BACKGROUND: Recent studies have associated non-alcoholic fatty liver disease (NAFLD) with increased risk of cardiovascular disease, using tests of subclinical atherosclerosis. AIM: To evaluate the influence of NAFLD on subclinical atherosclerosis and coronary artery disease (CAD). METHODS: We reviewed Pubmed and EMBASE. According to inclusion and exclusion criteria, we selected 14 studies and were classified in two groups. Ten studies aimed the presence of subclinical atherosclerosis and four studies the presence of coronary artery disease. To assess subclinical atherosclerosis, we selected studies with pathological carotid intima-media thickness (CIMT) and with presence of carotid plaques. We considered coronary artery disease when patients showed at least 50% stenosis at one or more major coronary arteries. NAFLD was assessed by ultrasound (US) and liver biopsy. RESULTS: NAFLD showed a higher prevalence of pathological CIMT [35.1% (351/999) vs. 21.8% (207/948); p < 0.0001], with OR 2.04 (95% CI: 1.65-2.51). Similarly, the presence of carotid plaques was higher in NAFLD diagnosed by US [34.2% (101/295) vs. 12.9% (51/394); p < 0.0001] [OR 2.82 (95% CI: 1.87-4.27)] and diagnosed by liver biopsy [64.8% (70/108) vs. 31.3% (59/188); p < 0.0001] [OR 4.41 (95% CI: 2.63-7.40)]. On the other hand, four studies assessed CAD in patients underwent coronary angiogram. Subjects with NAFLD showed 80.4% (492/612) of CAD, while it was detected in 60.7% (356/586) (p < 0.0001) in patients without NAFLD. Therefore, NAFLD was associated with a remarkably higher likelihood of CAD, using random effects model [OR 3.31 (95% CI: 2.21-4.95)] or fixed effects model [OR 3.13 (95% CI: 2.36-4.16)]. CONCLUSIONS: NAFLD increases the risk of subclinical atherosclerosis and coronary artery disease. The right management of these patients could modify the natural history both liver and cardiovascular disease.
BACKGROUND: Recent studies have associated non-alcoholic fatty liver disease (NAFLD) with increased risk of cardiovascular disease, using tests of subclinical atherosclerosis. AIM: To evaluate the influence of NAFLD on subclinical atherosclerosis and coronary artery disease (CAD). METHODS: We reviewed Pubmed and EMBASE. According to inclusion and exclusion criteria, we selected 14 studies and were classified in two groups. Ten studies aimed the presence of subclinical atherosclerosis and four studies the presence of coronary artery disease. To assess subclinical atherosclerosis, we selected studies with pathological carotid intima-media thickness (CIMT) and with presence of carotid plaques. We considered coronary artery disease when patients showed at least 50% stenosis at one or more major coronary arteries. NAFLD was assessed by ultrasound (US) and liver biopsy. RESULTS: NAFLD showed a higher prevalence of pathological CIMT [35.1% (351/999) vs. 21.8% (207/948); p < 0.0001], with OR 2.04 (95% CI: 1.65-2.51). Similarly, the presence of carotid plaques was higher in NAFLD diagnosed by US [34.2% (101/295) vs. 12.9% (51/394); p < 0.0001] [OR 2.82 (95% CI: 1.87-4.27)] and diagnosed by liver biopsy [64.8% (70/108) vs. 31.3% (59/188); p < 0.0001] [OR 4.41 (95% CI: 2.63-7.40)]. On the other hand, four studies assessed CAD in patients underwent coronary angiogram. Subjects with NAFLD showed 80.4% (492/612) of CAD, while it was detected in 60.7% (356/586) (p < 0.0001) in patients without NAFLD. Therefore, NAFLD was associated with a remarkably higher likelihood of CAD, using random effects model [OR 3.31 (95% CI: 2.21-4.95)] or fixed effects model [OR 3.13 (95% CI: 2.36-4.16)]. CONCLUSIONS: NAFLD increases the risk of subclinical atherosclerosis and coronary artery disease. The right management of these patients could modify the natural history both liver and cardiovascular disease.
Authors: Ansel Shao Pin Tang; Kai En Chan; Jingxuan Quek; Jieling Xiao; Phoebe Tay; Margaret Teng; Keng Siang Lee; Snow Yunni Lin; May Zin Myint; Benjamin Tan; Vijay K Sharma; Darren Jun Hao Tan; Wen Hui Lim; Apichat Kaewdech; Daniel Huang; Nicholas Ws Chew; Mohammad Shadab Siddiqui; Arun J Sanyal; Mark Muthiah; Cheng Han Ng Journal: Clin Mol Hepatol Date: 2022-03-02