Introduction: Cirrhotic cardiomyopathy (CCM) is defined as systolic and/or diastolic subclinic cardiac dysfunction at rest and an impaired contractile respon-siveness to stress. Because of augmented peripheral va-sodilatation in liver cirrhosis (LC), it is associated with low afterload. Left ventricular (LV) deformation by Speckle Tracking Echocardiography (STE) is still load-dependent, and does not reflect directly myocardial energy consumption. Since myocardial work (MW) in-corporates both LV deformation and load, it might be a better alternative for the assessment of LV function in CCM.

Methods: 80 subjects were assessed by 2D conventio-nal and STE: 40 patients with liver cirrhosis (LC) (58 ± 8 years, 23 males), free of any cardiovascular disease or diabetes, and 40 age and gender matched normal, con-trol subjects. Left ventricular ejection fraction (LVEF) and systolic/diastolic blood pressure (SBP/DBP) were measured. A new approach was used to evaluate myo-cardial work by 2DSTE: global constructive work (GCW) during shortening in systole adding negative work during lengthening in IVR; global wasted work (GWW), performed during lengthening in systole adding work performed during shortening in IVR; glo-bal work efficiency (GWE), as the constructive work divided by the sum of constructive and wasted work in% and global work index (GWI), as the GCW added to GWW. Similarly, a regional, segmental analysis was performed (18 segments model).E/E’ ratio, left atrial volume index (LAVi), and systolic pulmonary arterial pressure (sPAP) were also assessed.

Results: Patients with LC had significantly lower SBP (111 ± 14 vs. 126 ± 14, p=0.001) than controls, with si-milar LVEF. GCW (2068 ± 386 vs. 2302 ± 335, p=0.005) and CWI (1927 ± 379 vs. 2123 ± 353, p=0.01) were significantly decreased in patients with LC, probably due to decrease in afterload, which shifts LV work to a lower level of energy. GWE and GWW were similar to controls. By segmental analysis (18 segments model), apical and mid antero-lateral segments were the first affected in terms of myocardial work, with higher WW, low WE, but without a compensatory increase in CW in other segments, suggesting a regional myocardial dys-function. All patients with LC presented significantly elevated ale E/E’ratio (8.5 ± 2.5 vs. 7.5 ± 2.2, p=0.05), LAVi (45.9 ± 14.5 vs. 31.8 ± 6.8, p=0.001), sPAP (26 ± 9 vs. 21 ± 8) compared to controls, suggesting increased left ventricular filling pressures in LC patients.

Conclusions: Augmented peripheral vasodilatati-on and the decrease in afterload in LC patients cause a decrease in myocardial work in terms of GCW and GWI, compared to normal individuals. Apical and mid antero-lateral segments are the first affected, with an increase in wasted segmental work. Assessment of glo-bal and regional MW by STE might be a potential new tool to assess CCM, and to understand the relationship between LV remodelling and increased filling pressure under different loading conditions.