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Cardiovascular manifestations of systemic lupus erythematosus
Insights
Systemic lupus erythematosus (SLE) significantly impacts cardiac function, leading to increased cardiovascular risks. Understanding and treating these cardiac issues in SLE patients is crucial for improving survival rates.
Area of Science:
- Cardiology
- Rheumatology
- Immunology
Background:
- Systemic lupus erythematosus (SLE) is associated with significant cardiovascular morbidity and mortality.
- Pathologically, SLE involves pancarditis affecting the pericardium, myocardium, endocardium, and coronary arteries.
Purpose of the Study:
- To review the cardiovascular manifestations of SLE.
- To discuss the pathological findings and clinical underdiagnosis of cardiac involvement in SLE.
- To explore the impact of treatments, including steroids, on cardiovascular outcomes.
Main Methods:
- Review of autopsy and clinical studies on cardiovascular involvement in SLE.
- Analysis of reported prevalence of various cardiac conditions in SLE patients.
- Examination of treatment strategies and their associated risks.
Main Results:
- High autopsy prevalence of pericarditis (mean 62%) and myocarditis (mean 40%) in SLE, often underdiagnosed clinically.
- Libman-Sacks lesions (mean 43%) and infective endocarditis (1.1-4.9%) are noted.
- Coronary disease, valvular disease (e.g., aortic insufficiency, mitral regurgitation), hypertension (14-69%), and heart failure (5-44%) are common. Steroid use may exacerbate some cardiovascular issues.
Conclusions:
- SLE significantly affects cardiac function, with high rates of pericarditis and myocarditis often missed clinically.
- Various cardiac complications, including coronary and valvular disease, hypertension, and heart failure, are prevalent in SLE.
- Improved diagnosis and management of cardiovascular manifestations are essential for enhancing SLE patient survival, despite potential treatment-related risks.
Abstract:
SLE affects most aspects of cardiac function, and recent studies have reported increasing cardiovascular morbidity and mortality. Pathologically, SLE is characterized by a pancarditis involving pericardium, myocardium, endocardium, and coronary arteries. In autopsy series, pericarditis has been found in 43% to 100% (mean 62%, Table I), and myocarditis was found in 8% to 78% (mean 40%, Table II), but both have been underdiagnosed clinically. Libman-Sacks lesions have been noted in 25% to 100% (mean 43%) and infective endocarditis in 1.1% to 4.9% of clinical and autopsy studies (Table III). Coronary disease may be due to arteritis, which should be treated with high-dose steroids, or it may be due to atherosclerosis, which is amenable to medical or surgical therapy. Valvular disease has been treated surgically, but with a combined surgical mortality as high as 25%. Aortic insufficiency and mitral regurgitation are the most common valvular problems, although aortic and mitral stenosis have also been reported. Hypertension has been noted in 14% to 69%, and heart failure in 5% to 44%. Evidence for a lupus cardiomyopathy, which may be subclinical, is reviewed. While steroids may ameliorate SLE pancarditis, they have also been associated with hypertension, LV hypertrophy, purulent and constrictive pericarditis, mitral regurgitation, and perhaps accelerated atherosclerosis. It remains to be seen if improved diagnosis and treatment of the cardiovascular manifestations of SLE can enhance survival.