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Background In HFrEF patients, high pulmonary vascular resistances (PVR) reflect a combined increase of pre- and post-capillary pressures, associated with worse outcome. Mitral regurgitation (MR) may play a role in this complex physiopathology. We sought to investigate MR impact on lung DLCO and pulmonary vascular hemodynamic in HFrEF patient. Methods 22 HFrEF patients (age 67±11; LV EF) underwent right heart catheterization, rest and exercise echocardiography, right ventricle 3D assessment and lung alveolo-capillary membrane DLCO. We identified 2 subgroups according to normal (3 WU, n=5) PVR. Results Abnormal PVR patients showed increased pulmonary artery pressures and TPG, reduced CO and pulmonary artery compliance. Total DLCO was not significantly different between groups. The membrane component (Dm) and the alveolar volume (Va) were significantly reduced in abnormal PVR group, while the capillary volume (VC) showed a strong trend toward higher values. Abnormal PVR group had a very high percentage of moderate-to-severe MR. The TASPE/SPAP ratio and the circumferential component of RV systolic function were significantly reduced in abnormal PVR group. Normal PVR (n=17) Abnormal PVR (n=5) p NTproBNP, ng/L 3021±2527 7023±8785 0.55 MR moderate-to-severe, n (%) 3 (19%) 4 (80%) 0.025 TAPSE/SPAP, mm/mmHg 0.4761±0.1695 0.2956±0.0739 0.019 3D RV global EF, % 40.616±9.350 29.486±14.062 0.119 3D RV longitudinal EF, % 15.611±7.773 12.086±9.694 0.497 3D RV circumferential EF, % 31.0567±6.5744 21.1746±11.5823 0.019 Lung diffusion of CO (DLCO), ml/min/mmHg 19.021±4.643 15.233±1.761 0.197 Dm ml/min/mmHg 26.8±8.2 17.8±4.1 0.047 VC, ml 110±77 247±152 0.121 Graphics Conclusion The presence of severe MR, in this cohort of HFrEF patients, is associated with alveolar-capillary membrane remodeling (lower Dm), worse hemodynamic profile (higher PA pressures, lower PA compliance and higher PA resistance) and worse right ventricle to pulmonary circulation coupling (lower TAPSE/SPAP and lower 3D RV circumferential EF), confirming the use of therapeutic strategies aimed at correction of valvular disease.

Background The TAPSE/SPAP ratio has gained a role as an easy-to-use surrogate of right ventricle-to-pulmonary circulation (RV-PC) coupling, showing a strong prognostic significance in heart failure (HF) patients. The hemodynamic determinants of TAPSE/SPAP ratio, as assessed by invasive approach, have not been fully elucidated. Aim To identify the right heart hemodynamic variables correlated with TAPSE/SPAP in a HF with reduced EF (HFrEF) cohort, at rest and during exercise. Methods 24 HFrEF patients (age 67±11 years LV EF 27±7) underwent to rest and exercise echocardiography and performed right heart catheterization within 24 hours. Bivariate correlations between TAPSE/SPAP ratio (at rest and exercise), right heart hemodynamic variables, RV systolic function and NTproBNP have been explored. Results TAPSE/SPAP ratio at rest showed a moderate correlation with pulmonary artery wedge pressure (PAWP: r=0.432; p=0.039), pulmonary artery pressures (PAP systolic: r=0.474; p=0.026; PAP diastolic: r=0.434; p=0.043; mPAP: r=0.476; p=0.025), pulmonary vascular resistance and compliance (r=0.475; p=0.041), while a stronger correlation was identified with right atrial (RAP systolic: r=0.571; p=0.017; RAP diastolic: r=0.675; p=0.006) and right ventricular pressures- in particular diastolic ones (RVP systolic: r=0.584; p=0.004; RAP diastolic: r=0.646; p=0.002). No significant correlation was found with NTproBNP and RV 3D EF. Exercise TAPSE/SPAP ratio significantly correlated with right atrium (RAP systolic: r=0.564; p=0.036) and right ventricle systolic pressures only (RVP systolic: r=0.765; p TAPSE/PAPS correlation graphics Conclusions TAPSE/SPAP ratio at rest showed a stronger correlation with invasively derived diastolic right heart pressure rather than pulmonary vascular bed pressures. A similar correlation was also observed for exercise TAPSE/SPAP ratio. This tight correlation with RV, rather than vascular pressures, supports the significance of the ratio as a marker of RV adaptation to vascular overload.