Abstract
BackgroundRecent studies have suggested the importance of non-alcoholic fatty liver disease (NAFLD) and systemic inflammation in the development of atherosclerosis. The aim of this study was to compare the risk for coronary artery calcification (CAC) development according to the status of NAFLD and inflammation over four years of follow-up in subjects without baseline CAC.MethodsA total of 1,575 participants in a health screening program were divided into four groups according to baseline NAFLD state and high-sensitivity C-reactive protein (hs-CRP) (median 0.06 mg/L) levels as follows: no NAFLD and hs-CRP <0.06 mg/L, no NAFLD and hs-CRP ≥0.06 mg/L, NAFLD and hs-CRP <0.06 mg/L, and NAFLD and hs-CRP ≥0.06 mg/L. Coronary artery calcium score (CACS) was repeatedly measured by multi-detector computed tomography at four-year intervals and CAC development during those intervals was monitored in subjects with baseline CACS = 0.ResultsOver four years, 148 subjects (9.4%) developed CAC. The proportion of subjects who developed CAC was significantly higher in subjects with NAFLD at baseline compared with those without NAFLD at baseline (6.8 vs. 12.4%, p<0.01), and it was also higher in subjects with hs-CRP ≥0.06 mg/L compared with those with hs-CRP <0.06 mg/L (7.2 vs. 11.5%, p<0.01). In addition, the proportion of subjects who developed CAC was highest in subjects with NAFLD and hs-CRP ≥0.06 mg/dL, followed by subjects with NAFLD, subjects without NAFLD and hs-CRP ≥0.06 mg/L, and subjects without NALFD and hs-CRP <0.05 mg/L at baseline, in that order (13.7, 10.0, 8.3, and 5.8%, respectively; p for trend<0.01). The odds ratio for CAC development was highest in subjects with NAFLD and hs-CRP ≥0.06 mg/L (1.67, 95% CI 1.01–2.77), though it was attenuated after adjustment for body mass index.ConclusionsThe concomitant presence of NAFLD and systemic inflammation as assessed by hs-CRP increases the risk of CAC development over four years.
Highlights
Non-alcoholic fatty liver disease (NAFLD) is defined as a condition of fat deposition in the liver that comprises over 5% of the total liver weight in individuals without known viral or other liver diseases, and without a history of excessive daily alcohol consumption [1,2]
The proportion of subjects who developed CAC was significantly higher in subjects with NAFLD at baseline compared with those without NAFLD at baseline (6.8 vs. 12.4%, p
The proportion of subjects who developed CAC was highest in subjects with NAFLD and hs-CRP !0.06 mg/dL, followed by subjects with NAFLD, subjects without NAFLD and hs-CRP !0.06 mg/L, and subjects without NALFD and hs-CRP
Summary
Non-alcoholic fatty liver disease (NAFLD) is defined as a condition of fat deposition in the liver that comprises over 5% of the total liver weight in individuals without known viral or other liver diseases, and without a history of excessive daily alcohol consumption (defined as a daily intake of over 20 g for females and 30 g for males) [1,2]. Nonalcoholic fatty liver disease itself may promote CVD by contributing to insulin resistance and atherogenic dyslipidemia, which are important risk factors for cardiovascular disease [6,7]. Increased release of chemical messengers from visceral adipose tissue, including inflammatory cytokines, leads to adipose tissue inflammation that aggravates insulin resistance and facilitates atherosclerosis development and cardiovascular disease [7,8]. Kolak et al [9] observed adipose tissue inflammation in individuals with NAFLD independent of obesity, suggesting that the release of mediators from NAFLD causes adipose tissue inflammation, and systemic inflammation and CVD. Recent studies have suggested the importance of non-alcoholic fatty liver disease (NAFLD) and systemic inflammation in the development of atherosclerosis. The aim of this study was to compare the risk for coronary artery calcification (CAC) development according to the status of NAFLD and inflammation over four years of follow-up in subjects without baseline CAC
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