The initial cause of LSE is poorly understood. LSE is thought to occur in the context of a hypercoagulable state which leads to endothelial injury and subsequent deposition of thrombi and inflammatory molecules in affected valves. The vegetations that are thus formed consist of immune complexes, platelet thrombi, fibrin, and mononuclear cells. The vegetations may dislodge and cause embolisms. Histopathology LSE involves formation of cardiac lesions that may take the form of vegetations or thickening of the valvular leaflets. The vegetations are small and formed from strands of fibrin, neutrophils, lymphocytes, and histiocytes. Vegetations are most often small-to-moderate in size (10mm). The mitral valve is typically affected, and the vegetations occur on the ventricular and atrial surface of the valve. Though the left-sided heart valves (mitral and aortic) are most commonly affected, any of the heart valves as well as adjoining structures may become involved.<unk><unk><unk>  lesions rarely produce significant valve dysfunction and the lesions only rarely embolize. However, there is data to suggest an association between<unk>  and a higher risk for embolic cerebrovascular disease in people with SLE.
Libman–Sacks endocarditis
Loeffler endocarditis
Nonbacterial thrombotic endocarditis
Infective endocarditis
Subacute bacterial endocarditis
Tuberculous pericarditis
Nocardiosis
Coronary artery aneurysm