Case Presentation: A 37 year old female with a past medical history of Hypertension, Ischemic Cardiomyopathy (EF=40-45%), Systemic Lupus Erythematosus, and Antiphospholipid Antibody Syndrome presented to the Emergency Department with complaints of pleuritic chest pain that had been persistent for two days duration which radiated down her left arm. Initial laboratory workup noted a normal BMP & CBC. Troponin was noted to be elevated at 0.25 ng/mL. Lipid profile (LDL=72) was within normal limits as was A1C (5.3). Initial ECG was concerning for ST-elevation MI in the lateral leads(V2-V4) with no bundle branch block. Chest X-ray was unremarkable, however bedside ECHO noted a depressed ejection fraction of 40% with wall motion abnormality in the distribution of the LAD. A CT-Angiogram of the chest was performed to rule out aortic dissection. The patient was emergently transferred to the cardiac cath lab for percutaneous coronary intervention with drug-eluting stent placement. Cardiac cath noted a mid-LAD lesion that was 99% occluded. She tolerated the procedure well and was discharged to home on Ticagrelor and Aspirin.
Discussion: Systemic Lupus Erythematous is notoriously known for being the “great imitator” due to it’s ability to affect any organ system. Antiphospholipid Antibody syndrome commonly presents in the setting of Lupus and is associated with the formation of vascular thrombosis. In this case, the patient waited two days before receiving medical attention. A large retrospective analysis showed Antiphospholipid Syndrome was responsible for 100,000 of myocardial infarctions (MIs) in the United States annually, or nearly 4% of MIs. Given the patient in this case had no obvious traditional risk factors ,a delay in diagnosis and treatment could have been fatal given her delay in seeking care. A high index of suspicion of life threatening thrombosis is critical in these patients for the potential for favorable outcome.
Conclusions: Antiphospholipid Antibody Syndrome is a systemic autoimmune disease characterized by a hypercoagulable state commonly associated with recurrent pregnancy loss. However, there are other common clinical manifestations ranging from neurological involvement to cardiac involvement. Antiphospholipid antibodies have an ability to induce endothelial activation which can ultimately lead to development of accelerated atherosclerosis. We present a case of an otherwise healthy young female presenting with a myocardial infarction secondary to her antiphospholipid antibody syndrome due to plaque rupture in her mid-left anterior descending (LAD) artery.