Key result
HCV is linked to increased carotid plaques with no regression observed post-SVR.
Why the study?
The arterial pathology and mechanisms of increased CVD risk in HCV-infected individuals remain unclear.
Does successful treatment with direct-acting antivirals reverse subclinical arterial damage in treatment-naive chronic HCV patients?
Observational (n=30)
Does successful treatment with direct-acting antivirals reverse subclinical arterial damage in treatment-naive chronic HCV patients?
HCV infection is associated with accelerated atheromatosis rather than arterial stiffening, which does not appear to reverse 3 months after achieving sustained virological response.
SVR may not reverse carotid plaques within 3 months in HCV; leaves open whether atheromatosis regresses with longer follow-up.
Background: The arterial pathology and mechanisms of increased cardiovascular disease (CVD) risk in HCV-infected individuals are not yet clear. The aim of this study was to identify types of arterial pathology in treatment-naive chronic HCV patients and to test their reversibility after successful treatment. Methods: Consecutive, never-treated, HCV-infected patients were compared with age and CVD-related risk factors, matched controls, healthy individuals (HI), patients with rheumatoid arthritis (RA) and people living with HIV (PLWH), in terms of arterial stiffening by pulse wave velocity, arterial atheromatosis/hypertrophy by carotid plaques/intima-media thickness and impaired pressure wave reflections by augmentation index. After three months of sustained virological response (SVR) administered using direct-acting antivirals, vascular examination was repeated in HCV-infected patients to test drug and viral-elimination effect in subclinical CVD. Results: Thirty HCV patients were examined at baseline; fourteen of them were re-examined post-SVR. Compared with HI, HCV patients had significantly more plaques, which is similar to that of RA patients and the PLWH group. No other differences were found in all other vascular biomarkers, and regression among HCV patients also revealed no differences 3 months post-SVR. Conclusions: Accelerated atheromatosis, rather than arterial stiffening, arterial remodeling and peripheral impaired hemodynamics is the underlying pathology leading to increased CVD risk in HCV patients.
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Ανδρουτσάκος et al. (2023) conducted an observational in HCV infection (n=30). Direct-acting antivirals vs. Healthy individuals, rheumatoid arthritis patients, and people living with HIV was evaluated on Arterial stiffening, arterial atheromatosis/hypertrophy, and impaired pressure wave reflections. HCV patients (n=30) had significantly more carotid plaques than healthy individuals, similar to RA and HIV patients, with no regression observed in 14 patients 3 months post-SVR.
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