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Introduction: Right ventricle (RV) pressure and/or volume overload causes left ventricle (LV) deformation.Objective: Assessment of RV and LV wall deformation in pulmonary arterial hypertension (PAH) patients accordingly to pressure or volume overload conditions.Methods: 20 patients, age 65.4 ±13.5, with PAH on specific therapy, median Nt-ProBNP 730, TAPSE 21.0±5.7, RV ejection fraction 36.7 ±18.4%, pulmonary artery pressure (PAP) 85.9±15mmHg. Patients grouped in 2 groups accordingly to pressure overload (PPH, n=15) or volume overload (VPH) including patients with more than moderate tricuspid regurgitation. RV and LV longitudinal global strain (GS), tricuspid annulus TDI S waves recorded and MPI calculated. Nt-ProBNP characterised the neurohormonal activation. Between groups comparisons achieved with Mann-Whitney non-parametric test.Results (see table): Patients with PVH had significantly: (1) higher PAP (p=0.05), Nt-Pro-BNP (p=0.042) and tricuspid MPI (n=0.027); (2) worst RV systolic function with decreased S-Tr (p=0.02), however with no change in RV-GS; (3) worst LV systolic function with lower LV-GS (0.034).Conclusion: Volume overload is associated with greater neurohormonal activation, lower tricuspid S wave, but does not alter the longitudinal RV strain compared with the pressure overloaded RV. However LV longitudinal strain is decreased.