Key result
Metabolic dysfunction-associated fatty liver disease linked to ~265% higher major cardiovascular events risk.
Why the study?
It remained unknown whether coronary CT angiography-derived pericoronary fat attenuation index mediated the relationship between MAFLD and major adverse cardiovascular events.
Does the presence of MAFLD increase the risk of MACEs and adverse CCTA-derived plaque characteristics in patients with stable chest pain?
Cohort (n=367)
Yes
Does the presence of MAFLD increase the risk of MACEs and adverse CCTA-derived plaque characteristics in patients with stable chest pain?
MAFLD is associated with an increased risk of MACEs and adverse coronary plaque characteristics, a relationship that is partially mediated by coronary inflammation as measured by FAI.
Answers are grounded in this paper and cite their sources.
MAFLD signals elevated MACE risk warranting vigilance; observational data leaves causal plaque mediation open for confirmation.
BACKGROUND: Coronary CT angiography (CCTA) derived pericoronary fat attenuation index (FAI) is a reliable quantitative biomarker of vessel inflammation. However, whether this novel index mediated the relationship between metabolic dysfunction-associated fatty liver disease (MAFLD) and major adverse cardiovascular events (MACEs) remains unknown. METHODS: From January 2019 to December 2022, consecutive patients with stable chest pain who underwent CCTA and unenhanced abdominal CT were prospectively enrolled. All participants were divided into two groups-with MAFLD and without MAFLD according to abdominal CT results. The primary end point was MACEs, defined as cardiac death, nonfatal myocardial infarction, and late revascularization. RESULTS: A total of 135 participants with MAFLD and 232 without MAFLD were included in our study. The multivariate logistic regression analysis revealed that MAFLD was significantly associated with obstructive coronary artery disease (OR = 1.86, p = 0.024), high-risk plaque features ≥ 2 (adjusted OR = 2.34, p < 0.001), CT derived fraction flow reserve ≤ 0.8 (adjusted OR = 1.88, p = 0.006), FAI ≥ -70.1HU (adjusted OR = 3.25, p < 0.001) after adjusted for traditional risk factors. Participants with MAFLD showed a lower 36-month MACE-free survival rate than participants without MAFLD (54.0% vs. 83.5%, log-rank p < 0.001). In addition, MAFLD was significantly associated with MACEs (HR = 3.65, 95%CI: 1.83, 7.26, p < 0.001). Furthermore, mediation analysis revealed that FAI mediated 46.8% for the relationship between MAFLD and MACEs. CONCLUSIONS: MAFLD is associated with CCTA derived plaque characteristics, including geometric, physiologic and inflammatory status. The relationship between MAFLD and MACEs might be partially mediated via coronary inflammation, which could be captured by FAI. CLINICAL TRIAL NUMBER: Not applicable.
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Wang et al. (2025) conducted a cohort in Stable chest pain suggestive of coronary artery disease (n=367). Metabolic dysfunction-associated fatty liver disease (MAFLD) vs. Without MAFLD was evaluated on Major adverse cardiovascular events (MACEs) (HR 3.65, 95% CI 1.83-7.26, p=<0.001). Metabolic dysfunction-associated fatty liver disease increased the risk of major adverse cardiovascular events compared to patients without the disease.
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