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Review

Update: Heart Failure in Systemic Lupus Erythematosus

by
Dominika Blachut
*,
Michalina Mazurkiewicz
,
Marcin Schulz
,
Julia Cieśla
,
Brygida Przywara-Chowaniec
and
Andrzej Tomasik
2nd Department of Cardiology, Medical University of Silesia in Katowice, 41-800 Zabrze, Poland
*
Author to whom correspondence should be addressed.
Appl. Sci. 2025, 15(3), 1590; https://doi.org/10.3390/app15031590
Submission received: 21 December 2024 / Revised: 3 February 2025 / Accepted: 4 February 2025 / Published: 5 February 2025
(This article belongs to the Special Issue Feature Review Papers in Section Applied Biosciences and Bioengineering)
Browse Figure
Versions Notes

Abstract

:
Systemic lupus erythematosus (SLE) is a disease that significantly increases cardiovascular risk. Although cardiovascular diseases are one of the leading causes of death in SLE patients, the correlation between SLE and heart failure (HF) remains unexplored. Myocardial dysfunction in SLE patients is frequently asymptomatic or nonspecific, which makes it difficult to identify HF using standard diagnostic techniques. In addition, there are serious difficulties in its early diagnosis. In this review, we summarize the latest reports on the epidemiology of heart failure in SLE patients. Current evidence on the impact of SLE treatment on the development of HF, as well as potential risk factors that increase the risk of HF, is presented. Potential methods of treatment and early detection of HF with special attention to potential biomarkers are also provided. Further research is needed to better understand the mechanisms of the correlation between HF and SLE and to develop effective treatment strategies.

1. Introduction

Systemic lupus erythematosus (SLE) is an autoimmune disease with multiorgan manifestation. Tissue damage attributed to SLE is caused by the presence of autoantibodies and immune complex deposition, which occurs primarily in the kidneys, heart, blood vessels, central nervous system, skin, lungs, muscles, and joints. Cardiac involvement is the second most common organic manifestation of SLE, after lupus nephritis, diagnosed in almost half of patients. The most well-known SLE cardiac manifestations are pericarditis and Libman-Saks endocarditis. Therefore, cardiovascular diseases are responsible for significant morbidity and mortality in patients with SLE [1,2]. Generally, patients with an SLE diagnosis have a higher overall cardiovascular risk compared with the general population. However, the correlation between SLE and heart failure (HF) remains unknown.
It has been extensively suggested that SLE patients may be burdened with a higher incidence of HF than the general population [3,4,5,6,7,8]. However, the increased prevalence of HF does not explain the occurrence of myocarditis, which is a rare comorbidity in SLE [9,10]. It is estimated that the incidence of HF in SLE may be up to 5 times higher than in the general population [3,4]. Moreover, reduced left ventricular ejection fraction (LVEF) in patients with SLE compared to the control groups has been observed in previous studies [11,12]. Although the exact pathogenesis of HF in SLE is not entirely understood, chronic inflammation, immune dysfunction, and cardiovascular risk factors play a significant role in the development of heart failure. What is more, HF may be the first manifestation of SLE. Treatment is another important issue, as cardiac involvement in SLE may present as end-stage heart failure, requiring orthotopic heart transplantation (OHT) [13]. Although cardiovascular diseases are one of the leading causes of death in patients with SLE, myocardial dysfunction is often asymptomatic or presents with nonspecific signs. Finally, the difficulties in identifying disease in its early stages using standard techniques preclude detection of early subclinical cases.
In summary, due to the complex pathogenesis of SLE, early detection of cardiac problems may prove burdensome, which leads to delayed introduction of targeted treatment. There is a strong need for a better understanding of the mechanisms leading to heart failure in SLE. Furthermore, more effective diagnostic and therapeutic methods are being sought. The existing literature on heart failure in SLE is scarce. Notwithstanding the growing number of studies, there is still a lack of guidelines for the management of SLE-related HF, which makes optimization of the treatment in this group demanding. Thus, further studies focused on the increased risk of HF in patients with SLE are needed [14,15,16,17]. This article summarizes the latest reports on the epidemiology, symptoms, and potential treatment methods of heart failure in patients with SLE. A detailed review of the scientific databases Clinical Key, PubMed, and EMBASE was performed to prepare the manuscript. Particular attention was paid to the reports from the last decade (2014–2024).

