Abstract

PurposeHeart rate reduction (HR) is a cornerstone in heart failure therapy as it improves patient outcomes. The aim of this study is to evaluate short-term effect of ivabradine on NT-Pro BNP and neopterin in heart failure patients and assess the association between HR and these biomarkers.MethodsSixty patients on standard heart failure therapy were randomly allocated into ivabradine group (n = 30) and non-ivabradine group (n = 30). Ivabradine 5 mg twice daily was given for 3 months. Lipid profile and kidney functions were performed and blood samples for NT-Pro BNP and neopterin were analysed at baseline and after 3 months of intervention in both groups.ResultsThere was a significant improvement in NYHA class in ivabradine group (p < 0.001). Ejection fraction was improved in ivabradine and non-ivabradine groups after intervention (p < 0.001), with a greater improvement in ivabradine group (p = 0.026). Heart rate was reduced in ivabradine group (p < 0.001) and non-ivabradine group (p < 0.001) yet greater reduction was seen in ivabradine group (p < 0.001). Serum creatinine and blood urea nitrogen were reduced in ivabradine group (Scr: p = 0.001, BUN: p = 0.001). NT-Pro BNP and neopterin levels significantly decreased in ivabradine group (NT-Pro BNP: p < 0.001, neopterin p < 0.001). Significant positive correlation was found between HR and biomarker levels after intervention (NT-Pro BNP: r = 0.475, p < 0.001, neopterin: r = 0.384, p = 0.002).ConclusionIvabradine therapy reduced levels of both biomarkers which correlated well with HR. Biomarker levels might provide a tool for assessing ivabradine effectiveness in HF.Trial registrationDate: June 26, 2020. Identifier: NCT04448899. Link: Ivabradine in Patients with Congestive Heart Failure—Full Text View—ClinicalTrials.gov.

Highlights

  • Heart failure (HF) is a complicated clinical condition that affects the ability of the ventricles to fill up or pump enough blood to meet requirements of the body [1, 2]

  • During follow-up, in ivabradine group, 2 patients did not adhere to treatment regimen and 2 discontinued the treatment due to incidence of acute HF

  • In non-ivabradine groups, 1 patient did not adhere to treatment regimen and 3 discontinued the treatment due to incidence of acute HF

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Summary

Introduction

Heart failure (HF) is a complicated clinical condition that affects the ability of the ventricles to fill up or pump enough blood to meet requirements of the body [1, 2]. Other causes of HF might include: cardiomyopathies, valvular heart disease, atrial fibrillation (AF), chronic kidney disease (CKD), chronic obstructive pulmonary disease (COPD), thyroid dysfunction and anaemia [1–4]. Hyperlipidemia has a major role in the progression of heart failure as demonstrated by previous studies. Hypercholesterolemia decreases coronary blood flow and induces apoptosis through diminished autophagy leading to LV dysfunction [5, 6]. Studies found that high levels of fats lead to disrupting electrophysiology of the heart which in turn leads to arrhythmias [5, 6]. Recent findings found that levels of oxidised LDL are increased in HF leading to decrease in EF [5]

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