Association of NT-proBNP and sST2 with Left Ventricular Ejection Fraction and Oxidative Stress in Patients with Stable Dilated Cardiomyopathy.
Elżbieta Lazar-PoloczekEwa RomukWojciech JachecKarolina Wróbel-NowickaAgata ŚwiętekCelina WojciechowskaPublished in: Biomedicines (2024)
The aim of this study was to analyze the relationship between levels of sST2, NT-proBNP and oxidative stress markers in patients with reduced ejection fraction (HFrEF) due to non-ischemic cardiomyopathy. A total of 88 patients with HFrEF were divided into four groups based on left ventricular ejection fraction (≤25% and >25%) and NYHA functional class (group 1-LVEF > 25% and NYHA class I or II; group 2-LVEF > 25% and NYHA class III or IV; group III-LVEF ≤ 25% and NYHA class I or II; group IV-LVEF ≤ 25% and NYHA class III or IV). In 39 (44.32%) patients LVEF was reduced below 25%, and 22 of them (56.41%) were in NYHA functional class III/IV. Of the 49 (55.68%) patients with LVEF ≥ 25%, only 18.37% were in NYHA functional class III/IV ( p < 0.001). Patients with LVEF ≥ 25% had lower levels of NT-proBNP, total oxidant status (TOS), total antioxidant capacity (TAC), and oxidative stress index (OSI). The levels of NT-proBNP but not sST-2 correlated positively with NYHA functional class ( p < 0.001) and negatively with LVEF ( p < 0.001). The levels of sST-2 were associated with increased TAC ( p = 0.009) and uric acid ( p = 0.040). These findings indicate that only NT-proBNP was related to the severity of heart failure, whereas sST2 correlated with total antioxidant capacity. Therefore, in stable patients with HFrEF due to dilated cardiomyopathy, sST2 may be an additional biomarker reflecting the redox status, but not the severity of heart failure.
Keyphrases
- ejection fraction
- heart failure
- aortic stenosis
- oxidative stress
- left ventricular
- uric acid
- dna damage
- acute myocardial infarction
- cardiac resynchronization therapy
- coronary artery disease
- newly diagnosed
- induced apoptosis
- diabetic rats
- transcatheter aortic valve replacement
- acute heart failure
- acute coronary syndrome
- signaling pathway
- endoplasmic reticulum stress
- drug induced