Rheumatology International

, Volume 27, Issue 1, pp 115–116

Premature myocardial infarction in a young woman with systemic lupus erythematosus


    • Department of Clinical Immunology and RheumatologyAnkara University School of Medicine
  • Türkan Mete
    • Department of Clinical Immunology and RheumatologyAnkara University School of Medicine
Letter to the Editor

DOI: 10.1007/s00296-006-0209-1

Cite this article as:
Düzgün, N. & Mete, T. Rheumatol Int (2006) 27: 115. doi:10.1007/s00296-006-0209-1


Premature myocardial infarctionYoung womanSystemic lupus erythematosus


Cardiovascular disease is a major cause of mortality in systemic lupus erythematosus (SLE). It may consist of pericarditis, myocarditis, endocarditis, and may affect coronary arteries. Most often, cardiac involvement is subclinical. Clinically significant cardiac lesions are limited [1, 2] Coronary artery disease may develop due to vasculitis, premature atherosclerosis or antiphospholipid antibodies in SLE. Premature atherosclerosis is the most frequent cause of coronary artery disease in the patients. The early onset and severity of atherosclerosis in various rheumatic diseases were described with experimental and clinical studies [3]. A significant correlation was found between SLE and premature or accelerated coronary atherosclerosis [4]. However, the mechanisms of premature atherosclerosis associated with SLE are still unknown.

Here, we present a young female patient with SLE, who developed myocardial infarction, the leading cause of her death.

Case report

A 30-year-old female who was known to have had SLE for 6 years, presented with dispne, palpitation and bilaterally oedema at lower extremities. She had taken steroid irregularly on her own. On examination, it was found she had tachycardia with high blood pressure (170/100 mmHg), pallor, alopesia, digital vasculitis and small ischaemic lesions on hand fingers, livedo reticularis on extremities and bilateral pitting oedema. Physical examination of the thorax showed a soft systolic murmur at the mitral area with normal heart sounds, and bilaterally decreased chest sounds over the lower lobes. Laboratory investigations showed normocytic normochromic anemia (hemoglobin 9.5 g/l), elevated erythrocyte sedimentation rate (100 mm/h) and impaired renal functions (blood urea nitrogen 82 mg/dl, serum creatinin 3.5 mg/dl). Serum albumin was 2.4 g/l. There was proteinuria (2.120 mg/day), with urine microscopy showing red blood cells and casts. ANA, anti-ds-DNA and p-ANCA were strongly positive, anti-phospholipid antibodies were negative, complement levels were low, C-reactive protein was 9.5 mg/dl (normal 0–5 mg/dl). Serum total cholesterol, LDL and HDL cholesterol and trigliserid were in lower than normal values

Chest radiography showed a bilaterally pleural effusion. “ST” changes were seen on precordial derivations of electrocardiogram. Echocardiography showed moderately enlarged heart cavities and a limited hypokinesia on inter ventricular septum. No pericardial effusion was present. Treatment was started with pulse cylophosphamide (750 mg/m2) and prednisolon (60 mg/day). Clinical improvement was observed within 3 weeks. Oedema on lower extremities regressed, digital vasculitis resolved; small necrotic zones became demarcated and autoamputated. Pleural effusion, hematological and serological abnormalities regressed. Her prednisolone dosage was decreased to 50 mg/day. She developed atypical chest pain. EKG, creatinin kinase-MB (CK-MB) and troponin levels were monitorised. EKG showed negative “T” valves. CK-MB level did not change, troponin level showed a trend towards an increase and nitrogliserin was started. Coronary angiography was not done, because of serum creatinin level was still high. CK-MB and troponin levels continued to a significant increase and EKG revealed inferior myocardial infarction pattern. She developed cardio-pulmonary arrest and died.


Premature coronary artery disease is a major cause of illness and death in patients with SLE. The prevalence of coronary-artery atherosclerosis in the patients is elevated, and the age at onset is reduced [5]. Bruce et al. reported that overall SLE patients have a five to sixfold increased risk of coronary heart disease and this excess risk is especially pronounced in younger women where the excess risk may be >50-fold [6]. Recently severe coronary atherosclerosis resulting in angina pectoris and/or myocardial infarction in young adults has been reported in SLE. [7, 8].

Coronary artery disease may develop due to vasculitis which should be treated with high-dose steroid. In the case of our patient, angina pectoris and myocardial infarction occurred while she was taking steroid treatment, at the same time period, digital vasculitis on hand fingers responded good to high dose steroid. This evidence may indicate that coronary disease is not due to coronary arteritis, but this probability cannot be excluded. Corticosteroid treatment may trigger atherosclerotic vascular disorder or this patient may present both coronary arteritis and early atherosclerosis. The role of steroids is not completely clear, low steroid doses may have a beneficial anti-inflammatory role whereas higher doses may exacerbate metabolic factors [6].

Various factors such as systemic hypertension, dyslipidemia, obesity, smoking, duration of therapy with glucocorticoids, inflammation and hypercoagulability associated with anticardiolipin antibodies are implicated in premature atherosclerosis [9, 10].

Here, the young female patient with SLE had some known possible contributing factors such as hypertension, smoking, steroid therapy, except hyperlipidemia and anticardiolipin antibodies, to precipitate premature coronary artery and myocardial disease. However, these certain risk factors alone do not fully explain the excess risk observed [6]. This patient had no the clinical manifestations of antiphospholipid syndrome such as recurrent fetal loss, cardiac valvular abnormalities, neurological manifestations, hematologic abnormalities as well as the presence of anticardiolipin antibodies.

Inflammation is thought to play an important role in both the pathogenesis of SLE, as well as atherosclerotic vascular disease [11]. Atherosclerosis is considered to be a chronic inflammatory disorder, and C reactive protein, a marker of systemic inflammation, is known as an independent prognostic marker for cardiovascular disease. This patient had high level of C reactive protein before myocardial infarction.

In this young SLE patient, there were both uncontrolled systemic inflammation and traditional risk factors including hypertension, smoking and corticosteroid usage which might contribute to myocardial infarction process. In the early stage of life, coronary artery disease in patients with SLE may indicate negative prognosis as that of this patient.

Copyright information

© Springer-Verlag 2006