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MAFLD as a predictor of adverse cardiovascular events among CHD patients with LDL-C<1.8 mmol/L
Jingjing Song1, Yupeng Liu2, Ye Liu1
1Heart Center and Beijing Key Laboratory of Hypertension, Beijing Chaoyang Hospital, Capital Medical University, Beijing, China.
Insights
Metabolic (dysfunction)-associated fatty liver disease (MAFLD) increases cardiovascular risk in coronary heart disease patients, even with low LDL-C. Advanced liver fibrosis in MAFLD patients further elevates this risk, highlighting the need for integrated management.
Area of Science:
- Cardiology
- Hepatology
- Metabolic Diseases
Background:
- Patients on statin therapy still experience adverse cardiovascular events.
- Metabolic (dysfunction)-associated fatty liver disease (MAFLD) shares metabolic risk factors with cardiovascular disease.
- Residual cardiovascular risk persists in coronary heart disease (CHD) patients, particularly those with low LDL-C.
Purpose of the Study:
- To investigate the association between MAFLD and adverse cardiovascular outcomes.
- To assess cardiovascular risk in CHD patients with LDL-C < 1.8 mmol/L.
- To determine the impact of liver fibrosis on cardiovascular events in MAFLD patients.
Main Methods:
- Propensity score matching (PSM) was used to analyze 800 MAFLD and 800 non-MAFLD patients with LDL-C < 1.8 mmol/L.
- Major adverse cardiac and cerebrovascular events (MACCEs) were the primary endpoint.
- MAFLD patients were stratified by advanced liver fibrosis using the Fibrosis-4 (FIB-4) index.
Main Results:
- MAFLD patients had a significantly higher incidence of MACCEs compared to non-MAFLD patients (9.6% vs. 6.6%, p < 0.05).
- MAFLD was an independent risk factor for MACCEs (HR 1.48, 95% CI 1.04-2.1).
- Advanced liver fibrosis in MAFLD patients was associated with increased risk of MACCEs, all-cause mortality, myocardial infarction, and stent thrombosis (HR 2.91, 95% CI 1.17-7.19).
Conclusions:
- MAFLD is an independent predictor of adverse cardiovascular outcomes in CHD patients with LDL-C < 1.8 mmol/L.
- Advanced liver fibrosis exacerbates cardiovascular risk in MAFLD patients.
- Screening and management of MAFLD and liver fibrosis are crucial for addressing residual cardiovascular risk.
Background And Aims:
Patients receiving statin therapy still suffer from adverse cardiovascular events. Metabolic (dysfunction)-associated fatty liver disease (MAFLD) is a newly proposed concept that shares common metabolic risk factors with cardiovascular disease. This study aimed to investigate the association between MAFLD and adverse cardiovascular outcomes in coronary heart disease (CHD) patients with LDL-C<1.8 mmol/L.
Methods And Results:
CHD patients with LDL-C<1.8 mmol/L were divided into MAFLD and non-MAFLD groups. Propensity score matching (PSM) was used to control for baseline differences between the two groups. The primary endpoint was major adverse cardiac and cerebrovascular events (MACCEs). All MAFLD patients were further stratified into two groups with and without advanced liver fibrosis, according to the Fibrosis-4 (FIB-4) index cutoffs, and the associations between advanced liver fibrosis status and cardiovascular outcomes were analyzed. After PSM, 800 MAFLD and 800 non-MAFLD patients with LDL-C<1.8 mmol/L were analyzed. MAFLD patients exhibited a significantly greater cumulative incidence and risk of MACCEs than non-MAFLD patients (9.6 % versus 6.6 %, p < 0.05; HR 1.48, 95 % CI 1.04-2.1, p < 0.05). Among MAFLD patients with LDL-C<1.8 mmol/L, advanced liver fibrosis staged by the FIB-4 index was associated with an elevated risk for MACCEs (HR 2.91, 95 % CI 1.17-7.19, p < 0.05), all-cause mortality, myocardial infarction (MI) and stent thrombosis.
Conclusion:
MAFLD was an independent risk factor for adverse cardiovascular outcomes in CHD patients with LDL-C<1.8 mmol/L. Additionally, advanced liver fibrosis predicts increased risks for adverse cardiovascular events among MAFLD patients. These findings suggest that MAFLD and liver fibrosis screening and management contribute to the residual cardiovascular risk of CHD patients.
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