1136 DAPAGLIFOZIN AND PULMONARY PRESSURES IN HFREF: A NON INVASIVE ASSESSMENT


 
 
 Gliflozins proved effectiveness in reducing hospitalization and mortality in patients with heart failure and reduced ejection fraction (HFrEF). Recent studies showed how SGLT2-i improve loading condition and afterload by increasing extracellular Na excretion, downregulating RAAS and reducing vascular resistances. This latter aspect seems the result of a combined action on endothelial cells and vascular tone: experimental studies hypnotized that SGLT2-i may inhibit Na-H exchanger on endothelial cells and directly interact with PKG pattern and K+ channels determining vasodilation.
 On the other hand, 40 to 72% of patients with HFrEF are estimated to have postcapillary pulmonary hypertension. Of note, increased Pulmonary Artery Systolic Pressure (PASP) and Pulmonary vascular resistances (PVR) are associated with a worse outcome among HFrEF patients. However, effect of gliflozins on pulmonary artery pressures have never been investigated.
 
 
 
 This pilot study aims to assess whether Gliflozins may have positive effects on pulmonary artery by a non-invasive evaluation.
 
 
 
 We retrospectively analysed transthoracic echocardiograms (TTE) of 24 patients with HFrEF who added gliflozins on top of optimal medical therapy.
 ETT before and after three months of Dapagliflozin therapy were compared, with particular attention to PASP and right chambers dimension and function.
 
 
 
 At three months, no significant differences in Left Ventricle (LV) dimensions were found (116 ml/mq vs 101.61, p=0.096), while there was an improvement in LV Ejection Fraction (27.9% vs 30,04 p=0.040). E wave velocity and mean E/e’ significantly decreased (respectively 52.9 vs 37,11 p=0.03 and 11.2 vs 8.01 p<0.01). Pulmonary valve Acceleration Time (PV AT) significantly increased from 74.54 (± 22.2) to 101.8 ± 24.74 (p<0.01) while no significative difference in mean PASP (30.48 vs 23.75, p=0.058) and FAC (36.2 vs 38.78, p=0.133) were observed. Left atrial volume indexed (LAVi) was also found to decrease significantly (p<0.01).
 
 
 
 Gliflozins positive action on cardiac remodeling, preload and afterload are well known. However, as long as we know, there are no studies investigating Gliflozins effects on pulmonary vascular resistances and pressures.
 We observed a significative improvement on pulmonary pressures when gliflozins are added on top of OMT. One could speculate that reduction in mean E/e’ and, particularly, in E wave velocity, may be the expression of decrease LA pressure and LA volume due to LV function improvement with decrease in LA overload. In this context, a drop in postcapillary pressures may explain the increase in PV AT, which is an indirect sign of pulmonary pressures. In respect to PASP, which was also reduced, but significantly, PV AT may be more sensitive, explaining the difference in significance of these two results. No significative relation between PV AT increase and E wave velocity, mean E/e’ ratio and LAVi decrease was found, nevertheless a larger population may be required. Further studies, with a larger numerosity, are need to confirm our hypothesis.
 
 
 
 Gliflozins, on top of OMT, appear to improve pulmonary pressures by reducing left atrial pressures after three months of therapy at a non-invasive evaluation.