2. Epidemiology of Heart Failure in Systemic Lupus Erythematosus

Regardless of the long-standing and widespread awareness of the increased cardiovascular risk in patients with SLE, more detailed epidemiological data on heart failure in this group are beginning to appear. Autopsies of SLE patients have demonstrated that almost half of them presented signs of myocardial involvement, whereas the disease had been diagnosed premortem in solely about 1/10 patients, which indicates the scale of the diagnostic problem in the coexistence of these diseases [18]. Despite medical advances, cardiovascular disease mortality has remained unchanged for 30 years [19], whereas the incidence of HF in SLE patients is estimated to be 5 times higher than in the general population [3,4]. Importantly, SLE may predispose to HF more strongly than diabetes (DM) or dyslipidemia [3]. However, some studies indicate that the incidence of HF in patients with SLE is 2.7 times higher than in the general population, which is comparable to the risk associated with DM. Other studies have also observed a 3.2–3.8 times higher risk compared to the general population. The hazard ratio decreases with age, reaching a value of about 1.25 for patients over 65 years of age [3,20,21]. Patients with SLE are characterized by a higher frequency of hospitalization due to HF, and this risk decreases with age, conversely to the general population [19,21]. Nevertheless, age remains an independent risk factor for HF [22].
Considering gender, women remain the dominant group of patients with SLE, but younger men have a higher (up to 3.5-fold) risk of developing HF [3,21,23]. Similarly, the Black race significantly increases the risk of developing HF, even 1.5-fold [8,24,25,26]. In the multivariable model proposed by Chen et al., inclusion ethnicity indicates a 4.2-fold increase in the risk of HF in SLE patients with SLE [20].
Available data indicate that most acute cardiac symptoms occur within the first 6 months of SLE diagnosis. Therefore, HF is more likely to be related to SLE than to atherosclerosis, which develops in the later decades of life [8,27,28]. The prevalence of subclinical left ventricular systolic as well as left ventricular diastolic dysfunction is estimated to be about 11–16% and 4–8%, respectively. However, data from studies using magnetic resonance imaging suggest a higher percentage [29,30,31,32].
Despite the widespread recognition of the increased cardiovascular risk in SLE patients, the first epidemiological data on heart failure are emerging, underlining the difficulty of its early detection. Analysis of autopsies in SL patients exhibits that myocardial involvement occurs much more frequently than previously thought and consequently how often cases of HF are undiagnosed or diagnosed with delay. Therefore, not only the identification but also the effective treatment of heart failure in this group is an urgent problem. Moreover, the comparison of the risk of HF in SLE with other metabolic diseases, such as diabetes or dyslipidemia, indicates a preeminent predisposition of patients with lupus to the development of heart failure.
In addition, the higher risk of HF in younger men and Black patients, as well as other demographic characteristics, may be crucial in identifying groups at increased risk. It is worth emphasizing that the subclinical changes in the heart, such as left ventricular systolic and diastolic dysfunction, may go unnoticed, which impedes the introduction of early treatment. Further studies are necessary to better understand the mechanisms leading to heart failure in SLE and to develop appropriate diagnostic and therapeutic strategies.

