Systolic and diastolic dysfunction in advanced liver disease: does cirrhotic cardiomyopathy really exist?

Digestive and Liver Disease(2024)

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摘要
Introduction Cirrhotic cardiomyopathy (CCM) has been increasingly recognized as a clinically significant comorbidity of chronic advanced liver disease (cALD), mainly because its association with an higher risk for both cardiovascular and liver-related events. Recently, a revised definition of CCM proposed systolic dysfunction (SD, as defined as impaired left-ventricle global longitudinal strain LV-GLS> -18% or hyper-contractility, LV-GLS < -22%), or relevant diastolic dysfunction (DD) as diagnostic criteria. However, the prevalence of CCM is not well defined and there is a lack of knowledge about risk factors of the three different phenotypes of CCM. Methods Cirrhotic patients of any aetiology and Child-Pugh (CP) class and without previous significant heart diseases were evaluated in three different centres. A complete standard Color- and Tissue-Doppler echocardiography was performed; LV-GLS was obtained. Results 62 subjects (50 males, median age 62 years, 24 CP A, 21B, 17 C) were evaluated. Age, sex, etiology of liver disease and metabolic risk factors were equally distributed among CP classes. DD and impaired LV-GLS were found in 7 (11.1%) and 11 (17.7%) subjects, respectively; in multivariate analysis, only age (OR 1.13,95%IC [1.02-1.26], p=0.023) and body mass index (OR 1.19,95%IC [1.01-1.40], p=0.039) were independent risk factors. An increasingly number of patients with advanced cirrhosis showed cardiac hyper-contractility (LV-GLS < -22%: 9.1% CP A, 57.1%CP B, 72.2% CP C, p<0.001), that was independently related alternatively to only CP score (OR 1.57, 95%IC [1.18-2.08], p=0.002) or MELD score (OR 1.19, 95%IC [1.06-1.35], p=0.005). Conclusion Our data are consistent with a high prevalence of cardiac hyper-contractility in cALD CP C. Both DD and SD, quite infrequent in our cohort, were found to be associated withclassical liver-unrelated metabolic risk factors, raising the question on the real patho-physiology of CCM.
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