Cardiac Involvement in Systemic Lupus Erythematosus

Abstract

Publisher Summary Systemic lupus erythematosus (SLE) is a chronic inflammatory disease with a still undefined etiology, characterized by the production of autoantibodies and autoreactive T cells which can trigger an inflammatory process in various organ systems. Among these, the most affected ones are skin, musculoskeletal, hematopoietic and nervous system, kidney, lung, blood vessels, and heart. All the cardiac structures can be involved: pericardium, endocardium and valves, myocardium, coronary arteries, and conduction tissue. Pericarditis is one of the most characteristic manifestations of the disease and is included in the American Rheumatism association (ARA)/American College of Rheumatism (ACR) classification criteria for SLE. The prevalences of valvular verrucae and thickening observed in transthoracic and transesophageal echocardiography are reported in the chapter. There are two major pathogenetic hypothesis. The primum movens could be represented by a thrombus. According to this hypothesis, antiphospholipid antibodies (aPL) and anti-endothelium antibodies could bind to endothelial cells, which lead to their activation and, in turn, platelet aggregation and thrombus formation. Alternatively, the primum movens could be immune complex deposition between the endothelium and the basal membrane, followed by the infiltration of inflammatory cells.