3. Pathophysiology and Risk Factors of Heart Failure in Systemic Lupus Erythematosus

Systemic lupus erythematosus may contribute to the development of heart failure through many mechanisms and heart-related diseases, especially myocarditis, cardiomyopathy, or valvular heart disease, as well as through genetic predisposition [33,34,35]. It is estimated that SLE may be responsible for even 50% of HF cases in this group of patients [3,11,19,23]. In particular, subclinical heart failure is frequently observed in SLE patients and occurs in almost two-thirds of patients, as demonstrated by cardiac magnetic resonance imaging [31].
The pathogenesis of HF coexisting with SLE is multifactorial and still undetermined. Cardiovascular risk factors significantly associated with cardiac dysfunction in SLE include atherosclerosis, dyslipidemia, chronic kidney disease and lupus nephritis, obesity, as well as chronic inflammation. On the other hand, hypertension, myocarditis, pericarditis, and valvular heart disease are the main cardiological causes of HF development in SLE patients [8,19,36,37,38]. Furthermore, several studies have shown that the deterioration of diastolic function was associated with age and independently correlated with increased aortic stiffness [39,40]. Buss et al., in echocardiography of SLE patients with asymptomatic HF, demonstrated dysfunction of both systolic and diastolic left ventricular function compared with the control group [41], which has been confirmed in further trials [11,29,30,41,42,43]. SLE as a potential factor in the development of HF was also shown in one of the large, randomized trials conducted in Asia, where Song revealed a potential association between SLE and an increased risk of congestive heart failure [34]. Moreover, a study from Korea showed that SLE is an independent risk factor for the development of HF. HF was observed in 358 SLE patients and 354 control subjects (incidence rate 3.11 and 0.61 per 1000 person-years, respectively), and the risk of occurrence was determined to be 4.60 (95% confidence interval: 3.96–5.35) [14]. These results support the recognition of SLE as an independent factor in the development of HF. Therefore, the pathogenesis of HF is based on inflammation, which is an integral part of SLE. Moreover, in SLE patients, the dominant type is HF with preserved ejection fraction (HFpEF). HF with reduced left ventricular ejection fraction (HFrEF) occurs less frequently [7,9].
As previously mentioned, the pathogenesis of HF in SLE is presumably related to microvascular myocardial dysfunction resulting from chronic inflammation [21,44]. The main pathophysiological changes associated with HF are attributed to the influence of proinflammatory cytokines (tumor necrosis factor α, interleukins 1, 6, 8, 10, and 15, complement component C3a, C-reactive protein, and expression of clusters of differentiation CD4 and CD8) in the myocardium. Expression of cytokines consistently causes a decrease in ventricular contractility and thus, the development of nonischemic cardiomyopathy. Pomara et al. observed a positive correlation between myocytes and anti-TNF antibodies, interleukins (IL-8, IL-10, IL-15), complement component C3a, and CD4 and CD8 expression [45].
Additionally, type I interferon is associated with the involvement of T cells and macrophages in immunological processes resulting in impaired endothelial function and secondary atherosclerosis [46,47]. Similarly, accelerated oxidation of low-density lipoprotein (LDL) and increased uptake by monocytes promote the development of atherosclerosis [19,46].
Another pathophysiological mechanism in the development of HF in SLE patients is endothelial activation leading to collagen deposition. This process results in increased stiffness and hypertrophy of cardiomyocytes as well as reduced relaxation capacity of the myocardium, which may consequently lead to the development of HFpEF. Additionally, circulating antibodies form immune complexes, enhancing the immune response in the myocardium. On the other hand, activated components of the complement system cause cardiomyocyte damage. In Libman-Sacks inflammation, fibrin and thrombocytes are deposited on the heart valves, causing their destruction [45,48,49,50]. The predominance of the HFpEF type in SLE patients may be related to the pathophysiology of the disease and closely related to the effect of endothelin-1 (ET-1). ET-1 secretion increases in response to elevated blood pressure, leading to disturbances specific to HFpEF: endothelial dysfunction, myocardial fibrosis, increased vascular stiffness, and diastolic dysfunction. On the other hand, in HFrEF, cardiomyocyte damage leads to eccentric left ventricular remodeling and systolic dysfunction, which is an infrequent process in SLE [51,52,53].
Pathophysiological research is supported by the results of interventional studies since it has been shown that appropriate anti-inflammatory treatment significantly improves physical fitness. These observations were confirmed by the improvement of echocardiographic results and cardiopulmonary exercise results, as well as by the betterment of serological parameters and heart failure biomarkers during the observation period [12].
In conclusion, HF in SLE patients may be caused by multiple mechanisms, including myocarditis, cardiomyopathy, valvular heart disease, as well as genetic factors. Crucially, SLE itself may be responsible for 50% of HF cases in this group of patients. The prevalence of subclinical heart failure may be underestimated, which indicates a strong need for early diagnosis and implementation of cardiac function monitoring in these patients. Chronic inflammation plays a key role in the pathogenesis of HF development in SLE patients. Available data suggest anti-inflammatory therapy as a method to improve cardiac function and physical fitness of patients, as indicated by echocardiographic and cardiac marker results. This fact may be of practical importance in future attempts to develop standards for monitoring and treatment of patients with SLE. However, further studies are needed to better understand the mechanisms leading to HF in SLE and to construct more effective therapeutic strategies. A summary of risk factors responsible for the development of heart failure in SLE is presented in Figure 1.

