Key result
Advanced liver fibrosis is linked to ~4-fold higher risk of vascular atherosclerosis.
Why the study?
Whether the severity of histology fibrosis stage is associated with more pronounced cardiovascular organ damage in individuals with ultrasonography-diagnosed NAFLD was unsettled.
Does advanced liver fibrosis assessed by noninvasive markers associate with increased cardiovascular organ damage in adults with hepatic steatosis?
Cross-Sectional (n=400)
No
Does advanced liver fibrosis assessed by noninvasive markers associate with increased cardiovascular organ damage in adults with hepatic steatosis?
Odds Ratio: 3.95 (95% CI 1.12–13.87)
p-value: p=0.03
Advanced liver fibrosis, as determined by noninvasive markers, is independently associated with increased cardiovascular organ damage (atherosclerosis and LVH) in patients with hepatic steatosis.
May prompt CV evaluation in steatosis with high fibrosis probability; leaves open causality and need for longitudinal validation.
Evidence suggests that advanced fibrosis, as determined by the noninvasive NAFLD fibrosis score (NFS), is a predictor of cardiovascular mortality in individuals with ultrasonography-diagnosed NAFLD. Whether the severity of histology (i.e., fibrosis stage) is associated with more pronounced cardiovascular organ damage is unsettled. In this study, we analyzed the clinical utility of NFS in assessing increased carotid intima-media thickness (cIMT), and left ventricular mass index (LVMI). In this cross-sectional study NFS, cIMT and LVMI were assessed in 400 individuals with ultrasonography-diagnosed steatosis. As compared with individuals at low probability of liver fibrosis, individuals both at high and at intermediate probability of fibrosis showed an unfavorable cardio-metabolic risk profile having significantly higher values of waist circumference, insulin resistance, high sensitivity C-reactive protein (hsCRP), fibrinogen, cIMT, and LVMI, and lower insulin-like growth factor-1 (IGF-1) levels. The differences in cIMT and LVMI remained significant after adjustment for smoking and metabolic syndrome. In a logistic regression model adjusted for age, gender, smoking, and diagnosis of metabolic syndrome, individuals at high probability of fibrosis had a 3.9-fold increased risk of vascular atherosclerosis, defined as cIMT>0.9 mm, (OR 3.95, 95% CI 1.12-13.87) as compared with individuals at low probability of fibrosis. Individuals at high probability of fibrosis had a 3.5-fold increased risk of left ventricular hypertrophy (LVH) (OR 3.55, 95% CI 1.22-10.34) as compared with individuals at low probability of fibrosis. In conclusion, advanced fibrosis, determined by noninvasive fibrosis markers, is associated with cardiovascular organ damage independent of other known factors.
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Sesti et al. (2014) conducted a cross-sectional in Hepatic Steatosis (NAFLD) (n=400). High probability of advanced liver fibrosis (NAFLD fibrosis score > 0.676) vs. Low probability of liver fibrosis (NAFLD fibrosis score < -1.455) was evaluated on Vascular atherosclerosis (carotid intima-media thickness > 0.9 mm) (OR 3.95, 95% CI 1.12-13.87, p=0.03). High probability of advanced liver fibrosis was associated with a 3.9-fold increased risk of vascular atherosclerosis (OR 3.95) and a 3.5-fold increased risk of left ventricular hypertrophy.
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