Introduction Individuals with non-alcoholic fatty liver disease (NAFLD) have a significantly increased risk of cardiovascular (CV) disease independent of other cardiometabolic risk factors. We explored the relationship between endothelial function, oxidative stress, vascular inflammation and insulin resistance in patients with NAFLD.

Method Patients with proven NAFLD but without cirrhosis were recruited into the study and the following parameters were assessed:

1. Endothelial function – change in reflective index post salbutamol using digital plethysmography, urine albumin:creatinine ratio, plasma vascular cell adhesion molecule-1 (VCAM-1) and plasma cyclic guanosine monophosphate (cGMP)

2. Oxidative stress – blood glutathione ratio (GSH:GSSG), plasma total anti-oxidant status and plasma lipid hydroperoxides

3. Inflammation – highly-sensitive plasma CRP

4. Insulin resistance – HOMA-IR

Results We studied 42 patients: 31 males and 11 females. We found 79% had T2DM or impaired fasting glucose. Mean age was 58 ± 8 years, BMI 33.2 ± 5.5 kg/m², BP 133/82 ± 12/7 mmHg, duration of NAFLD diagnosis 1.0 ± IQR 3.4 years, HbA1c 53 ± 13 mmol/mol, total cholesterol 4.43 ± 1.14 mmol/l, HDL 1.06 ± 0.32 mmol/l, LDLc 2.51 ± 1.02 mmol/l, and triglycerides 1.93 ± 0.85 mmol/l. There was moderate correlation between VCAM-1 and hsCRP (Spearman’s rho=0.392,p = 0.01); moderate correlation between hsCRP and blood glutathione ratio (Spearman’s rho=0.325, p = 0.04) and moderate correlation between HOMA-IR and aspartate aminotransferase [AST] (Spearman’s rho=0.489, p = 0.001).

Conclusion Markers of both vascular (VCAM-1) and systemic low grade inflammation (hsCRP) were associated with evidence of endothelial dysfunction and oxidative stress, whilst insulin resistance was associated with AST in non-cirrhotic patients with NAFLD. VCAM-1 as a marker of endothelial activation may be a potential CV risk predictor in this group of patients.

Disclosure of interest None Declared.