Introduction: Cirrhotic cardiomyopathy (CC) is defi-ned as a cardiac dysfunction that includes mainly di-astolic dysfunction (DD), generated by liver cirrhosis (LC). Its present diagnosis is based mostly on 2D con-ventional transthoracic echocardiography (TTE), with focus on diastolic dysfunction. However, there is no standardized algorithm for diagnosis of CC. Role of the new methods, such as speckle tracking echocardiogra-phy (STE), for the diagnosis of CC is still controversial.

Objective: In this context, the purpose of our study was to assess left atrial (LA) function by STE in LC, on top of conventional TTE, in order to establish the role of LA function for the diagnosis of CC.

Methods: 107 subjects were assessed by TTE and STE: 52 patients with LC (57 ± 9 yrs, 23 males), free of any cardiovascular disease or diabetes, and 55 age-matched normal subjects. TTE was used to measure LV inde-xed volumes and ejection fraction (LVEF), E/E’, ratio, left atrial volume index (LAVi), and systolic pulmo-nary arterial pressure (sPAP); STE to measure global longitudinal strain (GLS) and LA functions: reservo-ir function by strain from MVC to MVO (LASr) and positive strain rate (LASRr), conduit function by strain from MVO to onset of atrial contraction (LAScd) and early negative strain during conduit phase (LASRcd), LA pump function by negative strain at MVC (LASct) and late negative strain during atrial contraction phase (LASRct). NTproBNP was measured in all patients.

Results: LC patients vs controls had lower SBP (112 ± 12 mmHg vs. 122 ± 12 mmHg, p<0.001), higher LV vo-lumes and NTproBNP (215 ± 258 pg/ml vs. 44 ± 43 pg/ ml, p<0.001), but similar LVEF. They had lower GLS (-20.8 ± 3% vs. -22 ± 2%, p=0.05) and higher E/E’ (8.5 ± 2.3 vs. 7.6 ± 2.3, p=0.05), LAVi (44 ± 14 ml/m2 vs. 28 ± 6.5 ml/m2, p=0.001) and sPAP (27 ± 9 mmHg vs. 21 ± 8 mmHg, p=0.003), sugesting higher LV filling pressu-re. Meanwhile, they had lower LA functions: rezervoir (LASr 28 ± 9% vs. 35 ± 4%, p=0.011; LASRr 1.29 ± 0.4 vs. 1.54 ± 0.4, p=0.002), conduit (LAScd 14.7 ± 8.1% vs. 18.3 ± 6.7%, p=0.014; LASRcd -1.2 ± 0.42 vs. -1.7 ± 0.61, p=0.001), pump (LASRct -1.64 ± 0.47 vs. -1.93 ± 0.44, p=0.002). By using current algorithm for the di-agnosis of DD, 21% of LC patients had DD, 48% had no DD, and 31% had indeterminate grade. By adding assessment of LA reservoir function by STE (LASr <35%) to the DD algorithm, 50% of patients had DD, without any indeterminate cases.

Conclusions: LC patients have longitudinal systolic LV dysfunction, diastolic dysfunction with higher es-timated LV filling pressure, and lower LA reservoir, conduit, and pump functions. By adding LA deforma-tion analysis by STE to the current diagnosis algorithm, better characterization of CC is possible.