Systemic lupus erythematosus (SLE) is a chronic, multisystem autoimmune disorder characterized by the production of diverse autoantibodies and immune-mediated tissue injury. The disease exhibits considerable clinical heterogeneity and may involve nearly every organ system. Among its various systemic manifestations, cardiovascular involvement is particularly important because it substantially increases both morbidity and long-term mortality. Epidemiological evidence consistently demonstrates that patients with SLE have a significantly higher risk of cardiovascular disease (CVD) compared with age- and sex-matched individuals in the general population [1,2]. Traditional cardiovascular risk factors alone do not sufficiently account for this heightened risk, indicating an essential role of lupus-specific inflammatory and immunological mechanisms [3–5].

Cardiac manifestations in SLE may involve the pericardium, myocardium, and endocardium, producing a broad spectrum of clinical abnormalities. Pericarditis is the most frequent cardiac feature, while myocarditis, endocarditis, valvular thickening, pulmonary hypertension, and conduction disturbances also occur and may remain clinically silent for prolonged periods [6]. Associations have been described between certain autoantibodies, such as anti-Ro/SS-A, anti-La/SS-B, anti-cardiolipin (aCL), and anti–double-stranded DNA (anti-dsDNA), and specific cardiac lesions; however, these immunologic markers do not entirely explain the pathogenesis or diversity of cardiac involvement in SLE [7,8]. Notably, endothelial dysfunction has been documented even in early disease and in patients without overt cardiovascular symptoms, reinforcing the contribution of chronic inflammation, renal disease, diastolic hypertension, and metabolic abnormalities to premature vascular injury [9,10].

The cardiovascular risk profile of SLE is particularly striking among young women. The incidence of myocardial infarction has been reported to be nearly three times higher than in matched controls, and case-control studies have demonstrated a 9- to 50-fold increased risk compared with healthy women [1]. These findings highlight SLE as an independent risk factor for premature atherosclerosis. Viewing atherosclerosis as an inflammatory disease provides a more comprehensive understanding of this association. Chronic immune activation, immune-complex deposition, endothelial damage, oxidative stress, and the presence of antiphospholipid antibodies contribute to accelerated atherogenesis and thrombotic complications.

Given the high prevalence of subclinical disease, many cardiac manifestations remain undetected without dedicated evaluation. Consequently, routine cardiovascular assessment—including electrocardiography, echocardiography, and other noninvasive modalities—is essential in patients with SLE to identify early cardiac involvement and initiate timely management.

Considering these gaps and the clinical significance of cardiac abnormalities in SLE, the present prospective observational study was undertaken at a tertiary care centre. The objectives were: (1) to determine the prevalence and spectrum of cardiac manifestations in patients with SLE; (2) to analyse the clinical profile of SLE patients in relation to cardiac involvement; and (3) to assess the association of disease duration and disease activity with the presence of cardiac abnormalities.

This prospective observational study was conducted in the Department of Medicine at Himalaya Medical College and Hospital, Patna. All evaluations were carried out in the outpatient department, inpatient medical wards, and the Medical Intensive Care Unit (MICU). The study was carried out over a period of nine months, from October 2024 to June 2025, after obtaining prior approval from the Institutional Ethics Committee.

The sample size was estimated using the standard formula:

Where Z1−α/2 represents the standard normal deviate at a 90% confidence level (1.96), ppp denotes the anticipated prevalence of cardiac manifestations in SLE (taken as 50% based on Kini et al.), q=1−pq = 1-pq=1−p, and ddd signifies an absolute precision of 10%. The calculated sample size was 96; however, to improve statistical power and account for incomplete data, the sample size was rounded and finalized at 100 participants.

Patients diagnosed with systemic lupus erythematosus were screened for eligibility. Those fulfilling the EULAR/ACR classification criteria for SLE, aged above 12 years, and willing to provide written informed consent were included. Individuals with prior cardiovascular involvement attributable to causes other than SLE, and those with other autoimmune or overlap syndromes, were excluded to prevent diagnostic confounding.

