Does speckle tracking transthorasic echocardiography show subtle changes in left ventricular function in patient with heart failure with reduced ejection fraction treated by Sacubitril-Valsartan

Abstract

Abstract Introduction Pathophysiology of HF involves a maladaptive response during which the (RAAS) is activated. RAAS activation leads to VC, HT, increased aldosterone levels, increased sympathetic tone, and eventually, cardiac remodeling, all of which are detrimental to the progression of the disease. By blocking these maladaptive elements, ACEIs or ARBs play a major role in reducing morbidity and mortality due to HF, Simultaneously, the NP system is also activated, hence the elevated BNP and NT-pro BNP seen in HF exacerbations. This is a Compensatory mechanism that leads to VD, natriuresis and diuresis, lowers BP, lowers sympathetic tone, and reduces aldosterone levels. The NP system works antagonistically to the RAAS and has favorable effects on the pathogenesis of HF NP are broken down by an enzyme called neprilysin and blocking of its action by neprilysin inhibitor prevent the breakdown of NP leading to prolonged duration of the favorable effects of these peptides. Sacubitril/valsartan is a first-in-class medicine that contains a neprilysin (NEP) inhibitor (sacubitril) and (Ang-II) receptor blocker (valsartan). STE is a sensitive tool for assessing ventricular function, even subclinical myocardial alterations that traditional imaging techniques are not able to detect. Sub endocardial function is powered mostly by longitudinal contraction, it is impaired earlier than circumferential or radial component's. Therefore, Longitudinal function is in most cases the best early marker of LV dysfunction. Objective The aim of our study is to retrospectively detect if the patients treated by sacubitril/valsartan showed no improvement in LVEF assessed by TTE, is the same patient will shows improvement in LVEF assessed by 2D STE? Methods Our study will include 200 patients with HFrEF. All participants were subjected to the following: History taking, Physical examination, Serial 12-lead ECG, 2D echo to assess: -LVEDD, LVESD and LVEF%, LVEDVI (ml/m2), LVESVI (ml/m2), (LAVI) ml/m2, E/e′ ratio. 2D STE was done before and after 6 months of sacubitril/valsartan. Results Age 48 ± 9 years, 63% females, 9 (4.5%) were in NYHA FC I, 120 (60%) NYHA FC II, 64 (32%) of patients were in NYHA FC III & 7 (3.5%) were in FC IV. improved to NYHA FC I, 82 (41%) NYHA FC II 118 (59%), LVEDV, LVESV, LVEF, E/e′ were 139.3 ± 7.3, 89.7 ± 4.7, 34.9 ± 2.8, 11.2 ± 2.7, that all improved to 139.1 ± 10.5, 89.0 ± 4.4, 35.6 ± 2.6, 9.1 ± 2.3. 82 (41%) patient showed improvement in LVEF either by traditional TTE or STE, 118 (59%) patients showed no improvement of EF by traditional TTE, of them 74 (37%) patients was improved detected by STE while 44 (22%) patients showed no improvement in EF neither by TTE nor by STE. Conclusion STE is more accurate diagnostic tool for detecting early improvment in LVEF that not detected by traditional TTE in patient with HFREF treated by scubitril/valsartan. Additional Content An author video to accompany this abstract is available on https://academic.oup.com/eurheartjsupp. Please click on the arrow next to ‘More Content’ and then click on ‘Author videos’.