Primary Stenting in a Patient with Acute Myocardial Infarction and Primary Antiphospholipid Syndrome

Antiphospholipid syndrome (APS) is an uncommon thrombotic disorder characterized by antiphospholipid antibodies (aPL). The syndrome may be associated with arterial or venous thrombosis, thrombocytopenia, recurrent fetal loss, skin lesions, neurological complications and retinal occlusion.1 Premature myocardial infarction may also be seen as a part of APS. In coronary artery bypass graft (CABG) operations and coronary balloon angioplasty (PTCA), APS may lead to complications such as bypass graft closure2 and early failure of PTCA.3,4 Although the patients with APS frequently have positive lupus anticoagulant activity, only a minority of these patients have satisfying diagnostic criteria for systemic lupus erythematosis (SLE). Thus, APS without the clinical features of SLE is called primary antiphospholipid syndrome.5 We present a case of primary stenting in a patient with primary APS who had recurrent coronary thrombosis without any other thrombotic disorder. Case Report. A 38-year-old man who was referred to our center from another hospital was admitted to the coronary care unit (CCU) with chest pain and history of five times defibrillation within the last 2 hours. He had electrocardiography (ECG) performed 1 hour prior to admission; it showed ST-segment elevation in leads V2–6, I and aVL and ST-segment depression in leads III and aVF (Figure 1A). Anterior wall myocardial infarction was considered to be the diagnosis based upon this ECG. The patient had no history of heart disease and no risk factors except smoking. His blood pressure was 110/70 mmHg and heart rate was 70 beats/minute. Physical examination was completely normal. We performed a new ECG; it showed ST-segment elevation in II, III and aVF and ST-segment depression in I, aVL and V1–2 (Figure 1B). We diagnosed acute inferior wall myocardial infarction and administered intravenous streptokinase. We detected successful clinical reperfusion signs. The patient was treated with aspirin, beta-blocker and heparin after thrombolytic therapy. After an uneventful follow-up period, we performed coronary angiography on the tenth day of admission. Left main coronary artery (LMCA) was normal, the proximal left anterior descending coronary artery (LAD) had eccentric plaque, the circumflex artery was normal and the right coronary artery (RCA) showed moderate (50–70%) stenosis in the mid-segment. Left ventriculography was normal. We planned an exercise stress test to evaluate the significance of the stenosis in the RCA and discharged the patient. The patient was re-admitted 5 days later with atypical chest pain. There were no diagnostic ECG changes during chest pain. Exercise stress test was performed 2 days later. There were no clinical symptoms or significant changes in ST segment during the treadmill period. During the recovery phase, he suffered severe chest pain and the monitor of the treadmill device showed ST-segment elevation in leads V2–6. Ventricular fibrillation then developed. After defibrillation and transfer to the CCU, ST-segment elevation was observed in II, III and aVF. We diagnosed acute inferior reinfarction and performed emergency coronary angiography. The RCA was totally obstructed at the point where we detected moderate stenosis in the previous angiography (Figure 2A) and the proximal LAD had subocclusive thrombus at the location where we detected eccentric plaque in the previous coronary angiography (Figure 2B). The patient underwent PTCA with successful recanalization. A few minutes after PTCA, we detected a new thrombus formation at the occlusion site and decided to implant a coronary stent. We finished the procedure after successful implantation of a 2.5 x 18 mm AVE GFX stent (Arterial Vascular Engineering, Inc., Santa Rosa, California). Ticlopidine 250 mg twice daily was added to treatment. We administered continuous intravenous heparin for 7 days after stent placement and performed a control angiography on day 7. The stent in the RCA was completely patent and the proximal LAD had only eccentric plaque. Because of the recurrence of myocardial infarction and thrombus formation in 2 different coronary arteries at the same time, additional blood tests were performed after the discontinuation of heparin. Results of routine biochemical tests, including lipid profile, hemoglobin and blood platelet count (220,000/mm3), were within normal limits. Prothrombin time and activated partial thromboplastin time were normal. Protein C, protein S and fibrinogen levels were normal. Antinuclear antibody, anti-DNA and lupus anticoagulant were negative. Biological syphilis test was negative. IgG aPL was 10 GPL units (normal,

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