Abstract

Cardiovascular risk factors (CVRF) lead to systemic endothelial dysfunction. It has been suggested that in cirrhosis, cardiovascular risk is low and systemic endothelial function is enhanced. However, there is no prospective study evaluating the relationship between cardiovascular risk and systemic endothelial function in cirrhosis, which was investigated here. In 47 patients with cirrhosis (33 males; median Child-Pugh score 8; median age 55 years), we evaluated: laboratory parameters, hepatic and systemic hemodynamics, CVRF, 10-year global cardiovascular risk by Framingham score, and presence of carotid plaques. Systemic endothelial dysfunction was investigated non-invasively by flow-mediated dilatation (FMD) of the brachial artery by ultrasound and defined as FMD <10%. Cardiovascular risk (median 7%) was low in 25%, moderate in 26%, moderately high in 40%, and high in 9%. Fifty-three percent of patients had systemic endothelial dysfunction. Systemic endothelial dysfunction (low FMD) increased in parallel with CV risk (linear trend P=0.039) and was higher in patients overweight or obese. Conversely, FMD increased in parallel with Child-Pugh/Mayo Clinic Model for End-stage Liver Disease (MELD) score, bilirubin, serum sodium, plasma renin activity, leukocyte count, platelet count, and with lower arterial pressure, suggesting that enhanced FMD is a feature of advanced liver failure and inflammation. Cardiovascular risk, bilirubin, leukocyte count, and arterial pressure remained independently associated with systemic endothelial dysfunction. CV risk was not low in our studied patients with cirrhosis, and systemic endothelial dysfunction was frequent in this population. In cirrhosis, similar to general population, cardiovascular risk impaired systemic FMD, although liver failure attenuated endothelial dysfunction.

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