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Updated: Aug 16, 2025

Assessment of Vascular Function in Patients With Chronic Kidney Disease
Published on: June 16, 2014
Short-term effect of sacubitril/valsartan on endothelial dysfunction and arterial stiffness in patients with chronic
Velia Cassano1, Giuseppe Armentaro1, Marcello Magurno1
1Department of Medical and Surgical Sciences, University Magna Græcia of Catanzaro, Catanzaro, Italy.
Insights
Sacubitril/Valsartan treatment significantly improved endothelial function and arterial stiffness in heart failure with reduced ejection fraction (HFrEF) patients. This was achieved by reducing oxidative stress, platelet activation, and inflammation markers over six months.
Area of Science:
- Cardiology
- Pharmacology
- Biomedical Science
Background:
- Heart failure with reduced ejection fraction (HFrEF) is linked to endothelial dysfunction, increased arterial stiffness, and myocardial damage.
- Sacubitril/Valsartan is a key therapeutic agent for HFrEF, known to reduce cardiovascular disease progression and mortality.
Purpose of the Study:
- To assess the impact of Sacubitril/Valsartan on endothelial dysfunction, arterial stiffness, oxidative stress, and platelet activation in HFrEF patients.
- To evaluate changes in these parameters after six months of treatment.
Main Methods:
- 100 Caucasian HFrEF patients were enrolled, with assessments at baseline and after 6 months.
- Endothelial function was measured using the reactive hyperemia index (RHI).
- Arterial stiffness was assessed via carotid-femoral pulse wave velocity (PWV), augmentation pressure (AP), and augmentation index (AI).
- Oxidative stress, platelet activation, and inflammatory biomarkers were quantified.
Main Results:
- Significant improvements were observed in hemodynamic, clinical, and metabolic parameters after 6 months.
- A marked reduction in oxidative stress markers (8-isoprostane, Nox-2) and platelet activation biomarkers (sP-selectin, Glycoprotein-VI) was noted.
- Significant enhancements in arterial stiffness and endothelial function indices were recorded.
Conclusions:
- Six months of Sacubitril/Valsartan treatment effectively improves endothelial dysfunction and arterial stiffness in HFrEF patients.
- The therapeutic benefits are attributed to the reduction of oxidative stress, platelet activation, and circulating inflammatory biomarkers.
- The treatment demonstrated a favorable safety profile with no adverse effects observed.
Abstract:
Heart failure (HF) is associated to endothelial dysfunction that promotes the increase of arterial stiffness thus augmenting myocardial damage. Sacubitril/Valsartan is used in the treatment of HF reduced ejection fraction (HFrEF) and has been proven effective in reducing cardiovascular disease (CVD) progression and all-cause mortality. The aim of this study was to evaluate the effect of Sacubitril/Valsartan on endothelial dysfunction, arterial stiffness, oxidative stress levels and platelets activation in patients with HFrEF, at baseline and after 6 months of treatment. We enrolled 100 Caucasian patients. Endothelial function was evaluated by the reactive hyperemia index (RHI) and arterial stiffness (AS) by the measurement of carotid-femoral pulse wave velocity (PWV), augmentation pressure (AP) and augmentation index (AI). At baseline, among enrolled outpatients, 43% showed a NYHA class II and 57% a NYHA class III. At 6 months, there was a significant improvement of several hemodynamic, clinical and metabolic parameters with a significant reduction in oxidative stress indices such as 8-isoprostane (p < 0.0001) and Nox-2 (p < 0.0001), platelets activity biomarkers such as sP-selectin (p < 0.0001) and Glycoprotein-VI (p < 0.0001), and inflammatory indices. Moreover, we observed a significant improvement in arterial stiffness parameters and in endothelial function indices. Our study demonstrated that 6 months treatment with Sacubitril/Valsartan, in patients with HFrEF, improves endothelial dysfunction and arterial stiffness, by reducing oxidative stress, platelet activation and inflammation circulating biomarkers, without adverse effects.
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