Integrated Echocardiographic Phenotyping of Cirrhotic Cardiomyopathy: A Severity-Dependent Multi-Domain Analysis
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Abstract
Background: Cirrhotic cardiomyopathy is a recognized complication of chronic liver disease characterized by subclinical myocardial dysfunction despite preserved conventional systolic parameters. Advanced echocardiographic techniques may improve the identification of cardiovascular involvement and clarify its relationship with liver disease severity.
Objectives: To characterize cardiac involvement in cirrhosis using an integrated multi-domain echocardiographic approach and evaluate its association with liver disease severity assessed by MELD-Na score.
Methods: This cross-sectional observational study included 50 patients with established cirrhosis and 50 age- and sex-matched healthy controls. Comprehensive transthoracic echocardiography, including speckle-tracking strain imaging, diastolic function assessment, atrial mechanics, and right ventricular–pulmonary coupling evaluation, was performed. Patients with cirrhosis were stratified according to MELD-Na categories (≤9, 10–19, ≥20). Multivariable regression analyses adjusted for age, heart rate, mean arterial pressure, and hemoglobin were performed.
Results: Left ventricular ejection fraction was preserved in patients with cirrhosis; however, left ventricular global longitudinal strain was significantly reduced compared with controls (−17.4% vs −20.1%), as was right ventricular free-wall strain (−18.2% vs −22.0%). Left atrial reservoir strain was lower in cirrhotic patients (26.1% vs 34.2%), while average E/e′ was higher (11.9 vs 8.5). Across increasing MELD-Na categories, there was a progressive worsening of left ventricular global longitudinal strain (−18.8%, −17.2%, −15.9%), right ventricular free-wall strain (−20.1%, −18.0%, −16.2%), left atrial reservoir strain (30.4%, 25.8%, 21.6%), and TAPSE/PASP ratio (0.71, 0.55, 0.41), accompanied by rising E/e′ (9.6, 12.1, 14.3). On multivariable linear regression analysis, increasing MELD-Na score remained independently associated with worsening LV global longitudinal strain (β = 0.28, p = 0.002), impaired RV free-wall strain (β = 0.24, p = 0.004), reduced left atrial reservoir strain (β = −0.31, p = 0.003), lower TAPSE/PASP ratio (β = −0.015, p = 0.008), and higher E/e′ ratio (β = 0.19, p = 0.005) after adjustment for age, heart rate, mean arterial pressure, and hemoglobin level.
Conclusions: Cirrhosis is associated with a severity-dependent multi-domain cardiovascular phenotype involving ventricular mechanics, diastolic abnormalities, atrial dysfunction, and impaired RV–pulmonary interaction despite preserved conventional systolic function. Integrated echocardiographic phenotyping may improve cardiovascular assessment in advanced liver disease.
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