After enrolment, each patient underwent a detailed clinical evaluation, including demographic profiling, disease history, and systemic examination to document organ involvement. Disease-related variables such as the time since diagnosis and total disease duration (calculated from the onset of first symptoms) were recorded.    Laboratory investigations, including complete blood counts, renal and liver function tests, inflammatory markers, and extended autoimmune serology, were documented from routine clinical reports. Cardiovascular evaluation included ECG and 2D echocardiography for all patients, while cardiac MRI was performed only when clinically indicated by the treating physician. Cumulative doses of medications frequently used in SLE, including corticosteroids, hydroxychloroquine, mycophenolate mofetil, azathioprine, and cyclophosphamide, were obtained from treatment records. Importantly, no additional investigations were performed solely for research purposes, ensuring that patient care remained unaffected.

All data were anonymised using unique identification codes, and patient confidentiality was maintained throughout the study. Informed consent was obtained in a language preferred by the patient or their guardian. Adolescents aged 12–18 years provided assent in addition to guardian consent, and a witness signature was taken for participants who were illiterate. No financial incentives were provided, and no additional cost was incurred by participants for partaking in the study.

Data entry and management were performed using Microsoft Excel 2010, and statistical analysis was conducted using SPSS version 21. Quantitative variables were summarised using mean, median, standard deviation, and interquartile ranges, while qualitative variables were expressed as frequencies and percentages. Associations between categorical variables and cardiac manifestations were examined using the Chi-square test or Fisher’s exact test, as appropriate. A p-value of <0.05 was considered statistically significant.

Demographic Information: Table 1 summarizes the demographic and baseline clinical profile of the 100 SLE patients included in the study. A clear female predominance was observed, with 88% of participants being women, while males accounted for 12%, consistent with the known higher prevalence of SLE among females in reproductive age groups. Age distribution showed that 43% of patients were ≤25 years, whereas 57% were older than 25 years, indicating that the disease affects both younger and older adults, though slightly more common in the latter. The mean age of the cohort was 30.1 ± 9.6 years, reinforcing the fact that SLE largely affects individuals in early adulthood. The mean disease duration was 24.8 ± 27.4 months, reflecting a wide variability in chronicity among patients. The mean SLEDAI score of 15.6 ± 5.1 demonstrates that a significant proportion of the cohort had moderate to high disease activity at presentation.

Table 1: Demographic and Baseline Characteristics (N = 100)

Clinical Parameters – System Involvement and Outcomes

Table 2 details the spectrum of clinical symptoms observed across various organ systems. Among general symptoms, fever (70%), headache (54%), and photosensitivity (49%) were the most commonly reported, followed by weight loss in 36% and edema feet in 27%, reflecting active systemic inflammation and multisystem involvement typical of SLE. Respiratory symptoms included breathlessness (37%) and cough (32%), suggesting concurrent pulmonary or cardiovascular involvement. Cardiovascular symptoms were also significant, with palpitations reported in 53% and chest pain in 8%, indicating possible pericardial or conduction abnormalities. CNS symptoms showed seizures in 17%, psychosis in 4%, and focal deficits in 4%, suggestive of neuropsychiatric lupus in a subset of patients. Gastrointestinal complaints included nausea/vomiting (24%) and abdominal pain (13%), while dysphagia was relatively uncommon (6%). Musculoskeletal symptoms, particularly arthralgia (39%) and arthritis (11%), were also prominent features

Table 2: System-wise Clinical Presentation (N = 100)

Cutaneous and Mucocutaneous Manifestations: Table 3 presents the wide array of cutaneous and mucocutaneous findings observed in the cohort. Among rash types, malar rash was the most frequent (62%), aligning with its classic association with SLE, followed by maculopapular rash (6%), discoid lesions (4%), petechiae (4%), and severe forms such as TEN-like rash (3%). Subacute lupus rash was detected in 2% of patients, while 19% had no rash at all. Rash distribution patterns showed that the face was the most common site (61%), while extremities including arms (16%), legs (4%), and toes (9%) were less commonly involved. Scalp involvement was noted in 3%, and generalized rash in 2%.

Other cutaneous and mucocutaneous findings were also prevalent. Alopecia was seen in 84%, highlighting its strong association with active lupus. Oral/nasal ulcers were present in 58%, further contributing to disease activity scoring. Vasculitic ulcers (11%) and gangrene (9%) signify severe vascular involvement, while pallor (48%) reflects underlying anemia, a common hematologic manifestation of SLE. Lymphadenopathy was noted in 5%.

