NOT SO CLASSIC CORONARY CLOT: APLA SYNDROME PRESENTING AS ACUTE CORONARY SYNDROME L. Mile; M. Marak; M. Cannatella Department of Internal Medicine, LSU Health Sciences Center - Baton Rouge Introduction: Antiphospholipid antibody (APLA) syndrome, diagnosed by clinical and laboratory criteria, is often considered after unusual or recurrent clots. APLA is also frequently suspected in females of reproductive age with underlying autoimmune disease or recurrent miscarriage. The following is an unusual case of an older woman with multiple risk factors for coronary artery disease whose acute coronary syndrome (ACS) etiology was thrombophilia. Case: A 68 year old woman with a past medical history significant for morbid obesity, hypertension, type 2 diabetes mellitus, right middle cerebral artery (MCA) stroke, and remote DVT presented with acute typical chest pain. She was admitted for chest pain evaluation after initial ECG was reassuring and troponin was 0.0. Her repeat troponins at 6 and 12 hours were 5.0 and 25.0 respectfully, and left heart catheterization was performed on hospital day two. Angiography showed occlusions both in the distal left anterior descending and left circumflex artery concerning for possible dissection or clot. Hypercoagulable workup ensued. Her lupus anticoagulant and phospholipid IgM were positive while inpatient, and she was discharged on anticoagulation and aspirin. She was then lost to follow up for 7 months, at which time she presented with a new left MCA stroke. Repeat APLA antibody testing was persistently positive (beta-2 glycoprotein, phospholipid, and lupus anticoagulant). She also had developed pancytopenia and nonscarring alopecia in the six-month interim. Immunologic testing for systemic lupus erythematosus (SLE) was positive, and she was diagnosed with SLE and APLA syndrome. Discussion: This case illustrates the unusual etiology of thrombophilia as the cause of a non-ST elevation myocardial infarction (NSTEMI) in a patient with multiple risk factors for coronary disease. Additionally, her clotting disorder was likely the initial manifestation of her
causes infection in immunocompromised individuals. Given that patient is at a low risk for aspiration and that she is currently known to be immunocompetent, it is unusual that patient presents with both Strepgordonii and Cryptococcus infections.
SLE, and she did not meet the clinical criteria (SLICC criteria) until seven months after her acute clotting event. There is a paucity of evidence for the role of immunomodulatory agents in APLA syndrome without SLE, and in the absence of clinical criteria of SLE there was not an indication for serologic SLE testing. Recognition of concomitant SLE and APLA is paramount to early initiation of immunomodulatory agents to control antibody production and decrease cardiovascular risk.
28 J LA MED SOC | VOL 171 | NO. 1
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