomarkers.
Secondary analyses were exploratory without formal adjustment for multiple comparisons, increasing the risk of type I error.
Potential referral bias because CCTA examinations were performed only when clinically indicated.
Study population had generally low liver stiffness values and a limited number of participants with significant fibrosis.
Residual confounding cannot be excluded despite extensive multivariable adjustment.
Small number of participants with significant fibrosis
Exploratory nature of secondary analyses
Non-MASLD group comprised individuals with cardiometabolic risk factors rather than metabolically healthy controls
Cross-sectional nature cannot establish causal or temporal relationship

Implication

MASLD warrants CV risk vigilance in practice; extends cross-sectional plaque links on CCTA but leaves causality and interventions open.

Abstract

Background Metabolic dysfunction–associated steatotic liver disease (MASLD) and coronary artery disease (CAD) share common pathophysiologic pathways. However, the relationship between different stages of MASLD and distinct coronary atherosclerosis phenotypes remains unclear. We evaluated the association of hepatic steatosis and fibrosis with coronary artery disease outcomes using paired vibration-controlled transient elastography (VCTE) and coronary computed tomography angiography (CCTA). Methods 425 adults who underwent both VCTE and CCTA within a three-month interval were included. MASLD was defined as controlled attenuation parameter (CAP) ≥248 dB/m, and significant fibrosis was defined as Liver Stiffness Measurement (LSM) ≥8 kPa. Coronary outcomes were assessed according to Coronary Artery Disease Reporting and Data System guidance. The primary outcome was plaque presence; secondary outcomes included obstructive stenosis, calcified plaque, high segment involvement, and CAD severity. Multivariable logistic regression models were progressively adjusted for demographic, lifestyle, and cardiometabolic factors. Results MASLD was present in 47.3% of participants. Individuals with MASLD had a higher prevalence of overall plaque than those without (81.6% vs 60.7%, p<0.001), whereas obstructive stenosis did not differ between groups. MASLD was independently associated with higher odds of overall plaque presence after full adjustment (OR 2.22, 95% CI 1.04–4.73; p=0.038). In exploratory analyses, MASLD did not increase the odds of obstructive stenosis, calcified plaque, or CAD severity. In contrast, 1 kPa increase in LSM was associated with higher odds of obstructive stenosis (OR 1.14, 95% CI 1.00–1.30) and calcified plaque (OR 1.18, 95% CI 1.04–1.34), but not CAD presence and severity. Conclusion MASLD was independently associated with the presence of coronary atherosclerotic plaque. Exploratory analyses further suggested that greater liver stiffness may be associated with obstructive stenosis and calcified plaque, raising the possibility that more advanced liver disease relates to specific features of advanced coronary artery disease. Confirmation in larger prospective studies is warranted.

Discussion

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Cite This Study

Us et al. (2026) conducted a cross-sectional in Metabolic dysfunction-associated steatotic liver disease (MASLD) (n=425). Metabolic dysfunction-associated steatotic liver disease (MASLD) vs. No MASLD was evaluated on Overall coronary atherosclerotic plaque presence (OR 2.22, 95% CI 1.04-4.73, p=0.038). Metabolic dysfunction-associated steatotic liver disease was independently associated with more than twofold higher odds of overall coronary atherosclerotic plaque presence (OR 2.22).

synapsesocial.com/papers/6aabb8045f706d05830e7771 https://doi.org/10.1007/s12072-026-11147-8

Topics

Coronary artery disease

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Implication

MASLD warrants CV risk vigilance in practice; extends cross-sectional plaque links on CCTA but leaves causality and interventions open.

Coronary atherosclerosis across stages of metabolic dysfunction–associated steatotic liver disease: a VCTE–CCTA study

Key Points

Study Design

Structured PICO

Main Result

Limitations

Implication

Abstract

Discussion

Cite This Study

Topics

Coronary atherosclerosis across stages of metabolic dysfunction–associated steatotic liver disease: a VCTE–CCTA study

Key Points

Study Design

Structured PICO

Main Result

Limitations

Implication

Abstract

Discussion

Cite This Study

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