Cardiovascular Manifestations of Systemic Lupus Erythematosus: An Overview

Systemic Lupus Erythematosus(SLE) is a multisystem autoimmune disease with variable presentations. A proposed mechanism for the etiology of SLE involves development autoantibodies that result from defect in apoptosis. The specific “find-me” (adenosine triphosphate [ATP]/uridine [UTP]) or “eat-me” (phosphatidylserine) signals activated upon release red cell nuclei. In absence apoptosis, nuclei break down, causing inflammation and contributing to autoimmunity. Many signs symptoms are caused by either circulating immune complexes direct effects antibodies on cells. genetic predisposition exists, concordance rate monozygotic twins between 25% 70%. If mother has SLE, her daughter’s risk developing 1:40, son’s 1:250. course consists intermittent remissions punctuated flares, organ damage often progresses over time. Pericarditis most frequent cardiac manifestation; it can be documented ECG, auscultation friction rub, evidence pericardial effusion. It usually responds anti-inflammatory therapy infrequently leads tamponade. More serious manifestations myocarditis fibrinous endocarditis Libman-Sacks. endocardial involvement lead valvular insufficiencies, commonly mitral aortic valves, embolic events. not been proven glucocorticoid other immunosuppressive therapies improve lupus endocarditis. Still, usual practice administer trial high-dose steroids appropriate supportive treatment heart failure, arrhythmia, As discussed above, patients at increased myocardial infarction, due accelerated atherosclerosis, which probably results attack, chronic inflammation, oxidative arteries.