Libman-Sacks endocarditis affects patients with systemic lupus erythematosus (SLE). Small granular vegetations consisting of fibrin develop on the undersurface of the leaflets of mitral and aoic valves. Fragments of vegetations may detach, resulting in embolism. Eventually, vegetations heal by organization of fibrin and subsequent fibrosis, leading to distoion of valve leaflets and resultant insufficiency or stenosis. The pathogenesis is unclear but is probably related to thrombotic diathesis. Hemorrhagic pericarditis is usually a consequence of tuberculosis or metastatic spread of cancer to the pericardium. An exudate containing blood accumulates in the pericardial sac, producing pain and a characteristic auscultatory phenomenon known as a pericardial rub. SLE is associated instead with fibrinous pericarditis, which also manifests with chest pain and pericardial rub. Infective endocarditis is prevalent in patients with damaged or prosthetic valves and in intravenous drug abusers. It is associated with formation of bulky, friable vegetations that consist of masses of fibrin, neutrophils, and bacteria. Such vegetations cause extensive destruction of valve leaflets and may release fragments into the bloodstream, with resultant septic embolism. There is no association between SLE and mitral valve prolapse, which is a frequent, usually asymptomatic, valvular abnormality that occurs in 2% to 3% of the general population. Mitral valve prolapse is also associated with Marfan syndrome. Complications include sudden death, thromboembolism, and mitral regurgitation. Ref: Kaul M.S., Tapson V.F., St. Clair E. (2011). Chapter 89. Rheumatologic Diseases and the Cardiovascular System. In V. Fuster, R.A. Walsh, R.A. Harrington (Eds), Hurst's The Hea, 13e.