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.