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Nonalcoholic Fatty Liver Disease and Severity of Cardiovascular Disease Manifestations

Nonalcoholic fatty liver disease (NAFLD), characterized by the accumulation of fat in the liver cells in the absence of excessive alcohol intake and other liver disease, affects approximately 15% to 30% of the general population in various countries; its prevalence increases up to 70% to 90% in people with obesity, metabolic syndrome (MetS), or type 2 diabetes mellitus (T2DM). The histological manifestations of NAFLD range from simple steatosis, steatohepatitis (nonalcoholic steatohepatitis [NASH]), liver fibrosis, cirrhosis, and, rarely, hepatocellular carcinoma. The NAFLD is considered to be the hepatic manifestation of the MetS. The NAFLD is strongly associated with increased risk of cardiovascular disease (CVD), and NAFLD is not only a marker but also an early mediator of atherosclerosis. The risk of clinical manifestations of CVD is significantly higher in individuals with NASH than in those with simple steatosis, and the histological severity of NAFLD (ie, steatosis, necroinflammation, and fibrosis) predicts CVD independent of classical risk factors, insulin resistance, and components of the MetS. This suggests that NAFLD might itself confer a degree of CVD risk above and beyond that associated with the individual components of MetS. Key issues remaining to be investigated are the association of NAFLD presence and/or grade (stage) with the severity, and therefore, the prognosis of CVD manifestations (coronary artery disease [CAD], stroke, and peripheral arterial disease [PAD]) and our ability to tackle the negative effect of NAFLD on CVD morbidity and mortality. The results of the study by Agac et al, published in this issue of Angiology, suggest that the prevalence of NAFLD was very high (81.2%) among subjects with acute coronary syndromes (ACS) and that the SYNTAX (Synergy between PCI with Taxus and Cardiac Surgery) score (SS) may represent a prognostic marker in patients with both non-ST and ST segment elevation ACS. The SS is an angiographic variable that predicts 1-year mortality rates, cardiac death, myocardial infarction, and target vessel revascularization in patients undergoing percutaneous coronary intervention (PCI) and its value is significantly higher in patients with NAFLD than in those without NAFLD (18 + 8 vs 11+ 5, P 1⁄4 .001). Furthermore, in multivariate analysis, increased age (odds ratio [OR] 1.05; 95% confidence interval [CI] 1.00-1.10) and the presence of NAFLD (OR, 13.20; 95% CI, 2.52-69.15) were independent factors associated with the SS value. This suggests that the presence of NAFLD was associated with a more severe CAD, which is bound to have a worse prognosis. Among the limitations of this study are the cross-sectional design and therefore its inability to confirm findings on the rate of CVD events. Moreover, the use of the SS has been mainly validated in the Acute Catheterization and Urgent Intervention Triage StrategY trial only in patients with a non-ST-segment elevation ACS undergoing PCI, and its use in patients with ST elevation ACS might be challenged. Initially, the SS was shown to be an effective tool for predicting the risk of major ischemic events in patients with stable CAD and multivessel or left main disease undergoing PCI, and there are data suggesting a moderate intraobserver reproducibility (its calculation relies on the subjective assessment of lesions using coronary angiography). Nevertheless, the findings of this study are adequate to act as hypothesis generating and should encourage the design of bigger and long-term studies that will prospectively investigate the relationship between the presence and the histological stage of NAFLD with actual midor long-term prognosis of CVD. Moreover, these results might motivate the initiation of interventions to control and, if possible, to reverse the progress of NAFLD from steatosis to a more advanced stage, given that at present time, there is no globally accepted effective intervention for NAFLD. There are some data suggesting a close relationship of NAFLD with the severity of CAD. To begin with, there are very few data on NAFLD and ACS. The most common cause of ACS appears to be vulnerable plaque rupture. These are related to a positive remodeling of the vessel, a large lipid