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Invasive Hemodynamic Characterization of the Portal-hypertensive Syndrome in Cirrhotic Rats
Published on: August 1, 2018
Arterial Hypertension is Associated with a Lower Portal Hypertensive Burden in Compensated Cirrhosis: A Retrospective
Raffaele Buono1, Marzia La Franca1, Paolo Girardi2
1Unit of Internal Medicine and Hepatology (UIMH), Department of Medicine - DIMED, University of Padova, Padova, Italy.
Background And Aims:
While systemic arterial pressure typically declines with advancing cirrhosis, the relationship between arterial hypertension (AH) and clinical outcomes in compensated cirrhosis is not defined. We aimed to investigate the association between AH and non-invasive markers of portal hypertension and liver-related complications.
Methods:
We conducted a retrospective cohort study including 189 patients with compensated liver cirrhosis, stratified according to history of AH. Clinical, laboratory, endoscopic, and outcome data, including cirrhosis decompensation, liver transplantation, and mortality, were collected. Median follow-up time was 5 years, IQR 3.2-5.0 years. Spleen diameter was assessed at baseline and serially during follow-up.
Results:
Of the 189 patients, 111 had a history of AH. Compared with non-hypertensive patients, those with AH were older, had higher platelet counts, smaller spleen diameter, and fewer indirect signs of portal hypertension, including esophageal varices, congestive gastropathy, and portosystemic shunts (all p < 0.05). During follow-up, spleen size remained stable in hypertensive patients, whereas a progressive increase in spleen diameter was observed in patients without AH. Despite these differences, no significant differences were found between groups in terms of cirrhosis decompensation or overall mortality. However, patients without AH had a significantly higher rate of liver transplantation (p = 0.008).
Conclusion:
In compensated cirrhosis, AH is associated with fewer indirect signs of portal hypertension, including smaller and stable spleen size. These findings support the concept that patients with AH exhibit a distinct hemodynamic phenotype, characterized by less pronounced portal hypertensive state and circulatory dysfunction.
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