3.1. Arterial Hypertension (HA)

Arterial hypertension (HA) is one of the principal factors associated with the development of heart failure. Importantly, HA is more frequent in patients with systemic lupus erythematosus than in the general population. It is estimated that it affects up to half of patients with SLE. HA may be the effect of glucocorticosteroid (GC) treatment or a complication of chronic kidney disease [3,8,54].

3.2. Pericarditis

Pericarditis is the most common cardiac manifestation of SLE, occurring in 30–50% of patients. Moreover, the diagnosis of pericarditis is one of the diagnostic criteria for SLE [55]. However, in the course of this disease, pericardial involvement with severe myocardial dysfunction is scarce. Pericarditis, like other types of serositis, occurs more frequently during periods of SLE activity in other organs [1].

3.3. Myocarditis and Endocarditis

Myocarditis is associated with chronic inflammation and fibrosis, which secondarily leads to impaired systolic function of the myocardium. Complement components, chronic inflammation, and deposition of immune complexes are involved in these processes. Antibodies: anti-Ro (SS-A), antiribonucleoprotein, and antiphospholipid antibody may also be involved. Myocarditis is observed in about 10% of SLE patients. Moreover, postmortem studies have shown the presence of myocarditis in up to 2/3 of patients [56,57]. It predominantly affects younger patients and can range from asymptomatic to severe heart failure [8,56,58,59]. A type particularly associated with SLE is Libman-Sacks endocarditis, which may cause valvular dysfunction and be another factor in the development of HF [33,60,61,62].
Myocarditis in SLE patients is a serious condition, as it can lead to severe HF and dilated cardiomyopathy [56,63,64]. Cases of heart failure during pregnancy and the postpartum period caused by myocarditis have also been described [10,65]. However, myocarditis and dilated cardiomyopathy are late manifestations of myocardial dysfunction and are relatively infrequent [45,66]. In patients with HFpEF with a history of myocarditis, regional wall motion (RWM) abnormalities and significant diastolic dysfunction are observed. Thus, these parameters are sensitive markers of general myocardial dysfunction [67]. LVEF reduction after myocarditis occurs in about ¼ of patients. Most patients remain in the group with preserved ejection fraction. However, diastolic dysfunction is observed in almost 90% of patients [68,69]. Similarly, regional disturbances in the motion of the heart walls are found in the majority of patients [60]. Magnetic resonance imaging (MRI) remains the gold standard for diagnosis [70,71,72].

3.4. Coronary Artery Disease (CAD)

SLE is an extremely important risk factor for atherosclerosis and, secondarily, coronary artery disease (CAD). On the other hand, CAD is a causative factor in only 20% of HF cases in SLE patients. In contrast to the general population, younger patients, especially men, are more predisposed to HF coexisting with SLE—up to 50-fold, which is a possible cause of the tenuous association with CAD in this age group [3,8,11,19,23,73]. The increased risk of HF in younger patients may indeed be related to the underlying molecular processes in SLE, including chronic inflammation and microvascular disease, as well as the presence of common HF risk factors [3,19,74]. Nevertheless, the prevalence of HF associated with CAD is significantly higher than in the general population. [75]. Accelerated development of CAD mainly leads to ischemic cardiomyopathy and HFrEF [31]. Additionally, a history of myocardial infarction increases the risk of developing HF in SLE threefold [19].

