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Antiphospholipid Antibody Syndrome Causing Acute Myocardial Infarction in a Young Adult Benjamin Sussman, DO, B

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Antiphospholipid Antibody Syndrome Causing Acute Myocardial Infarction in a Young Adult Benjamin Sussman, DO, B Osteopathic Family Physician (2010) 2, 139-143 Antiphospholipid antibody syndrome causing acute myocardial infarction in a young adult Benjamin Sussman, DO, B. Brent Simmons, MD From the Department of Family and Community Medicine, Hahnemann University Hospital, Drexel University College of Medicine, Philadelphia, PA KEYWORDS: Myocardial infarction (MI) is more frequent in patients older than 45 years of age; however, it can occur Myocardial infarction; in young patients and it is important to include in the differential diagnosis of chest pain. In this case, Antiphospholipid a 29-year-old male presented to the emergency department with chest pressure. Electrocardiography antibody syndrome; revealed an acute ST elevation MI. The patient was found to have a mixed hypercoagulability disorder, Factor V Leiden; including antiphospholipid (aPL) antibody syndrome, which led to the infarction. aPL antibody Hypercoagulable state; syndrome is a common cause of acquired hypercoagulability in the general population. It is a clinical Anticoagulation; syndrome characterized by repeated arterial and venous thrombosis, recurrent fetal loss, and positive Young adult antibody tests. Asymptomatic patients with low titer aPL antibodies require no treatment. Asymptom- atic patients with moderate to high titer aPL antibodies are managed with low-dose aspirin, as are patients with a history of pregnancy-related complications. Patients with more severe manifestations, such as venous or arterial thrombosis, are managed with lifelong administration of warfarin. © 2010 Elsevier Inc. All rights reserved. Case report ach” felt fine. He denied any allergies. He was a nonsmoker, denied any illicit drug use, and was a social drinker. His A 29-year-old male presented to the emergency department father developed hypertension in his 60s, and his maternal with a two-day history of progressively increasing chest grandfather had coronary disease diagnosed in his 70s. He pain. He stated the pain was left-sided, substernal, and denied any family history of premature or sudden death of began while he was sitting. The pain at presentation was a anyone younger than age 55. 10 out of 10 on a pain scale and associated with nausea, At arrival to the emergency department, he was pale, sweating, shortness of breath, and radiation to his left arm diaphoretic, and tachycardic at 110 bpm, which then slowed and jaw. He denied fever, chills, abdominal pain, dizziness, to 83 bpm after a few minutes. His blood pressure was blurry vision, or headaches. It was described as dull in 110/70, respiratory rate was 22 breaths/min, temperature nature and felt like “a piano was sitting on my chest.” All was 98.5°F, and his oxygen saturation was 100% on room other review of systems was negative. He denied any trauma air. There was no peripheral edema and all his pulses were to his chest. He had never experienced chest pain like this. normal. Heart auscultation was regular without any mur- He had a past medical history of ulcerative colitis, which murs, rubs, or gallops. His lungs were clear without any was in remission, and he was supposed to be taking sul- fasalazine, but admitted he rarely used it because his “stom- rhonchi or rales. His abdominal, neurological, and rectal examinations were all normal. A portable chest x-ray was clear. A 12-lead electrocardiogram was performed and Corresponding author: Dr. Benjamin M. Sussman, Department of Family showed sinus rhythm with ST-segment elevation in the and Community Medicine, Drexel University College of Medicine, 10 Shurs Lane, Suite #203, Philadelphia, PA 19127. anterior precordial leads (Fig. 1). He was given aspirin, E-mail address: [email protected]. nitroglycerin sublingual tablets followed by intravenous 1877-573X/$ -see front matter © 2010 Elsevier Inc. All rights reserved. doi:10.1016/j.osfp.2010.06.008 140 Osteopathic Family Physician, Vol 2, No 5, September/October 2010 Figure 1 A 12-lead electrocardiogram showing sinus rhythm with ST-segment elevation in the anterior precordial leads. (IV) nitroglycerin, IV heparin, and eptifibatide. While this two days later he was resting comfortably when he com- was being done, the physician covering the acute myocar- plained again of chest pain. He then suffered a ventricular dial infarction (MI) service was alerted. fibrillation cardiac arrest while in the ICU and was success- The patient’s initial troponin I level was 10.27. His initial fully resuscitated. He was intubated during the cardiac arrest basic metabolic panel was unremarkable, as was his urine and, after recovering, was not able to be extubated. Fourteen analysis, prothrombin time, partial