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Original article

A prospective evaluation of pulmonary, systemic and hepatic haemodynamics in HIV–HCV-coinfected patients before and after antiviral therapy with pegylated interferon and ribavirin

Thomas Reiberger, Berit A Payer, Arnulf Ferlitsch, Wolfgang Sieghart, Florian Breitenecker, Maximilian C Aichelburg, Brigitte Schmied, Armin Rieger, Michael Trauner, Markus Peck-Radosavljevic, Vienna Hepatic Hemodynamic Lab and Vienna HIV & Liver Study Group

Corresponding author name: Markus Peck-Radosavljevic
Corresponding author e-mail: markus.peck@meduniwien.ac.at

Citation: Antiviral Therapy 2012; 17:1327-1334
doi: 10.3851/IMP2349

Date accepted: 14 March 2012
Date published online: 05 September 2012

Abstract

Background: Patients coinfected with HIV and HCV are at risk for developing portal hypertension (PHT), hyperdynamic circulation and pulmonary arterial hypertension (PAH). Data on the influence of antiviral therapy with pegylated interferon-α (PEG-IFN-α) and ribavirin (RBV) are limited.

Methods: Haemodynamic parameters, including hepatic venous pressure gradient (HVPG), pulmonary arterial pressure (PAPmean), cardiac output (CO) and systemic vascular resistance (SysVR), were prospectively evaluated before and after PEG-IFN-α+RBV therapy in 80 HIV–HCV-coinfected patients.

Results: Baseline evaluation showed a mean HVPG of 4.7 mmHg, CO of 6.15 l/min and PAPmean of 14.8 mmHg. PHT was present in 26% of patients, hyperdynamic circulation in 5% and PAH in 4%. Patients with advanced fibrosis (METAVIR stage F3/F4; n=32) had significantly higher CO (P=0.008), lower SysVR (P=0.035), higher PAPmean (P=0.018) and higher pulmonary vascular resistance (P=0.022) than patients with stage F0–F2 fibrosis (n=48). Both hyperdynamic circulation and PAH were significantly associated with liver stiffness, fibrosis stage and portal pressure; a non-significant trend was found for CD4+ T-cell counts and HIV RNA levels. No significant changes in PAPmean, CO and SysVR were observed after PEG-IFN-α+RBV treatment, although a significant decrease in HVPG was noted in patients with HCV eradication (P=0.013).

Conclusions: The overall prevalence of hyperdynamic circulation and PAH in HIV–HCV coinfection is low. Advanced fibrosis, increased liver stiffness, elevated portal pressure and probably CD4+ T-cell count and HIV viraemia represent risk factors for hyperdynamic circulation and PAH. PHT is present in 26% of HIV–HCV-coinfected patients evaluated for antiviral therapy. Successful HCV eradication significantly decreases HVPG.

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