Abstract

It is thought that chronic liver disease affects a person's risk of cardiovascular disease (CVD) development. The aim of this study was to assess the effect of Chronic Hepatitis B (HBV) infection, Chronic Hepatitis C (HCV) infection, and liver damage on cardiovascular risk and selected vascular parameters contributing to CVD risk. This case-control study included a group of 114 patients composed of 34 patients with HBV, 35 patients with HCV, and 45 patients as the control group. Cardiovascular risk was assessed by analyzing classic risk factors, and the SCORE system. The following arterial properties were analyzed using applanation tonometry with SphygmoCor Vx technology: central systolic blood pressure (cSBP), central pulse pressure, augmentation pressure, augmentation index, and carotid-femoral pulse wave velocity (PWV). Asymmetric dimethyloarginine (ADMA) blood levels were analyzed using ELISA as a marker of vascular function. In a univariable analysis we found no significant differences between the hepatitis B, hepatitis C, and control groups in terms of PWV (respectively: median 7.2 [Q25-Q75 6.4-8.5], 7.3 [6.9-8.7], 7.8 [6.5-8.9]), cSBP (115 [109-126], 118 [107-123], 116 [107-129]), ADMA (0.52 [0.47-0.60], 0.53 [0.45-0.62], 0.58 [0.51-0.63]), SCORE (0 [0-1], 0 [0-2], 0 [0-2]). No significant differences in cardiovascular variables were observed between cirrhotic and non-cirrhotic patients. A multivariable analysis confirmed the above findings. (PWV, p=0 . 29; cSBP, p=0.26; ADMA, p=0.19). We concluded that chronic hepatitis B or C was not independently associated with an adverse cardiovascular risk profile nor with an unfavorable pattern of vascular parameters contributing to CVD risk in our study population, even in the case of liver cirrhosis. The same was true for blood ADMA levels.

Highlights

  • Endothelial dysfunction is an early and, crucial element leading to development of CVD

  • Many patients suffering from chronic hepatitis B and C are people who, on the one hand exhibit extensive liver damage, but on the other, do not suffer from other risk factors of CVD such as diabetes or obesity

  • There are several of mechanisms through which, theoretically, the liver could influence the development of CVD; impact on arterial stiffness and endothelial dysfunction among them (ONI et al 2013)

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Summary

Introduction

Endothelial dysfunction is an early and, crucial element leading to development of CVD. It occurs even before the formation of atherosclerotic plaque and fatty streaks (VANHOUTTE 2009). As a person’s liver deteriorates, the endothelium of hepatic vessels deteriorates with it This is a heavily pronounced process in cirrhosis (IWAKIRI et al 2014). It has been demonstrated that serum ADMA levels grow in non-infectious liver disease (NIJVELDT et al 2003; LLUCH et al.2004; MOOKERJEE et al 2007a). Those levels correspond to the severity of damage (MOOKERJEE et al 2007b). MOOKERJEE et al (2007a) have shown that acute liver failure is characterized by an increase in ADMA, which correla

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