thromboplastin time, and weeks after his initial labs, lupus anticoagulant was still international normalized ratio (INR). He had a leukocyte positive as was a high titer B2-glycoprotein-I antibody (an count of 16.3 and a hemoglobin and hematocrit of 12.1 and antiphospholipid [aPL] antibody). Unfortunately, he contin- 35.9, respectively. His urine drug screen was negative for ued to have recurrent deep vein thrombosis while in the ICU phencyclidine, benzodiazepines, cocaine, amphetamines, and he eventually died from a pulmonary embolism. The tetrahydrocannabinol, opiates, and barbiturates. family declined an autopsy. The patient was taken to the catheterization lab, where he was found to have a near 100% occluded left anterior descending artery and a 90% occlusion of his right coronary arteries. Cardiac stenting was attempted but was unsuccess- Discussion ful because of the density of the clot. The cardiologist successfully performed a thrombectomy of his left anterior When approaching a patient such as this, it is vital to descending artery clot. His IV heparin was continued understand the differential diagnosis of MI in young adults. throughout the hospitalization. An echocardiogram per- The causes of MI in adults younger than 45 years can be formed later that morning showed a 40% ejection fraction divided into four groups: (1) atheromatous coronary artery and slight septal wall motion abnormalities. Because of his disease, (2) non atheromatous coronary artery disease, (3) young age, more laboratory tests were ordered for anaylsis, MI related to substance abuse, and (4) hypercoagulable which were run from his initial “preheparin” treatment, states.1 including lupus anticoagulant, factor V Leiden, prothrombin Atheromatous coronary disease begins in childhood. In a gene mutation, proteins C and S levels, homocysteine level, study of 760 young adults who died of various causes, and factor VIII levels. advanced coronary disease was found in 20% of men and While he was recovering in the intensive care unit (ICU), 8% of women between the ages of 30 and 34 years.2 The his hypercoagulable laboratory results returned. His factor etiology of atheromatous coronary artery disease in young V Leiden was heterozygous and he was positive for the persons is similar to older individuals, with high lipids, lupus anticoagulant. Antithrombin III, proteins C and S, diabetes, and smoking being major risk factors.1 Nonathe- homocysteine level, factor VIII level, and anti-nuclear an- romatous coronary artery disease can be caused by congen- tibody were normal. His chest pain had been resolved and ital abnormalities, such as myocardial bridging (a tunneling Sussman and Simmons Antiphospholipid Antibody Syndrome and Acute MI in a Young Adult 141 phenomenon that can result in arterial constriction) and aPL antibodies are found among young, otherwise coronary artery aneurysm.3 The third major cause—recre- healthy people at a prevalence of 1% to 5% for both anti- ational drug use—is common among young patients. Co- cardiolipin antibodies and lupus anticoagulant antibodies.8 caine use was found to be associated in 48% of young adults Among patients presenting with thrombosis, the prevalence who presented to the emergency department with nontrau- of aPL antibodies is much higher, in the range of 4% to matic chest pain.4 Patients with cocaine-related MI cannot 21%.7 Among patients with aPL antibodies, the absolute be distinguished clinically from other causes. Therefore, risk of developing new thrombosis is low (1% per year) in patients who lack cardiac risk factors, especially young otherwise healthy patients without prior thrombotic events; patients, should have urine cocaine screening routinely per- may be moderately increased (up to 10% per year) in formed. women with recurrent fetal loss without prior thrombosis; The fourth cause—hypercoagulability—is a rare but im- and is highest (10% in the first year) in patients with a portant cause of MI in young people, as illustrated in this case. history of venous thrombosis who have discontinued anti- 7 The differential diagnosis of the hypercoagulable state can be coagulant drugs within 6 months. Finally, among patients divided into congenital and acquired. Congenital causes in- with systemic lupus erythematosus, the prevalence of aPL clude antithrombin III deficiency, protein C deficiency, protein antibodies can be as much as 30% for anticardiolipin anti- 8 S deficiency, homocystinuria, dysfibrinogenemias, hyperlipid- bodies and as much as 34% for the lupus anticoagulant. emia, and factor V Leiden mutation.5 Acquired causes include The clinical spectrum of disease for aPL antibody syn- oral contraceptive use, lupus anticoagulant, myeloproliferative drome varies. It can present as vascular events, systemic disorders, essential thrombocythemia, polycythemia vera, par- manifestations (eg, livedo reticularis, thrombocytopenia, oxysmal
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