Table 3: Cutaneous and Mucocutaneous Manifestations (N = 100)

Cardiovascular and Respiratory Examination Findings: Table 4 highlights the clinical findings detected on cardiovascular and respiratory system examination. Cardiovascular examination revealed that the vast majority (95%) had no audible murmurs, whereas 2% had pansystolic murmurs, 1% exhibited a diastolic mitral murmur, and 2% showed a systolic murmur or loud P2, suggestive of possible valvular dysfunction or pulmonary hypertension. These findings correspond to known cardiac manifestations in SLE, including Libman–Sacks endocarditis, pericardial involvement, and pulmonary arterial hypertension.

Respiratory examination findings showed bilateral basal crepitations in 7% of patients, suggestive of underlying pleural disease or interstitial lung involvement. The remaining 93% had normal breath sounds, indicating that overt pulmonary findings were present only in a minority, despite respiratory symptoms reported in Table 2.

Table 4: Cardiovascular and Respiratory Examination Findings (N = 100)

Associated Systemic Manifestations (N = 100): Table 5 outlines the distribution of major systemic manifestations observed among the SLE patients. Pericarditis was present in 46%, while pericardial effusion was the most frequent cardiac manifestation, affecting 78% of the cohort, highlighting the strong cardiovascular involvement in SLE. Pleural involvement was less common, with pleural effusion and pleurisy each reported in 6% of patients. Musculoskeletal complaints were also notable: myalgia occurred in 52% and myositis in 13%, reflecting muscular inflammation as a common extrarenal feature. Hematological involvement was striking, with anemia documented in 88%, underscoring its high prevalence in active SLE. Neuropsychiatric lupus manifestations were present in a subset, with NPSLE-related seizures observed in 13% and cognitive impairment in 6% of patients

Table 5: Associated Systemic Manifestations (N = 100)

Autoantibody Profile (N = 100): Figure 1 summarises the autoantibody patterns in the study population. Anti-dsDNA positivity (44%) was the most common, consistent with its strong association with lupus activity and renal involvement. Anti-RNP/Sm and anti-Sm antibodies were present in 27% and 24% respectively, supporting the diagnosis of SLE and possible overlap syndromes. SSA (Ro) and SSB (La) antibodies were found in 21% and 8%, indicating a subset of patients at risk for photosensitivity, cutaneous lupus, and neonatal lupus. Anti-histone antibodies were positive in 15%, while nucleosome antibodies were seen in 11%, both of which correlate with disease activity. Ribosomal-P positivity (19%) reflects the subset prone to neuropsychiatric manifestations. Antiphospholipid markers such as ACLA (12%), β2-glycoprotein IgG/M (9%), and lupus anticoagulant (6%) suggest a smaller proportion with secondary antiphospholipid syndrome. Additionally, p-ANCA and Scl-70 were both detected in 6%, indicating occasional overlap with vasculitis and scleroderma-associated antibodies.

Figure 1: Autoantibody Profile (N = 100)

Association of Cardiac Involvement With Disease Parameters

Pericardial Effusion vs. Renal Involvement: Table 6 evaluates the association between pericardial effusion and renal involvement. Among patients with renal involvement (n=46), 40 patients (87%) had pericardial effusion, whereas only 6 (13%) did not. In contrast, among those without renal involvement (n=54), 38 patients (70%) had effusion, and 16 (30%) did not. The association between renal involvement and pericardial effusion was statistically significant (Chi-square = 4.82; p = 0.028).

Table 6: Pericardial Effusion vs Renal Involvement

Mean Disease Duration and SLEDAI in Relation to Pericardial Effusion: Table 7 compares the mean disease duration and SLEDAI score between patients with and without pericardial effusion. The mean disease duration was higher in the effusion group (25.9 ± 28.1 months) than in those without effusion (19.8 ± 23.2 months), though this difference was not statistically significant (p = 0.31), indicating that pericardial effusion may occur regardless of chronicity. In contrast, disease activity measured by SLEDAI was significantly higher in the effusion group (16.1 ± 5.2) compared to those without effusion (13.0 ± 4.7), with a p-value of 0.03, indicating a statistically meaningful association.

