Lupus (SLE) is a chronic autoimmune disease where the body’s immune system mistakenly attacks its own healthy tissues and organs, causing widespread inflammation. This systemic attack means that lupus can affect nearly any part of the body, including the skin, joints, kidneys, and nervous system. The inflammation significantly affects the cardiovascular system, making heart involvement a major concern for individuals living with SLE. Cardiovascular complications are a leading cause of illness and death in lupus patients, manifesting through two primary mechanisms: direct inflammatory damage to heart structures and accelerated long-term vascular risk.
Direct Inflammatory Damage to Heart Structures
Lupus-related inflammation can directly target the three layers of the heart: the outer lining, the muscle, and the inner valves. Pericarditis, the inflammation of the pericardium (the sac surrounding the heart), is the most common cardiac manifestation in lupus, affecting approximately 20% to 40% of patients. This condition typically causes a sharp chest pain that often worsens with deep breathing, coughing, or lying flat, and it is usually responsive to anti-inflammatory medication.
The heart muscle (myocardium) can also become inflamed in myocarditis, which occurs in an estimated 10% to 15% of symptomatic patients. Myocarditis weakens the heart’s pumping ability, potentially leading to heart failure, a rapid heartbeat, and shortness of breath. This serious complication requires immediate attention and aggressive immunosuppressive therapy to preserve cardiac function.
The inner lining of the heart and its valves can develop non-infectious growths, known as vegetations, in Libman-Sacks endocarditis. These sterile growths are composed of immune complexes, fibrin, and platelets, typically forming on the mitral and aortic valves. While often asymptomatic, these vegetations can lead to valve dysfunction, causing blood to flow backward (regurgitation) or narrowing the valve (stenosis).
The presence of these vegetations significantly increases the risk of embolic events, such as a stroke, if a piece breaks off and travels through the bloodstream. Echocardiographic studies suggest that Libman-Sacks endocarditis is present in about 11% to 15% of living SLE patients, with a higher prevalence in those who also have Antiphospholipid Syndrome.
Accelerated Vascular Risk in Lupus Patients
Beyond acute inflammatory conditions, lupus creates a chronic, systemic environment that dramatically speeds up atherosclerosis (the hardening and narrowing of the arteries). This accelerated atherosclerosis is a primary driver of long-term cardiovascular morbidity and mortality in SLE patients. Chronic systemic inflammation, a hallmark of lupus, damages the endothelial cells lining the blood vessels, promoting the buildup of fatty plaque.
This accelerated plaque formation puts young women with lupus at a disproportionately high risk, with one study suggesting they are up to 50 times more likely to experience a heart attack than women of a similar age without the disease. The traditional cardiovascular risk factors, such as high cholesterol and smoking, do not fully account for this extreme increase in risk, highlighting the specific role of the autoimmune process.
The risk is further compounded by common co-occurring conditions and treatment side effects. Lupus nephritis (kidney inflammation) can lead to hypertension, while the long-term use of corticosteroids, a common treatment for SLE, can also contribute to elevated blood pressure and cholesterol levels. Another significant factor is the frequent co-occurrence of Antiphospholipid Syndrome (APS), an autoimmune clotting disorder that increases the risk of blood clots, heart attacks, and strokes.
Identifying Cardiac Involvement
Recognizing cardiac involvement in lupus can be challenging because symptoms are often non-specific or even absent. The most noticeable symptom is typically chest pain, which can be sharp and positional in pericarditis, or feel like pressure or tightness if coronary arteries are affected. Patients may also experience unexplained shortness of breath, especially during physical activity, which can signal myocarditis or heart failure.
Other signs include heart palpitations, indicating an abnormal heart rhythm, and persistent fatigue that is disproportionate to their lupus disease activity. Because a significant portion of cardiac damage can occur without obvious symptoms, physicians rely on diagnostic tools for surveillance. An echocardiogram (ultrasound of the heart) is frequently used to visualize the heart’s structure, check for fluid, assess valve function, and measure the heart muscle’s pumping strength.
An electrocardiogram (EKG) helps detect rhythm abnormalities, while blood tests can measure inflammatory markers and specific autoantibodies associated with lupus. For more detailed imaging of the heart muscle and surrounding tissue, a Cardiac MRI may be employed. Regular monitoring, even in the absence of symptoms, is important because early detection allows for timely treatment intervention to prevent irreversible heart damage.
Treatment Strategies for Lupus-Related Heart Conditions
Treatment for lupus-related heart conditions involves a dual strategy: controlling the underlying autoimmune disease and managing the specific cardiac complication. Therapy rests on suppressing systemic inflammation with immunosuppressive medications. Hydroxychloroquine, an antimalarial drug, is routinely used for its general anti-inflammatory and potential cardioprotective effects, and is recommended for almost all lupus patients.
For active inflammatory conditions like pericarditis, nonsteroidal anti-inflammatory drugs (NSAIDs) or corticosteroids are often prescribed to quickly reduce inflammation, with colchicine sometimes added to prevent recurrence. Severe myocarditis requires high-dose corticosteroids, sometimes combined with other immunosuppressants like mycophenolate mofetil or cyclophosphamide, to resolve the acute muscle inflammation.
Managing the risk of accelerated atherosclerosis and clotting is equally important. This involves the aggressive control of traditional cardiovascular risk factors, including blood pressure and cholesterol, often with medications like statins and antihypertensives. Patients with a high risk of blood clots, particularly those with Antiphospholipid Syndrome, are often prescribed antiplatelet drugs like aspirin or anticoagulants to prevent heart attacks and strokes.