3.5. Valvular Heart Disease

The prevalence of valvular heart disease in patients with symptomatic SLE is estimated at less than 5%, while in the asymptomatic group it may be found in up to 2/3 of patients. Valvular heart disease may increase the risk of developing HF threefold. In addition, an association between the presence of antiphospholipid antibodies and valvular heart disease has been identified [3,8,76]. In addition, mitral and tricuspid regurgitation may coexist with the presence of antibodies against double-stranded DNA (dsDNA), indicating valvular dysfunction associated with disease activity [77].

3.6. Pulmonary Hypertension (PH)

A significant problem in SLE, related to right ventricular dysfunction, is pulmonary hypertension (PH). The incidence of PH in SLE patients is estimated at about 4–40% [78]. It is widely known that the presence of antiphospholipid antibodies predisposes to the development of pulmonary hypertension. Nevertheless, the impact of PH on the risk of developing HF in patients with SLE has not been precisely assessed [79,80].

3.7. Cardiac Arrhythmias

Various types of cardiac arrhythmias are common and often lead to HF in the general population as well [15,16,17]. Atrial fibrillation, complete atrioventricular block, and QT prolongation are the most common arrhythmias observed in SLE patients. They are estimated to affect 30 to 70% of patients [19]. History of myocarditis, leading to inflammatory infiltration or fibrotic scarring of the conduction system, may be the cause of numerous arrhythmias. QT prolongation may be the result of anti-Ro/SSA antibody action, which may lead to serious ventricular arrhythmias and consequently to sudden cardiac death [81,82].

3.8. Other Causes

Left ventricular hypertrophy (LVH) is found in about 1/5 of patients with SLE. LVH may be caused by hypertension and corticosteroid use. Correlation between disease duration and left ventricular mass has been previously demonstrated. LVH may be another predisposing factor to heart failure through impaired systolic and diastolic function [29,30,83,84].
Another cause of HF in the course of SLE is Macrophage Activation Syndrome (MAS). Heart failure and right ventricular dysfunction are the main MAS features [85,86]. The role of MAS in the development of HF should be further explored in future studies.