Table 7: Mean Disease Duration and SLEDAI

Systemic lupus erythematosus (SLE) is a chronic inflammatory autoimmune disorder that predominantly affects women of child-bearing age. Its prevalence ranges from 40–200 per 100,000 individuals, with higher rates in Black populations. Cardiac involvement is a major contributor to SLE morbidity, occurring in more than 50% of patients over the disease course. The risk of myocardial infarction is substantially elevated—up to nine times higher than the general population, and nearly fifty times higher compared with healthy women. Although cardiac manifestations are well recognized, the underlying pathogenesis is complex and involves immunological, inflammatory, and vascular mechanisms.

Autoimmune vascular injury in SLE predisposes to premature atherosclerosis, which, in addition to traditional coronary risk factors, contributes to cardiovascular morbidity. Pericarditis is the most frequent cardiac manifestation and typically presents as positional chest pain. Myocarditis is less common but significant for its potential to cause arrhythmias, ventricular dysfunction, or dilated cardiomyopathy. Coronary vasculitis is rare; however, accelerated ischemic coronary artery disease frequently presents atypically. Importantly, many cardiac manifestations remain clinically silent for prolonged periods, necessitating imaging modalities such as echocardiography for early detection. Given these complexities, understanding the burden of cardiac complications in SLE is essential.

The present study was conducted at a tertiary care hospital to investigate the spectrum of cardiac manifestations in SLE, describe the overall clinical profile, and analyse their relationship with disease duration and disease activity.

Demographic Characteristics: In this cohort, females constituted the majority (89.29%), giving a female-to-male ratio of 8.33:1—consistent with typical epidemiological trends. Over half of the patients (57.14%) were aged more than 25 years, and the mean age was 29.69 ± 9.98 years. Many were homemakers, reflecting prevalent socioeconomic demographics in Indian SLE populations.

Clinical Presentation: Patients demonstrated a wide variety of clinical features. Among general symptoms, fever (69.64%), headache (53.57%), and photosensitivity (48.21%) were frequent. Respiratory symptoms included cough (30.36%) and breathlessness (35.71%). Cardiovascular complaints such as palpitations (51.79%) and chest pain (7.14%) suggested possible pericardial or inflammatory involvement. Neuropsychiatric manifestations—seizures (16.07%), psychosis (3.57%), focal deficits (3.57%)—highlighted the presence of NPSLE in a notable subset.

Cutaneous and mucocutaneous involvement remained prominent: malar rash (60.71%), oral ulcers (51.79%), alopecia (87.5%), and vasculitic ulcers (10.71%). Rash types included discoid, maculopapular, petechial, and TEN-like lesions. Rash was most frequently located on the face (60.71%). Musculoskeletal manifestations included arthralgia (37.5%) and arthritis (8.93%).

Cardiac Manifestations in SLE: Cardiac involvement may affect the pericardium, myocardium, or endocardium. Pericarditis affects up to 25% of patients at onset or during relapses, while asymptomatic pericardial effusion may be present in up to 40%. Myocarditis is rare but has serious implications for cardiac function. Libman–Sacks endocarditis—which produces non-infective vegetations on valvular surfaces—affects approximately 10% of patients.

In the present study, pansystolic murmur, diastolic mitral murmur, and systolic murmurs (including loud P2) were each reported in 1.79% of patients. Pericardial effusion was significantly more prevalent in this cohort (80.36%) than the 40–55% reported in other studies, suggesting high disease activity. Other systemic features included myositis (12.50%), myalgia (50%), anemia (87.50%), mucosal ulcers (57.14%), alopecia (82.14%), and malar rash (62.50%).

Our findings are consistent with those of Doria et al. [11], who noted that pericarditis is the most common cardiac abnormality in SLE, followed by valvular lesions, myocardial dysfunction, and coronary involvement. Echocardiography is considered indispensable for detecting asymptomatic abnormalities and is recommended for periodic evaluation in SLE patients. Premature atherosclerosis, as noted in their work, is a leading cause of coronary artery disease (CAD) in SLE.

The prevalence of clinically manifest ischemic heart disease ranges between 8–16%, but subclinical CAD is far more common. Perfusion defects have been reported in up to 38% of adults and 16% of pediatric SLE patients. Using various noninvasive techniques, atherosclerosis has been detected in 28–40% of SLE patients and strongly correlates with age and disease duration.

