Aortic flow propagation velocity, epicardial fat thickness, and osteoprotegerin level to predict subclinical atherosclerosis in patients with nonalcoholic fatty liver disease

Abstract

Objective:Nonalcoholic fatty liver disease is the most common cause of liver dysfunction in Western countries and an independent risk factor for atherosclerotic heart disease. Appropriate noninvasive parameters are lacking for optimal risk stratification of cardiovascular disease in these patients. We evaluated several recently discovered noninvasive parameters for atherosclerosis in patients with nonalcoholic fatty liver disease: epicardial fat thickness, aortic flow propagation velocity, and osteoprotegerin level.Methods:Forty-one patients (27 men and 14 women; mean age, 37.9±8.9 years) with nonalcoholic fatty liver disease and 37 control subjects (17 men and 20 women; mean age, 34.5±8.6 years) were enrolled in this observational case-control study. Patients with nonalcoholic fatty liver disease diagnosed at a gastroenterology outpatient clinic were included. Patients with cardiac pathology other than hypertension were excluded. Epicardial fat thickness and aortic flow propagation velocity were measured by echocardiography. The serum concentration of osteoprotegerin was measured using a commercial enzyme-linked immunosorbent assay kit.Results:Nonalcoholic fatty liver disease patients exhibited a significantly lower aortic flow propagation velocity (155.17±30.00 vs. 179.00±18.14 cm/s, p=0.000) and significantly higher epicardial fat thickness (0.51±0.25 vs. 0.29±0.09 cm, p=0.000) than control subjects. Osteoprotegerin levels were higher, but not significant, in patients with nonalcoholic fatty liver disease (28.0±13.0 vs. 25.2±10.8 pg/mL, p=0.244). Binary logistic regression analysis showed that aortic flow propagation velocity (OR, –0.973; 95% CI, 0.947–0.999) and waist circumference (OR, –1.191; 95% CI, 1.088–1.303) were independent predictors of nonalcoholic fatty liver disease.Conclusion:In this study, epicardial fat thickness and osteoprotegerin level were higher and aortic flow propagation velocity was lower in patients with nonalcoholic fatty liver disease. Early detection of abnormal epicardial fat thickness and aortic flow propagation velocity may warrant a search for undetected cardiovascular disease in patients with nonalcoholic fatty liver disease. (Anatol J Cardiol 2016; 16: 974-9)

Non-alcoholic fatty liver disease: A growing public health problem in Turkey

“…Furthermore, NAFLD leads to significant changes in vessel functionality. A study by Oguz et al (41) showed that patients with NAFLD had a significantly lower aortic flow propagation velocity. Another study demonstrated that coronary flow velocity reserve is significantly impaired in patients with NAFLD (42,43).…”

Cardiovascular Risk in Fatty Liver Disease: The Liver-Heart Axis—Literature Review

“…Several articles described a significant association between EFT and NAFLD. Oguz et al conducted a cross-sectional study concluding that EFT and osteoprotegerin level were increased while aortic flow propagation velocity was decreased in patients with NAFLD (105). Another study involving 868 subjects from the PLIC Study conducted by Baraghetti et al reported that hepatic steatosis and EFT were related to an increased incidence of extra-cardiac plaques (106).…”

The association between epicardial adipose tissue and non-alcoholic fatty liver disease: A systematic review of existing human studies

“…A total of 58 articles were excluded because they did not meet the inclusion criteria. Finally, 18 articles (thirteen cross-sectional studies (Fracanzani et al, 2016[ 7 ]; Brouha et al, 2018[ 3 ]; Cho et al, 2017[ 4 ]; Kim et al, 2016[ 18 ]; Psychari et al, 2016[ 33 ]; Petta et al, 2015[ 32 ]; Granér et al, 2015[ 8 ]; Topuz et al, 2014[ 39 ]; Turan, 2020[ 40 ]; Lai et al, 2012[ 19 ]; Ledda et al, 2021[ 21 ]; Iacobellis et al, 2008[ 15 ]; Meng et al, 2018[ 27 ]) and five case-control studies (Iacobellis et al, 2014[ 12 ], Colak et al, 2012[ 5 ], Yilmaz et al, 2011[ 43 ], Sunbul et al, 2014[ 37 ], Oğuz et al, 2016[ 30 ]), published between 2008 and 2021, which met our inclusion criteria were reviewed. Out of these, fourteen studies measured EAT thickness using echocardio-graphy; in the rest, EAT volume was assessed using CT or MRI methods (Brouha et al, 2018[ 3 ]; Granér et al, 2015[ 8 ]; Ledda et al, 2021[ 21 ]; Meng et al, 2018[ 27 ]).…”

“…The characteristics of studies are shown in the Table 1 (Tab. 1) (References in Table 1: Brouha et al, 2018[ 3 ]; Cho et al, 2017[ 4 ]; Colak et al, 2012[ 5 ]; Fracanzani et al, 2016[ 7 ]; Granér et al, 2014[ 8 ]; Iacobellis et al, 2008[ 15 ]; Iacobellis et al, 2014[ 12 ]; Kim et al, 2016[ 18 ]; Lai et al, 2012[ 19 ]; Ledda et al, 2021[ 21 ]; Meng et al, 2018[ 27 ]; Oğuz et al, 2016[ 30 ]; Petta et al, 2015[ 32 ]; Psychari et al, 2016[ 33 ]; Sunbul et al, 2014[ 37 ]; Topuz et al, 2014[ 39 ]; Turan, 2020[ 40 ]; Yilmaz et al, 2011[ 43 ]).…”