# Update: Heart Failure in Systemic Lupus Erythermatosus
## 6 Potential HF Biomarkers in SLE Patients  
Cardiovascular risk in SLE is often underestimated; therefore, there is a strong need to use reliable biomarkers to identify patients at high risk of cardiovascular disease. The N-terminal prohormone of brain natriuretic peptide (NT-proBNP) is a dominant marker in both diagnostics and risk assessment in heart failure. Concentration of NT-proBNP increases in response to volume and pressure overload. NT-proBNP in SLE may correlate with organ dysfunction and disease durability [99; 125]. However, it does not always allow for detection of early stages of heart failure with preserved left ventricular ejection fraction. In such cases, stress hemodynamic assessment is necessary. [12] Already in childhood, patients with SLE had significantly increased BNP levels compared to healthy controls. Furthermore, BNP levels were increased in SLE patients without cardiovascular symptoms [51]. There are reports in the literature of fatal cases associated with acute HF, most likely caused by tumor necrosis factor (TNF) [122]. NT-proBNP levels may also be elevated in atherosclerosis, acute coronary syndromes, ischemic stroke, or renal failure [125]. Troponins are the dominant marker of acute coronary syndromes, but they are also useful in the assessment of HF. However, there is a lack of data on the correlation between high-sensitivity troponin T (hs-TropT) and echocardiographic markers of cardiac function in detecting early abnormalities or assessing subclinical disease. SLE patients without diagnosed or symptomatic disease show higher hs-TropT values, which may indicate subclinical cardiac dysfunction. [PERSON] et al. demonstrated a correlation between hs-TropT and left ventricular stiffness abnormalities associated with an abnormal E/e' ratio [126]. Additionally, parameters of systolic function disorders (LVEF, LVES) positively correlated with higher hs-Trop concentration [127]. Asymmetric dimethylarginine (ADMA) enzyme is an endogenous inhibitor of nitric oxide (NO) synthase, blocking the release of NO from endothelial cells. This process leads to the inhibition of NO's vasodilatory effects. Reduced NO levels can cause endothelial dysfunction, which leads to atherogenesis and secondarily to heart failure. ADMA activity is associated with a fourfold higher risk of cardiovascular diseases. Additionally, it negatively correlates with left ventricular ejection fraction (LVEF) and positively with the New York Heart Association (NYHA) cardiac function score, BNP levels, and the incidence of HF. Higher levels of ADMA are observed in chronic heart in patients with SLE [46; 128; 129]. The colony-stimulating factor 1 (CSF1) is a cytokine produced by the activation of macrophages, lymphocytes, and mesenchymal cells, which influences the differentiation of monocytes and macrophages. It has been suggested that CSF1 may be a potential risk factor for cardiac dysfunction. In patients with SLE and atherosclerosis, M-CSF may be a biomarker of adverse cardiovascular events [130]. [PERSON] et al. assessed the levels of soluble serum protein ST2 (sST2), chemokine CXCL-10, and high-sensitivity troponin (hs-troponin) in 57 patients with SLE. Levels of sST2, CXCL-10, and hs-troponin were significantly higher in patients with active SLE as assessed by the Systemic Lupus Erytheratosus Disease Activity Index (SLEDAI) and with existing organ damage. CXCL-10 correlated negatively with diastolic dysfunction, especially with echocardiographic parameters: E/A, E/e' lateral, and E/e' septal, whereas E/e' correlated positively with CXCL-10. A negative correlation between sST2 and E/e' lateral and a positive correlation with E/e' was also observed. ST2 and CXCL-10 proteins may be potential biomarkers of subclinical diastolic dysfunction [127]. Similar conclusions were presented by [PERSON] et al., who showed a higher concentration of sST2 and a correlation with disease activity [131]. Galectin-3 was also considered as a potential biomarker. Significantly higher levels of this protein were shown in chronic heart failure.