• Media type: E-Article
  • Title: Hepatic Steatosis Is Associated With Aortic Valve Sclerosis in the General Population : The Study of Health in Pomerania (SHIP) : The Study of Health in Pomerania (SHIP)
  • Contributor: Markus, Marcello Ricardo Paulista; Baumeister, Sebastian Edgar; Stritzke, Jan; Dörr, Marcus; Wallaschofski, Henri; Völzke, Henry; Lieb, Wolfgang
  • Published: Ovid Technologies (Wolters Kluwer Health), 2013
  • Published in: Arteriosclerosis, Thrombosis, and Vascular Biology, 33 (2013) 7, Seite 1690-1695
  • Language: English
  • DOI: 10.1161/atvbaha.112.300556
  • ISSN: 1079-5642; 1524-4636
  • Origination:
  • Footnote:
  • Description: Objective We aimed to analyze the association between hepatic steatosis and aortic valve sclerosis in the general population. Approach and Results Cross-sectional data of 2212 men and women, aged 45 to 81 years, from the baseline examination of the population-based Study of Health in Pomerania (SHIP-0) were analyzed. Hepatic steatosis was primarily defined as the presence of a hyperechogenic ultrasound pattern of the liver. Aortic valve sclerosis was determined by echocardiography. In our sample, hepatic steatosis was present in 877 (39.7%) individuals. Among participants with hepatic steatosis, aortic valve sclerosis was more common (n=323; 36.8%) compared with participants without hepatic steatosis (n=379; 28.4%; P <0.001). After adjustment for potential confounders, individuals with hepatic steatosis had 33% higher odds of aortic valve sclerosis compared with those without hepatic steatosis (95% confidence interval, 6%–66%; P =0.014). Additional adjustment for high-sensitive C-reactive protein, serum ferritin levels, and white blood cells slightly reduced the association to 32% (95% confidence interval, 4%–66%; P =0.021). Conclusions Our findings add evidence that hepatic steatosis and aortic valve sclerosis are interrelated after adjustment for major confounders. The release of proatherogenic substances by the steatotic liver or its contribution to insulin resistance and dyslipidemia may contribute to the development of calcification and sclerosis of the aortic valve.