is a new treatment for heart failure with reduced ejection fraction which has a spectacular effect on survival  The effect of this drug on myocardial work are unknown  Sacubitril-Valsartan increases myocardial constructive work and work efficiency  Pressure-strain loops are a recently introduced tool for the non invasive estimation of myocardial work.  Constructive work a prognostic of major adverse cardiac events in patients with heart failure receiving Sacubitril-Valsartan

Background. Heart failure with reduced ejection fraction (HFrEF) is a heterogeneous syndrome. In heart failure (HF) classifications, right ventricle (RV) function was for a long time unrecognized in favor of left ventricular ejection fraction (LVEF). The response to sacubitril/valsartan might differ according to phenotypes and the impact of right ventricular characteristics on this response remains controversial.Objectives. First, we applied clustering analysis in a HFrEF population undergoing sacubitril/valsartan treatment according to guidelines, to identify phenotypes and their associated clinical outcomes. Secondly, we evaluated RV-remodeling. Materials and methods.It is a prospective, observational, single-center study conducted on 108 symptomatic patients (mean age 66 ±12.8 years, 22.2% women). First, the clustering analysis was applied in a HFrEF population undergoing sacubitril/valsartan treatment, according to the guidelines, in order to identify phenotypes and clinical outcomes associated with them. Secondly, we evaluated RV-remodeling.Results. Two distinct clusters were identified. Among the differences between phenotypes, RV (tricuspid annular plane systolic excursion (TAPSE) 16 ±4 mm compared to 19 ±4 mm, p < 0.001; RV free wall strain −19 ±5% compared to −21 ±4%, p = 0.046; RV fraction area change (FAC) 31 ±9% compared to 38 ±9%, p < 0.001), LV-filling pressure (E-wave deceleration time 138 (median: 41) ms compared to 180 (median: 94) ms, p < 0.001; E/e' 16.7 (median: 8.0) ms compared to 13.0 (median: 9.7) ms, p = 0.02) and creatinine level (106 ±34 µmol/L compared to 90 ±19 µmol/L, p = 0.002) were substantially different at the initiation of therapy. Major adverse cardiac events (MACEs) or death occurred in 38 out of 107 patients: 51. 1% in cluster 1 compared to 24.2% in cluster 2 (p = 0.0074). A significant improvement in RV-functional parameters was observed under treatment. The TAPSE improved and correlated with the change in left ventricular (LV) function. Yet, it did not correlate with systolic pulmonary artery pressure (sPAP) and LV end-diastolic diameter.Conclusions. The HFrEF phenotype characterized by more severe RV dysfunction has a worse prognosis during sacubitril/valsartan therapy. Both RV-and LV functions significantly improve when the patient is treated with sacubitril/valsartan.

The benefit-risk ratio of a pharmacoinvasive strategy (PI) in patients ≥70 years of age with ST-segment elevation myocardial infarction (STEMI) remains uncertain resulting in its limited use in this population. This study compared efficacy and safety of PI with primary percutaneous coronary intervention (pPCI). Data from 2,841 patients (mean age: 78.1 § 5.6 years, female: 36.1%) included in a prospective multicenter registry, and who underwent either PI (n = 269) or pPCI (n = 2,572), were analyzed. The primary end point was in-hospital major adverse cardiovascular events (MACE) defined as the composite of all-cause mortality, nonfatal MI, stroke, and definite stent thrombosis. Secondary end points included all-cause death, major bleeding, net adverse clinical events, and the development of in-hospital Killip class III or IV heart failure. Propensity-score matching and conditional logistic regression were used to adjust for confounders. Within the matched cohort, rates of MACE was not statistically different between the PI (n = 247) and pPCI (n = 958) groups, (11.3% vs 9.0%, respectively, odds ratio 1.25, 95% confidence interval 0.81 to 1.94; p = 0.31). Secondary end points were comparable between groups at the exception of a lower rate of development of Killip class III or IV heart failure after PI. The rate of intracranial hemorrhage was significantly higher in the PI group (2.3% vs 0.0%, p = 0.03). In conclusion, the present study demonstrated no difference regarding inhospital MACE following PI or pPCI in STEMI patients ≥70 years of age. An adequatelypowered randomized trial is needed to precisely define the role of PI in this high-risk subgroup.