Introduction: Liver cirrhosis (LC) is associated with increased cardiovascular events after liver transplant. However, there is no specific pre transplant protocol for cirrhotic cardiomyopathy detection. We assessed the mechanisms of cardiac involvement in patients with LC and correlated these findings with hepatic dysfunction. Methods: We studied 100 subjects by conventional and speckle tracking echo: 50 with LC (57 ± 10 years, 23 non-alcoholic), free of any cardiovascular disease or diabetes, and 50 matched normals. LV systolic function was assessed from ejection fraction, cardiac output (CO), LV mass, longitudinal, circumferential and radial strain; diastolic function from left atrial volume, E/A, E/E’, early/late strain rate (SRe, SRl); right heart function from FAC, TAPSE, right atrial volume, systolic PAP, RV systolic strain/SR, early/late diastolic SR (RVSRe, RVSRl). Child and MELD scores were used for hepatic dysfunction. QTc interval, NT pro-BNP, and β crosslaps were measured. Arterial function was assessed from IMT, local wave speed, elastic modulus, and stiffness index (β); endothelial function from FMD. Results: LV, RV systolic, arterial and endothelial functions were similar to normals. LC patients had higher LV mass (114 ± 19 vs 81 ± 17 g/m2, p < 0.001) and CO (3.2 ± 1.5 vs 2.7 ± 0.8 l/m2, p < 0.01), LV diastolic dysfunction (TDE, E/A, SRl, E/E’), dilated LA (37 ± 15 vs 23 ± 8 ml/m2, p < 0.001) and RA (27 ± 12 vs 18 ± 6 ml/ m2, p < 0.001), increased PAPs (25 ± 9 vs 19 ± 8 mm Hg, p < 0.01), and RV diastolic dysfunction (RVDTE 215 ± 63 vs 157 ± 58 msec, p < 0.001; RVSRe 0.98 ± 0.3 vs 1.2 ± 0.5 1/s, p < 0.01). Meanwhile, NT pro-BNP (209 ± 213 vs 48 ± 43, p < 0.001), β crosslaps (0.6 ± 0.2 vs 0.4 ± 0.1, p = 0.001), QTc (434 ± 30 vs 402 ± 25 ms, p < 0.001) were increased. Child and MELD scores correlated with LAV and RVSRe (r = 0.50, p < 0.001). Findings were similar for alcoholic and non-alcoholic LC. Conclusions: Patients with LC had higher CO, LV mass and subclinical biventricular diastolic dysfunction, with larger LA and RA volumes, and higher NT pro-BNP. These findings are correlated with the degree of liver dysfunction. Since arterial and endothelial functions were not affected, our findings suggest that patients with LC had intrinsic myocardial disease, probably due to increased myocardial fibrosis induced by liver dysfunction.