Open Access Case Report Article ID: JCMC-3-128

    Aortic Valve Thrombosis in Antiphospholipid Syndrome Causing Coronary Artery Embolic Disease

    Jeremy R Burt*, Kimberly M Beavers and Vincent E Grekoski

    Antiphospholipid syndrome (APS) is a disorder characterized by the presence of anti-phospholipid antibodies which can include Lupus anticoagulant and Anticardiolipin antibody [1]. These antibodies bind to cardiolipin and have been shown in some cases to require β2- glycoprotein I in order to bind to cardiolipin [2]. Symptoms of this disorder include vascular thrombosis without inflammation in the vessel wall, premature birth, spontaneous abortion, and death in a morphologically normal fetus at or beyond the 10th week of gestation [1]. APS has a strong correlation to systemic lupus erythematosus (SLE) with studies showing that 30% of patients with SLE will develop APS; however, APS can still be found in patients without SLE at a low frequency [3].

    This disorder can cause cardiovascular complications which include marantic vegetation and valvular stenosis and/or regurgitation [1]. The exact mechanism of valve disease in APS is not fully understood, but the current belief is that there is an interaction between valve antigen and antiphospholipid antibodies which result in the observed thrombosis and valve thickening [4]. It is known that one third to one half of patients with APS have valve disease and that APS patients with valve disease have an increased risk for thromboembolic events [5].


    Published on: Aug 24, 2016 Pages: 32-34

    Full Text PDF Full Text HTML DOI: 10.17352/2455-2976.000028
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