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Cardiac remodelling identified by cardiovascular magnetic resonance in patients with hepatitis C infection and liver disease
Authors:Phillip J Ngu  Michelle Butler  Alan Pham  Stuart K Roberts  Andrew J Taylor
Institution:1.Department of Cardiovascular Medicine,Alfred Hospital,Melbourne,Australia;2.Baker IDI Heart and Diabetes Institute, Heart Centre,Alfred Hospital,Melbourne,Australia;3.Department of Anatomical Pathology,Alfred Hospital,Melbourne,Australia;4.Department of Gastroenterology,Alfred Hospital,Melbourne,Australia
Abstract:Chronic cardiac dysfunction in patients with chronic liver disease (CLD) in the absence of alcohol consumption or other cardiac disease is well described. Whilst functional and morphological features of this condition remain unclear, diastolic dysfunction has been implicated by echocardiography. We aimed to evaluate myocardial structure, function and tissue composition with cardiac magnetic resonance (CMR) imaging in patients with hepatitis C and histological evidence of liver disease on biopsy. Contrast-enhanced CMR imaging for morphological, functional and tissue characterization was performed on 16 patients with CLD and 21 healthy controls. Cardiac structure and function was assessed with standard cine imaging, with Late Gadolinium Enhancement (LGE) and myocardial T1 mapping (pre- and post-contrast) performed to evaluate regional and diffuse myocardial fibrosis respectively. Compared to controls, patients with CLD demonstrated lower left ventricular end-diastolic volume (LVEDV) (138 ± 36 vs. 167 ± 44 mL, p < 0.05), reduced stroke volume (88 ± 20 vs. 109 ± 29 mL, p = 0.016), lower post-contrast myocardial T1 time and higher Partition Coefficient consistent with diffuse myocardial fibrosis (466 ± 78 vs. 545 ± 134 ms and 0.247 ± 0.110 vs. 0.123 ± 0.057 %, p < 0.05 for both). There were no differences in other cardiac parameters including left ventricular mass and ejection fraction (p = NS for all comparisons). No patients in either group had evidence of LGE. Compared to controls, patients with hepatitis C and histological evidence liver involvement have lower LVEDV, SV and increased diffuse myocardial fibrosis, all of which are associated with diastolic dysfunction. LVEF and LV mass were preserved. This may explain in part previous functional observations made by echocardiography.
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