caa a22 4500 445794755 CHVBK 20180317145121.0 cr unu---uuuuu 170323e20111201xx s 000 0 eng 10.1007/s10620-011-1767-y doi (NATIONALLICENCE)springer-10.1007/s10620-011-1767-y Mechanisms Linking Nonalcoholic Fatty Liver Disease with Coronary Artery Disease [Elektronische Daten] [W. Nseir, A. Shalata, A. Marmor, N. Assy] The most common cause of death in patients with nonalcoholic fatty liver disease (NAFLD) is coronary artery disease (CAD), not chronic liver disease. Fatty liver increases cardiovascular risk by classical (dyslipidemia, hypertension, diabetes) and by less conventional mechanisms. Common pathways involved in the pathogenesis of fatty liver and CAD includes hepatic insulin resistance and sub clinical inflammation. The hepatic insulin resistance state of fatty liver infiltration is characterized by increased FFA, which causes lipotoxicity and impairs endothelium-dependent vasodilatation, increases oxidative stress, and has a cardio toxic effect. Additional metabolic risk factors include leptin, adiponectin, pro inflammatory cytokines [such as IL-6, C-reactive protein and plasminogen activator inhibitor-1 (PAI-1)], which together lead to increased oxidative stress and endothelial dysfunction, finally promoting coronary artery disease (CAD). When classical risk factors are superimposed on fatty liver accumulation, they may further increase the new metabolic risk factors, exacerbating CAD. The clinical implication is that patients with NAFLD are at higher risk (steatohepatitis, diabetes, obesity, atherogenic dyslipidemia) and should undergo periodic cardiovascular risk assessment including the Framingham score, cardiac effort test, and measurement of intimae-media thickening of the carotids arteries. This may improve risk stratification for CAD. Springer Science+Business Media, LLC, 2011 Fatty liver nationallicence Cardiovascular disease nationallicence Coronary artery diseases nationallicence Mechanism nationallicence NAFLD nationallicence Steatohepatitis nationallicence Nseir W. Departments of Internal Medicine, Holy Family Hospital, Nazareth, Israel aut Shalata A. Liver Unit, Ziv Medical Center, POB 1008, 13100, Safed, Upper Galilee, Israel aut Marmor A. Department of Cardiology, Ziv Medical Center, Safed, Israel aut Assy N. Liver Unit, Ziv Medical Center, POB 1008, 13100, Safed, Upper Galilee, Israel aut Digestive Diseases and Sciences Springer US; http://www.springer-ny.com 56/12(2011-12-01), 3439-3449 0163-2116 56:12<3439 2011 56 10620 https://doi.org/10.1007/s10620-011-1767-y text/html Onlinezugriff via DOI 1 review-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/s10620-011-1767-y text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Nseir W. Departments of Internal Medicine, Holy Family Hospital, Nazareth, Israel aut NATIONALLICENCE 700 1- Shalata A. Liver Unit, Ziv Medical Center, POB 1008, 13100, Safed, Upper Galilee, Israel aut NATIONALLICENCE 700 1- Marmor A. Department of Cardiology, Ziv Medical Center, Safed, Israel aut NATIONALLICENCE 700 1- Assy N. Liver Unit, Ziv Medical Center, POB 1008, 13100, Safed, Upper Galilee, Israel aut NATIONALLICENCE 773 0- Digestive Diseases and Sciences Springer US; http://www.springer-ny.com 56/12(2011-12-01), 3439-3449 0163-2116 56:12<3439 2011 56 10620 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer