Jeremy R Burt*, Kimberly M Beavers and Vincent E Grekoski
Department of Radiology, Florida Hospital Orlando, USA
Received: 07 June, 2016; Accepted: 19 August, 2016; Published: 24 August, 2016
Jeremy R Burt, MD, Department of Radiology, Florida Hospital, 601 E Rollins Street, Orlando, FL, 32803, Tel: 407-303-8178; Fax: 407-303-9702l; E-mail:
Burt JR, Beavers KM, Grekoski VE (2016) Aortic Valve Thrombosis in Antiphospholipid Syndrome Causing Coronary Artery Embolic Disease. J Cardiovasc Med Cardiol 3(1): 032-034. DOI: 10.17352/2455-2976.000028
© 2016 Burt JR, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
CMR: Cardiac MR; TTE: Transthoracic Echocardiography; RI: Magnetic Resonance Imaging; CT: Computed tomography; APS: Antiphospholipid Syndrome; SLE: Systemic Lupus Erythmatosus
Antiphospholipid syndrome (APS) is a disorder characterized by the presence of antiphospholipid antibodies which are known to promote thrombus formation and heart valve complications. In this case, a 20 year old African American male presenting with chest pain was found to have APS as well as Budd-Chiari Syndrome. He was then evaluated through the use of cardiac magnetic resonance imaging and cardiac catheterization, which revealed an aortic valve thrombus as well as myocardial infarction from coronary artery emboli. This is the first time this condition has been documented in the literature and serves as an example of successful detection and treatment. The patient underwent coronary artery bypass grafting and the thrombus was surgically removed. The patient was discharged with lifelong prescription for anticoagulant medication.
Antiphospholipid syndrome (APS) is a disorder characterized by the presence of anti-phospholipid antibodies which can include Lupus anticoagulant and Anticardiolipin antibody . These antibodies bind to cardiolipin and have been shown in some cases to require β2- glycoprotein I in order to bind to cardiolipin . 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 . 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 .
This disorder can cause cardiovascular complications which include marantic vegetation and valvular stenosis and/or regurgitation . 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 . It is known that one third to one half of patients with APS have valve disease4 and that APS patients with valve disease have an increased risk for thromboembolic events .
Thromboembolic events commonly found in APS include deep vein thrombosis, stroke, pulmonary embolism, thrombosis of renal vessels, and livedo reticularis . Myocardial infarction is relatively uncommon in APS patients  and an APS case involving infarctions due to a coronary artery embolism from aortic valve thrombosis has not been previously published. In patients without APS, valvular disease is the third most common cause of coronary embolism. The only documented cases of coronary embolism due to aortic valve vegetation were caused by prosthetic heart valve complications .
In this study, a patient presenting with coronary artery embolic disease due to aortic valve thrombosis and APS is documented with cardiac MR (CMR).
A 20-year-old African American male with a history of migraine, pancreatitis and ulcerative colitis presented to the ER with acute chest pain, dyspnea, and vertigo. He had no history of heart attack or stroke. The patient underwent multiple tests including laboratory testing for troponin, anticardiolipin antibodies (aCL), lupus anticoagulant (LA), and anti-beta2-glycoprotein-1 (anti-B2GP1), blood counts, renal and liver function testing. He also had an EKG, cardiac catheterization, CMR, transthoracic echocardiography, and abdominal computed tomography (CT).
Laboratory tests revealed elevated troponin, thrombocytopenia, and elevated liver function tests. Electrocardiogram revealed significant ST segment depression in the anterolateral leads. The patient was admitted and underwent cardiac catheterization which showed long filling defects in the large first diagonal branch (Figure 1A,B) and distal right coronary arteries (Figure 1C) suspicious for embolic disease. The patient underwent transthoracic echocardiography which revealed mild mitral and tricuspid regurgitation with normal systolic function. No cardiac mass, vegetation or thrombus was identified.
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