Recommended Citation
Gowda A, Solis J, Trier A, Noor A. Lupus Turmoil - Rare Cardiac Manifestations of SLE. Presented at Scientific Day; May 20, 2026; Milwaukee, WI.
Abstract
Introduction/Background:
Cardiac involvement in systemic lupus erythematosus (SLE) has variable manifestations. Pericarditis is the most common cardiac manifestation (20%), whereas myocarditis is rare, occurring in approximately 1–2% of cases. Cardiac tamponade is also rare, but possible in lupus pericarditis. Heart failure develops in 2-3% of patients. While stress cardiomyopathy can occur, sustained heart failure with reduced ejection fraction (HFrEF) due to inflammatory myocarditis is uncommon.
Description:
A 40-year-old woman with SLE complicated by lupus nephritis induced end-stage renal disease had multiple admissions for renal failure and progressive cardiac decline. Chest x-ray initially showed new, sudden onset cardiomegaly. Transthoracic ECHO (TTE) showed a large pericardial effusion with tamponade physiology and newly reduced ejection fraction (26%). Despite worsening ECHO features, she declined pericardiocentesis. Later admissions were marked by recurrent uremia, persistent large pericardial effusion, and worsening biventricular dysfunction despite intermittent hemodialysis, steroids, colchicine, and plasmapheresis. Later, she presented with fever, confusion, and severe cardiomegaly; echocardiography demonstrated LVEF of 18–19% with persistent effusion. Right and left heart catheterization revealed normal coronaries, elevated filling pressures, and low cardiac output. The patient was later amenable to pericardiocentesis; however, it was cancelled after interval reduction in effusion size following consistent dialysis. Cardiac MRI demonstrated extensive myocardial fibrosis, consistent with autoimmune myocarditis and acute pericarditis in SLE, confirming inflammatory lupus cardiomyopathy causing sustained HFrEF. She transitioned to guideline directed heart failure therapy.
Discussion:
This case shows rare cardiac manifestations of SLE: recurrent large pericardial effusion with tamponade physiology and persistent HFrEF. Although the patient’s tamponade can be attributed to either uremia or lupus pericarditis, her heart failure is due to autoimmune inflammatory myocarditis. New cardiomegaly in SLE should prompt timely evaluation of pericardial effusion and tamponade. Early rheumatologic management and initiation of dialysis are essential in patients with lupus nephritis and uremia. Cardiac MRI was critical in diagnosing autoimmune myocarditis over stress cardiomyopathy. Early recognition and multidisciplinary care are essential to improve outcomes in rare, high-risk cardiac complications of SLE.
Presentation Notes
Presented at Scientific Day; May 20, 2026; Milwaukee, WI.
Full Text of Presentation
wf_yes
Document Type
Poster
Open Access
Available to all.
Lupus Turmoil - Rare Cardiac Manifestations of SLE
Introduction/Background:
Cardiac involvement in systemic lupus erythematosus (SLE) has variable manifestations. Pericarditis is the most common cardiac manifestation (20%), whereas myocarditis is rare, occurring in approximately 1–2% of cases. Cardiac tamponade is also rare, but possible in lupus pericarditis. Heart failure develops in 2-3% of patients. While stress cardiomyopathy can occur, sustained heart failure with reduced ejection fraction (HFrEF) due to inflammatory myocarditis is uncommon.
Description:
A 40-year-old woman with SLE complicated by lupus nephritis induced end-stage renal disease had multiple admissions for renal failure and progressive cardiac decline. Chest x-ray initially showed new, sudden onset cardiomegaly. Transthoracic ECHO (TTE) showed a large pericardial effusion with tamponade physiology and newly reduced ejection fraction (26%). Despite worsening ECHO features, she declined pericardiocentesis. Later admissions were marked by recurrent uremia, persistent large pericardial effusion, and worsening biventricular dysfunction despite intermittent hemodialysis, steroids, colchicine, and plasmapheresis. Later, she presented with fever, confusion, and severe cardiomegaly; echocardiography demonstrated LVEF of 18–19% with persistent effusion. Right and left heart catheterization revealed normal coronaries, elevated filling pressures, and low cardiac output. The patient was later amenable to pericardiocentesis; however, it was cancelled after interval reduction in effusion size following consistent dialysis. Cardiac MRI demonstrated extensive myocardial fibrosis, consistent with autoimmune myocarditis and acute pericarditis in SLE, confirming inflammatory lupus cardiomyopathy causing sustained HFrEF. She transitioned to guideline directed heart failure therapy.
Discussion:
This case shows rare cardiac manifestations of SLE: recurrent large pericardial effusion with tamponade physiology and persistent HFrEF. Although the patient’s tamponade can be attributed to either uremia or lupus pericarditis, her heart failure is due to autoimmune inflammatory myocarditis. New cardiomegaly in SLE should prompt timely evaluation of pericardial effusion and tamponade. Early rheumatologic management and initiation of dialysis are essential in patients with lupus nephritis and uremia. Cardiac MRI was critical in diagnosing autoimmune myocarditis over stress cardiomyopathy. Early recognition and multidisciplinary care are essential to improve outcomes in rare, high-risk cardiac complications of SLE.
Affiliations
Aurora Sinai Medical Center, St. Luke's Medical Center