Abstract
Background: Left ventricular ejection fraction (LVEF) is calculated from volumetric change without representing true myocardial properties. Strain echocardiography has been used to objectively measure myocardial deformation. Myocardial strain can give accurate information about intrinsic myocardial function, and it can be used to detect early-stage cardiovascular diseases, monitor myocardial changes with specific therapies, differentiate cardiomyopathies, and predict the prognosis of several cardiovascular diseases. Sacubitril/valsartan has been shown to improve mortality and reduce hospitalizations in patients with heart failure with reduced ejection fraction (HFrEF). The effect of sacubitril/valsartan angiotensin receptor neprilysin inhibitor (ARNI) on left ventricular (LV) ejection fraction (EF) and torsion dynamics in HFrEF patients has not been previously described. Methods: The study involved 73 patients with HFrEF, for all patients Full history was taken, full clinical examination was done. Baseline vital signs, ECG, NYHA classification, conventional echocardiography and STE were done at baseline study and after 6 and 11 months.Basal and apical LV short-axis images were acquired for further off-line analysis. Using commercially available two-dimensional strain software, apical, basal rotation, and LV torsion were calculated. Results: ARNI group of patients showed improvement of symptoms, LV global longitudinal strain (LVGLS)% and diastolic parameters including, E/A, E/e', TV, untwist onset and rate after 6 months of therapy in comparison to the traditionally treated patients. The improvement continued for 11 months with in additional significant improvement of systolic parameters in the form of LVGLS%, EF%, Twist, Apical and basal rotations, main dependent parameters for improvement of EF% was LVGLS% and Apical rotation. Conclusion: To the best of our knowledge, this is the first study to demonstrate that therapy with sacubitril/valsartan in HFrEF patients could create a state of gradual and chronic LV deloading which cause relieving of myocardial wall tensions and decreasing the LV end diastolic pressure this state could cause cardiac reverse remodeling and reestablishment of starling forces proprieties of LV myocardium, which lead to increase of LV EF.