LETTER T. Ku¨ru¨ m Æ M. Soy Æ E. Karahasanog˘lu G. O ¨ zbay Æ N. C. Sayin A case of primary antiphospholipid syndrome who developed acute myocardial infarction followed by early-onset pre-eclampsia Received: 24 May 2002 / Accepted: 25 August 2002 Ó Clinical Rheumatology 2003 Primary antiphospholipid syndrome (PAPS) is a non- inflammatory autoimmune disease associated with an increased risk of vascular thrombosis [1]. Here we de- scribe a 29-year-old woman with PAPS who developed acute myocardial infarction (MI) followed by an early- onset pre-eclampsia (EOPE), who was treated by thrombolytic therapy. The patient was admitted to the emergency unit with acute chest pain radiating to her left shoulder for 4 h. Her medical history consisted of pregnancy ending in spontaneous labour 4 years ago, and a first-trimester abortion 2 years ago. In addition, she had developed EOPE, characterised by hypertension (180/120 mmHg), oedema, ascites, proteinuria (6 g/day) and severe fetal growth retardation that ended with medical abortion 4 weeks ago. There was no premature ischaemic heart disease (IHD) or autoimmune rheumatic disease in her family. Her ECG (Fig. 1) showed acute anterior wall MI. Serum creatine kinase MB (CK-MB) and troponin-I levels were 12.2 ng/ml (N: 0–4.3) and 12.4 ng/ml (N: 0–1), respectively. Medical therapy including tissue plasmi- nogen activator (tPA) was begun. ST segment elevations were lowered, the chest pain diminished and reperfusion arrhythmia (accelerated idioventricular rhythm) appeared in the second hour of the tPA therapy. On angiography the coronary arteries were found to be normal, but anteroseptal and apical hypokinesia was observed. Transthoracic echocardiography demonstrat- ed moderate severe mitral regurgitation, decreased midseptal and apicoseptal wall motion. ESR was 64 mm/h and CRP was 1.25 mg/dl. CBC and C3, C4, serum urea, creatinine, ALT, AST, albumin, globins, triglycerides, total and HDL, LDL and VLDL choles- terols levels were within normal limits. No proteinuria was detected on urine analysis. In further examinations Clin Rheumatol (2003) 22: 160–161 DOI 10.1007/s10067-002-0674-1 T. Ku¨ru¨m (&) Æ M. Soy Æ E. Karahasanog˘lu, G. O ¨ zbay Æ N. C. Sayin Trakya University Faculty of Medicine, Department of Cardiology, 22030, Edirne, Turkey Tel.: +90 535 396 19 64 Fax: +90 284 235 27 30 e-mail: turhankurum1@superonline.com DI DII DIII aVR aVL aVF V1 V2 V3 V4 V5 V6 Fig. 1 Electrocardiogram of the limb and precordial leads of the patient on admission. Note the ST segment elevations in V2–V6 precordial leads