Effect of sacubitril valsartan on cardiac function and endothelial function in patients with chronic heart failure with reduced ejection fraction

Abstract

OBJECTIVE: The aim of the present study was to observe the effect of sacubitril valsartan on cardiac function and vascular endothelial function in patients with chronic heart failure with reduced ejection fraction (HFrEF). METHODS: A total of 80 patients with HFrEF were randomly divided into an observation group and a control group, with 40 patients in each group. Sacubitril valsartan was added to the conventional treatment in the observation group, and perindopril was added to the conventional treatment in the control group. Both groups were treated continuously for 12 weeks. The left ventricular ejection fraction (LVEF), left ventricular end-diastolic diameter (LVEDD), flow-mediated vasodilatory function (FMD) of the brachial artery, and levels of plasma Ang II, endothelin 1 (ET-1), and calcitonin gene-related peptide (CGRP), together with the serum nitric oxide (NO) and NO synthase (NOS) were compared before and after treatment in the groups. RESULTS: Before the treatment, the levels of LVEF, LVEDD, FMD, Ang II, ET-1, CGRP, NO, and NOS in the observation group were not significantly different from those in the control group (P > 0.05). However, the levels of LVEF, FMD, CGRP, NO, and NOS in both groups were significantly higher after the treatment than those before the treatment (P < 0.05) and significantly higher in the observation group than those in the control group. The difference was statistically significant (P < 0.05). Meanwhile, the levels of LVEDD, Ang II, and ET-1 in both groups decreased significantly after the treatment (P < 0.05) and were significantly lower in the observation group than those in the control group. The difference was statistically significant (P < 0.05). CONCLUSION: Sacubitril valsartan might improve endothelial function while increasing cardiac function in HFrEF patients.

LCZ696, an Angiotensin Receptor-Neprilysin Inhibitor, Ameliorates Endothelial Dysfunction in Diabetic C57BL/6 Mice

“…Thus, these findings suggest that the elevated bioavailability of NPs by neprilysin inhibition during treatment with LCZ696 may have a beneficial impact on NO synthesis and exert superior effects on preventing cardiovascular complications compared with standalone ARBs. One clinical study also dem onstrated that LCZ696 improved the endothelial function in patients with chronic heart failure with a reduced ejection fraction 25) . In addition, ex vivo and in vitro experiments that had been conducted in normoglycemic conditions strengthened the concept that the combination of neprilysin inhibitor and ARB treatment has potential benefits in enhancing endothelial NO synthesis as a result of reducing oxidative stress, inflammation, or inhibiting vasoconstrictors such as endothelin-1 and angiotensin II 14-21, 26, 27) .…”

Peptides from Harpadon nehereus Bone Ameliorate Angiotensin II-Induced HUVEC Injury and Dysfunction through Activation of the AKT/eNOS and Nrf2 Pathway

“…In addition to oxidative stress, Ang II has been reported to induce endothelial cell dysfunction by inhibiting nitric oxide synthase (eNOS) activity and stimulating ET-1 secretion. , eNOS is a key rate-limiting enzyme in the synthesis of NO, which promotes vasodilation and blood pressure reduction. ET-1 is an important vasoconstriction factor and is one of the risk factors for endothelial cell dysfunction and hypertension.…”