Cardiac disease prevalence varies in the literature: Badui et al. reported a frequency of 70% [12], while Ostanek et al. reported 68% [13]. In comparison, our study documented cardiac abnormalities in 52% of patients. Pericardial involvement is the commonest lesion reported across multiple studies, with prevalence estimates ranging from 11–54%—consistent with findings from our cohort.

Badui et al. [12] observed that common cardiac complications included pericarditis/pericardial effusion (39%), arterial hypertension (22%), ischemic heart disease (16%), myocarditis (14%), heart failure (10%), pulmonary hypertension (9%), valvular disease (9%), pleural effusion (7%), and cerebrovascular accident (3%). These distributions mirror the multisystem involvement seen in our patients.

Associated Systemic Findings: Neurological manifestations included focal deficits (5.36%), NPSLE seizures (12.5%), psychosis (5.36%), cognitive impairment (5.36%), and headaches (17.86%). Vasculitic skin involvement—ulcers (10.71%) and gangrene (8.93%)—was also observed. Serositis in the form of pleurisy, pleural effusion, and pericarditis was common.

Immunological Profile: Autoantibody positivity patterns were consistent with classical SLE: RNP/Sm (26.79%), Sm (25%), SSA (19.64%), SSB (7.14%), Scl-70 (5.36%), PCNA (5.36%), dsDNA (42.86%), histone (14.29%), nucleosome (10.71%), and ribosomal-P antibodies (17.86%). Antiphospholipid antibodies were also present: ACLA (10.71%), β2-glycoprotein (14%), and lupus anticoagulant (5.36%). These findings reinforce the heterogeneity of serological profiles in SLE.

Disease Activity Index: The mean SLEDAI score was 15.21 ± 5.24, suggesting moderate to high disease activity. Higher SLEDAI scores were significantly associated with pericardial effusion (p = 0.025), although no significant relationship was observed with valvular involvement.

Correlation of Clinical Parameters With Cardiac Manifestations: Renal involvement showed a significant association with pericardial effusion (p = 0.028), indicating a possible parallel between multisystem involvement and cardiac complications. No significant associations were observed with specific autoantibodies (RNP, Sm, dsDNA) or hematologic abnormalities (leucopenia, thrombocytopenia).

Previous studies have shown inconsistent relationships between SLE disease activity and cardiac manifestations. Li et al. [14] reported an association between pulmonary arterial hypertension (PAH) and increased disease activity. Conversely, Huang et al. [15] found PAH to be more frequent in patients with lower SLEDAI scores. Some studies have shown correlations only with myocarditis and PAH, but not with valvular, pericardial, or coronary involvement.[16-22] This suggests that cardiac involvement in SLE does not always coincide directly with disease flares. Consistent with our findings, many authors have reported that cardiac abnormalities tend to coexist with renal and hematologic manifestations.

The present study demonstrates that cardiac involvement is highly prevalent among patients with systemic lupus erythematosus and frequently occurs in association with multisystem disease activity. Pericardial effusion emerged as the most common cardiac manifestation, occurring at a substantially higher frequency than reported in many earlier studies, suggesting more aggressive or active disease in our cohort. Higher SLEDAI scores were significantly associated with pericardial effusion, and renal involvement also showed a strong correlation, underscoring the interplay between systemic inflammation and cardiovascular complications.

Although murmurs and valvular abnormalities were less frequently detected clinically, their presence highlights the need for vigilant cardiovascular assessment, given the known propensity of SLE to cause subclinical myocardial, pericardial, and valvular disease. Autoantibody profiles did not show significant correlations with cardiac manifestations, reaffirming that serology alone cannot predict cardiovascular involvement.

Overall, the findings emphasize that cardiovascular evaluation should be an integral component of routine clinical monitoring in SLE, even in asymptomatic individuals. Early detection through echocardiography and careful assessment of disease activity may enable timely intervention and potentially reduce long-term morbidity. Further longitudinal studies are needed to clarify causal pathways and assess the prognostic significance of subclinical cardiac abnormalities in SLE.

CONFLICT OF INTEREST: NONE TO DECLARE

SOURCES OF FUNDING: NONE

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