Abstract

BackgroundArterial blood pressure (BP) is a reliable marker of circulatory dysfunction in cirrhotic patients. There are no prospective studies evaluating the association between different levels of arterial BP and ascites development in compensated cirrhotic patients. Therefore, we evaluated the relationship between arterial BP and ascites development in compensated cirrhotic patients.Materials and MethodsA total of 402 patients with compensated HCV-related cirrhosis were prospectively followed during 6 years to identify ascites development. At baseline, patients underwent systolic, diastolic and mean arterial pressure (MAP) measurements. Any history of arterial hypertension was also recorded. The occurrence of events such as bleeding, hepatocellular carcinoma, death and liver transplantation prior to ascites development were considered as competing risk events.ResultsOver a median of 156 weeks, ascites occurred in 54 patients (13%). At baseline, MAP was significantly lower in patients with ascites development (75.9 mm/Hg [95%CI, 70.3–84.3]) than those without ascites (93.6 mm/Hg [95% CI: 86.6–102.3]). After adjusting for covariates, the 6-year cumulative incidence of ascites was 40% (95%CI, 34%–48%) for patients with MAP<83.32 mm/Hg. In contrast, cumulative incidences of ascites were almost similar among patients with MAP values between 83.32 mm/Hg and 93.32 mm/Hg (7% [95% CI: 4%–12%]), between 93.32 mm/Hg and 100.31 mm/Hg (5% [95% CI: 4%–11%]) or higher than 100.31 mm/Hg (3% [95% CI: 1%–6%]). The MAP was an independent predictor of ascites development.ConclusionsThe MAP is closely related to the development of ascites in compensated HCV-related cirrhosis. The risk of ascites development increases in 4.4 fold for subjects with MAP values <83.32 mm/Hg.

Highlights

  • Chronic hepatitis C virus (HCV) infection is a leading cause of end-stage liver disease worldwide [1]

  • mean arterial pressure (MAP) was significantly lower in patients with ascites development (75.9 mm/Hg [95%confidence intervals (CI), 70.3–84.3]) than those without ascites (93.6 mm/Hg [95% CI: 86.6– 102.3])

  • Cumulative incidences of ascites were almost similar among patients with MAP values between 83.32 mm/Hg and 93.32 mm/Hg (7% [95% CI: 4%–12%]), between 93.32 mm/Hg and 100.31 mm/Hg (5% [95% CI: 4%–11%]) or higher than 100.31 mm/Hg (3% [95% CI: 1%–6%])

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Summary

Introduction

Chronic hepatitis C virus (HCV) infection is a leading cause of end-stage liver disease worldwide [1]. Once HCV-related cirrhosis has developed, the annual risk of clinical decompensation has been estimated at ,6% (range, 4–8%) per year. [12] In compensated cirrhosis, circulatory dysfunction is a crucial step for ascites development. Arterial hypotension is a reliable marker of circulatory dysfunction in cirrhotic patients. Hepatorenal syndrome may occur in the setting of marked circulatory dysfunction, which is characterized by arterial hypotension and activation of neurohumoral systems. [12,16,18] A previous study has reported that arterial blood pressure is an independent predictor of survival in cirrhotic patients with ascites. Arterial blood pressure (BP) is a reliable marker of circulatory dysfunction in cirrhotic patients. There are no prospective studies evaluating the association between different levels of arterial BP and ascites development in compensated cirrhotic patients. We evaluated the relationship between arterial BP and ascites development in compensated cirrhotic patients

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