4. Electrocardiographic (ECG) and Echocardiographic Changes in SLE

ECG abnormalities observed in SLE may indicate subclinical cardiac involvement. They may take the form of typical ECG changes that occur in cardiovascular diseases in the general population, as well as abnormalities associated with antibodies characteristic of SLE. On the other hand, Azharudeen et al. found prolonged QTc and QTd intervals that were not significantly associated with disease activity, anti-Ro antibodies, interleukin 1β, and interleukin 6 levels in SLE patients treated with hydroxychloroquine and prednisolone [87]. Therefore, ECG abnormalities in SLE patients may be indicative of subclinical cardiac dysfunction. Furthermore, ECG abnormalities may occur even in a relatively stable clinical condition, which poses a formidable diagnostic challenge.
As far as echocardiography is concerned, subclinical ventricular dysfunction in SLE may manifest as systolic dysfunction and/or diastolic dysfunction [41]. In SLE patients, enlargement of the left atrium, left ventricle in diastole, and increased left ventricular mass index (LVMI) as well as reduced left ventricular systolic and diastolic function, expressed by E/A (the ratio of E-wave to A-wave velocities of mitral inflow) and E/e’ (the ratio of the E-wave velocity of mitral inflow to the e’ velocity of mitral annular motion during diastole) indices, were observed [88]. A study conducted in India, including 50 patients with SLE, showed that 12% of patients had diastolic dysfunction [89]. In other studies, Global Longitudinal Strain (GLS) abnormalities were observed even in patients with good clinical condition. GLS measures the percentage deformation (shortening) of myocardial fibers in the longitudinal axis using speckle-tracking echocardiography. GLS disturbances were more pronounced in the active disease stage, suggesting that SLE may significantly affect cardiac function, even in the absence of cardiovascular disease. Diastolic dysfunction and GLS abnormalities were observed in patients with long-term disease activity, confirming the higher risk of cardiovascular disease in this group [36,41,42,43,84].
Both systolic and diastolic ventricular dysfunction in SLE is a particularly important issue in the context of subclinical changes, which can nowadays be detected using modern diagnostic methods such as STE and GLS assessment. These techniques seem to be promising tools in the assessment of early cardiac dysfunctions, invisible in conventional echocardiography. Studies present increasingly strong evidence of a correlation between disease activity and the severity of GLS dysfunctions, which may indicate that SLE affects cardiac function already in the subclinical phase. Therefore, speckle tracking echocardiography (STE) and GLS parameter assessment seem to be promising methods for assessing subclinical cardiac dysfunction in SLE [36,42]. Left ventricular GLS may be a marker of future cardiovascular events, which should be investigated in multicenter, prospective studies [42].
Reduced left ventricular function on cardiac MRI and its correlation with SLE activity and inflammation. It is worth noting that in cardiac magnetic resonance imaging of SLE patients, a correlation was observed between reduced left ventricular function and disease activity as well as inflammation [90]. The study was conducted on a small number of patients, but it confirms that patients with SLE show a lower LVEF than the control group.
Positron emission tomography (PET) is a tool for assessing myocardial perfusion and inflammation. The literature describes lower myocardial flow reserve (MFR) values measured by PET in patients with autoimmune rheumatic diseases. In cases where MFR was below 1.5, patients had a worse prognosis, including a higher risk of HF [70]. There is a lack of data for SLE.

5. Treatment of Systemic Lupus Erythematosus and Heart Failure

It is believed that immunosuppressive therapy, by inhibiting inflammation, may reduce the risk of cardiovascular diseases. Most studies have focused on the risk of atherosclerosis and the secondary development of coronary artery disease; thus, there is a deficiency of data on the effect of SLE treatment on HF development. However, in individual reports, an improvement in left ventricular ejection fraction has been observed after cytotoxic therapy [58,64].

5.1. Antimalarial Drugs (AM)

The cardioprotective effect of hydroxychloroquine has been demonstrated in many retrospective studies [8,91,92,93]. For antimalarial drugs (AM), which are one of the main groups of drugs used in SLE, an association with the development of cardiomyopathy has been described in several cases. Cardiomyopathy associated with AM was manifested by diastolic dysfunction, conduction disturbances, and ventricular hypertrophy. Thus, the assessment of markers of heart damage such as cardiac troponin or NT-proBNP may prove useful in everyday practice, since they may be elevated in asymptomatic patients and indicate the risk of taking AM drugs [94,95,96,97,98,99,100]. Another complication of AM use is the risk of impaired ventricular repolarization, which increases the risk of serious arrhythmias such as torsade de pointes, atrioventricular blocks, and the accumulation of metabolic products related to the inhibition of lysosomal enzymes [98,101,102]. In patients taking AM, smoking is also unpredictable, as it interferes with the action of hydroxychloroquine by increasing the expression of TLR-9. Furthermore, SLE patients who do not smoke are potentially at lower risk of HFrEF [103]. However, the data on this issue are inconsistent and insufficient to provide strong evidence [91,100,104,105].

5.2. Glucocorticoids (GCs)

The use of glucocorticoids (GCs) is associated with the risk of dyslipidemia, overweight, obesity, metabolic syndrome, and diabetes as secondary complications. Therefore, it increases the overall cardiovascular risk, and thus the probability of developing heart failure [19,106,107,108]. GCs affect the process of atherogenesis, and the duration of use and dose are the main predictors of cardiovascular complications [11,108]. Therefore, SLE patients treated with glucocorticoids are 8 times more likely to develop HF [19]. Corticosteroids can have a negative impact on the cardiovascular system in SLE by contributing to an increase in epicardial adipose tissue [71].

