This study confirmed that MAFLD is correlated with cardiovascular risk factors, coronary atherosclerotic plaques, and degree of stenosis. In addition, after correction for traditional cardiovascular risk factors, MAFLD was independently correlated with noncalcified plaques and mixed plaques, indicating that there is a correlation between MAFLD and CAS. In the subgroup analysis, there was a trend toward a correlation of MAFLD with significant stenosis, especially among patients who were young, female, nonsmokers with low BMI, without MetS, and with high LDL-C.
The results of this study confirmed that MAFLD was correlated with hypertension, diabetes, obesity, and dyslipidemia, which are common risk factors for CVD. Previous studies have also confirmed that NAFLD is correlated with CVD. A study involving 17,350 patients demonstrated that [14] NAFLD was correlated with an elevated 10-year risk of developing CVD as estimated using the Framingham risk score (FRS) and was not correlated with classical CVD risk factors and MetS. Another study of patients with fatty liver with an average follow-up of 6.5 years found that the risk of CVD doubled [15]. Since NAFLD was renamed MAFLD, hypertension, diabetes, obesity, and dyslipidemia have been included in the diagnostic criteria. Therefore, the relationship between MAFLD and CVD is closer than that between NAFLD and CVD. The complex mechanism between NAFLD and CVD has not been fully elucidated, but inflammation is an important link; the mechanism that links MAFLD and CVD must be further studied.
This study found that MAFLD was correlated with Overall plaque in the coronary arteries. After exclusion of recognized risk factors for coronary heart disease, such as age, sex, hypertension, diabetes, smoking, and hyperlipidemia, MAFLD was still independently correlated with noncalcified plaques and mixed plaques. Niikura et al. [16] found that NAFLD was closely correlated with increased carotid intima-media thickness, CAS, and increased arterial stiffness. A meta-analysis of 27 studies indicated that after excluding traditional cardiovascular risk factors and MetS, nonalcoholic fatty liver and subclinical AS were still independently correlated [17]. The latest evidence suggests that NAFLD is a risk factor for the development of cardiovascular complications of AS, such as stroke and myocardial infarction [18–20]. AS is one of the causes of CVD, and inflammation plays an important role in intimal thickening of the arterial wall, arteriosclerosis and luminal stenosis [21]. Studies have confirmed that an increase in CRP in fatty liver patients indicates an inflammatory process [22], but the underlying mechanism is more complicated and may be related to chronic fat overload-induced liver cell death in NAFLD. Hepatocyte death causes the release of molecules that trigger macrophage activation, and an increase in macrophages and Kupffer cells leads to an increase in the circulating levels of systemic inflammatory markers, including the interleukin (IL)-1, IL-6 and IL-20 subfamilies [23, 24]. MAFLD patients should be screened for atherosclerotic cardiovascular disease (ASCVD).
Most studies of NAFLD and CAS have suggested that NAFLD is only correlated with noncalcified plaques or mixed plaques [25, 26]; however, the results of this study suggest that MAFLD is correlated with both noncalcified and mixed plaques, indicating that MAFLD is more closely correlated with CVD than is NAFLD. This closer correlation may be because the diagnostic criteria for MAFLD better identify lean or normal weight fatty liver patients with metabolic abnormalities, a population that is not identified by the diagnostic criteria for NAFLD but is at high risk of developing CVD. A recent study revealed that MAFLD patients had a higher risk of ASCVD than did NAFLD patients [7], and a retrospective study of 13,083 patients with complete ultrasound and laboratory data demonstrated that patients who met the diagnostic criteria for MAFLD were more likely to have multiple metabolic comorbidities, including CVD, than were patients with NAFLD [27]. Therefore, clinicians should use the diagnostic criteria for MAFLD to identify patients with metabolic dysfunction at an early stage and intervene in a timely manner to reduce the incidence of CVD.
In this study, the number of noncalcified plaques was 1.6 times higher in the MAFLD group than in the non-MAFLD group, and the number of combined mixed plaques was 1.5 times higher in the MAFLD group than in the non-MAFLD group. A prospective study with 3 years of follow-up [28] found that the probability of major cardiovascular events within 3 years was significantly higher in patients with noncalcified plaques and mixed plaques than in patients with calcified plaques (23%, 38%, and 6%), indicating that the prognosis of patients with noncalcified plaques and mixed plaques is poor. Mixed plaques include both calcified and noncalcified plaques. Noncalcified plaques are unstable plaques, and unstable plaque rupture predisposes individuals to a greater risk of acute coronary syndrome events [29]. Patients with MAFLD combined with CAS may have a higher risk of major cardiovascular events and acute coronary syndrome events. This study found that there were significantly more patients with multiple coronary artery stenoses in the MAFLD group than in the non-MAFLD group and that multiple coronary artery stenoses may lead to more adverse cardiovascular events and poor patient prognosis. Therefore, MAFLD patients should be screened for ASCVD. Patients with CAS should be screened for MAFLD to improve metabolic dysfunction in a timely manner to avoid adverse cardiovascular events.
This study has limitations. First, this retrospective study could not clarify the causal relationship between MAFLD and coronary plaque formation. Second, because image reconstruction artifacts associated with radioactive materials (such as calcium metal) can obscure the coronary artery lumen, such artifacts may lead to an underestimation or overestimation of coronary artery stenosis (inaccurate assessment of the vascular lumen under high calcium conditions).
In summary, this retrospective study found that MAFLD was correlated with traditional cardiovascular risk factors, CAS, coronary artery stenosis, and multiple coronary artery lesions, and further analysis revealed that MAFLD was an independent risk factor for noncalcified and mixed coronary atherosclerotic plaques.