5.3. Biological Disease-Modifying Antirheumatic Drugs (bDMARDs)

Biological disease-modifying antirheumatic drugs (bDMARDs) may potentially reduce the risk of developing heart failure. Nonetheless, there is a scarcity of research on their use in SLE, and most of the available trials refer to rheumatoid arthritis (RA) [109,110]. Cardioprotective effects in RA have been suggested for rituximab [98,99,109]. Similarly, improvement of echocardiographic parameters and biomarkers of heart failure has been reported for belimumab [12]. Therapy targeting the interferon pathway may induce a positive therapeutic and cardioprotective response, mainly by inhibiting the development of atherosclerosis [111]. Despite promising preliminary studies, evidence of the cardiovascular effects of bDMARDs in SLE is limited, which is another issue that needs to be addressed in future studies.

5.4. Intravenous Immunoglobulin (IVIg)

Intravenous immunoglobulin (IVIg) has an immunomodulatory effect by increasing the suppressor activity, blocking the Fc receptor, and influencing the complement components. Furthermore, IVIg is involved in the regulation of T and B lymphocytes, the interferon pathway, and inhibits the elimination of immune complexes [112,113,114]. Data on IVIg treatment in SLE are scarce and mainly concern myocarditis [66]. Several studies have shown that IVIg reduces inflammation and increases LVEF in patients with HF [115,116,117,118,119,120,121], although two studies did not show any changes in the above-mentioned parameters [69,122].

5.5. Other Drugs

There are no data on the association of mycophenolate mofetil, cyclophosphamide, or azathioprine therapy with HF development [123], although a higher incidence of congestive heart failure has been reported with azathioprine [35]. Due to significant similarities in the pathophysiology of autoimmune diseases, methotrexate may have a cardioprotective effect, as in rheumatoid arthritis [4,124].

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. Winau 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 failure 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].
Chorin 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 Erythematosus 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 Mok 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. Galectin-3 increases the proliferation of pericytes, myofibroblasts, and fibroblasts and the secretion of procollagen I, which leads to cardiac hypertrophy, its remodeling, and contractility disorders due to increased fibrosis, the presence of mast cells, and the expression of TGF-β and Smad3 [132,133]. A summary of potential biomarkers of HF in SLE patients is provided in Table 1.

7. HF Treatment in Systemic Lupus Erythematosus

In the absence of contraindications, heart failure treatment should be carried out in accordance with the recommendations of global scientific societies [15,16,17,48,49], although there are no dedicated guidelines. However, one study reported that patients with SLE and HF were less likely to receive full heart failure treatment according to guidelines [7]. Immune disorders and chronic inflammation, as well as glucocorticosteroids and immunosuppression as standard treatment, are additional factors in the development of HF. Intravenous immunoglobulins or electrotherapy are occasionally used. According to the guidelines, cardiac resynchronization therapy or the use of a left ventricular assist device should be considered. In patients with unsatisfactory results of conservative treatment, a potential solution may be heart transplantation [13,15,16,17,134,135]. Single cases of heart transplantation have been described in SLE patients, where the main causes of HF were myocarditis, infective endocarditis, dilated cardiomyopathy, and ventricular dysfunction [13,136,137,138,139]. The majority of transplant centers consider SLE a contraindication to transplantation because of the risk of disease relapse in the transplanted organ. However, OHT may be considered in selected patients with SLE and end-stage heart disease. The overall immunosuppressive strategy may be similar to that used in the general population [13]. In patients with left ventricular dysfunction, significant improvement in LVEF, diastolic function, and right ventricular systolic pressure was demonstrated after kidney transplantation [140,141].

8. Conclusions

In summary, heart failure is a serious complication in patients with systemic lupus erythematosus. The occurrence of HF is associated with many pathophysiological mechanisms that require further research. Early diagnosis and appropriate diagnostic processes are crucial to improving the quality of life and increasing the survival of patients with SLE. The increased cardiovascular risk in patients with systemic lupus erythematosus is widely known, but there are insufficient clinical studies to determine the scale of the heart failure phenomenon. Apart from routine cardiovascular risk assessment, there are currently no recommendations for the diagnosis and treatment of heart failure in systemic lupus erythematosus. Control of disease activity seems to be the fundamental way to reduce the risk of developing heart failure. Patients diagnosed with SLE should be under cardiological supervision. Further research is needed to better understand the mechanisms of the correlation between HF and SLE and to develop effective treatment strategies.

Author Contributions

Conceptualization, D.B. and B.P.-C.; methodology, A.T.; formal analysis, A.T.; investigation, M.M. and M.S.; resources, M.M., M.S. and J.C.; data curation, D.B.; writing—original draft preparation, D.B., M.M., M.S. and B.P.-C.; writing—review and editing, A.T.; supervision, A.T.; project administration, D.B.; funding acquisition, D.B. and B.P.-C. All authors have read and agreed to the published version of the manuscript.

Funding

This research was funded by the Medical University of Silesia in Katowice, grant number PCN-191/N/1/K and PCN-1-182/K/0/K.

Institutional Review Board Statement

Not applicable.

Informed Consent Statement

Not applicable.

Data Availability Statements

No new data were created or analyzed in this study.

Conflicts of Interest

The authors declare no conflicts of interest.

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Applsci 15 01590 g001
Figure 1. Summary of risk factors responsible for the development of heart failure in SLE. Source: own study.
Figure 1. Summary of risk factors responsible for the development of heart failure in SLE. Source: own study.
Applsci 15 01590 g001
Table 1. A summary of potential biomarkers of HF.
Table 1. A summary of potential biomarkers of HF.
Name of the BiomarkersSignificant Value in HFComment
NT-proBNPconfirmedConfirmed association with diagnosis and severity of HF
hs-TropTconfirmedMarker of early cardiac function abnormalities
ADMAinsufficient dataA marker potentially associated with chronic HF
sST2insufficient dataMarker positive correlation with E/e ratio disturbances
CXCL-10insufficient dataMarker negatively correlated with diastolic dysfunction (E/A, E/e’ lateral, and E/e’ septal)
CSF-1insufficient dataPotential marker of cardiac dysfunction
Galectin-3insufficient dataPotential marker of cardiac dysfunction
NT-proBNP—N-terminal prohormone of brain natriuretic peptide; hs-TropT—high-sensitivity troponin-T; ADMA—asymmetric dimethylarginine; sST2—sST2 protein; CXCL-10—CXCL-10 protein; E/A—the ratio of E-wave to A-wave velocities of mitral inflow; E/e’—the ratio of the E-wave velocity of mitral inflow to the e’ velocity of mitral annular motion during diastole; CSF-1—the colony stimulating factor 1.
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Blachut, D.; Mazurkiewicz, M.; Schulz, M.; Cieśla, J.; Przywara-Chowaniec, B.; Tomasik, A. Update: Heart Failure in Systemic Lupus Erythematosus. Appl. Sci. 2025, 15, 1590. https://doi.org/10.3390/app15031590

AMA Style

Blachut D, Mazurkiewicz M, Schulz M, Cieśla J, Przywara-Chowaniec B, Tomasik A. Update: Heart Failure in Systemic Lupus Erythematosus. Applied Sciences. 2025; 15(3):1590. https://doi.org/10.3390/app15031590

Chicago/Turabian Style

Blachut, Dominika, Michalina Mazurkiewicz, Marcin Schulz, Julia Cieśla, Brygida Przywara-Chowaniec, and Andrzej Tomasik. 2025. "Update: Heart Failure in Systemic Lupus Erythematosus" Applied Sciences 15, no. 3: 1590. https://doi.org/10.3390/app15031590

APA Style

Blachut, D., Mazurkiewicz, M., Schulz, M., Cieśla, J., Przywara-Chowaniec, B., & Tomasik, A. (2025). Update: Heart Failure in Systemic Lupus Erythematosus. Applied Sciences, 15(3), 1590. https://doi.org/10.3390/app15031590

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