Transesophageal and transthoracic echocardiography and Doppler-examinations in systemic lupus erythematosus

• Published in: Scandinavian journal of rheumatology 2001, Vol.30 (5), p.275-281
• Main Author: Omdal, Per Lunde, Knut Rasmussen, Svein Ivar Mellgren, Gunnar Husby, Roald
• Format: Article
• Language: English
• Subjects: Adrenal Cortex Hormones - adverse effects; Adrenal Cortex Hormones - therapeutic use; Adult; Aged; Aortic Valve - abnormalities; Aortic Valve - diagnostic imaging; Biological and medical sciences; Calcinosis - etiology; Cardiovascular system; Echocardiography, Doppler; Esophagus - diagnostic imaging; Female; Fibrosis; Heart Diseases - diagnostic imaging; Heart Diseases - etiology; Humans; Investigative techniques, diagnostic techniques (general aspects); Lupus Erythematosus, Systemic - complications; Lupus Erythematosus, Systemic - diagnostic imaging; Male; Medical sciences; Middle Aged; Mitral Valve - abnormalities; Mitral Valve - diagnostic imaging; Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis; Systemic Lupus Erythematosus Heart Disease Echocardiography; Ultrasonic investigative techniques
• ISSN: 0300-9742; 1502-7732
• DOI: 10.1080/030097401753180354

Objective : To search for cardiac abnormalities in systemic lupus erythematosus (SLE). Methods : 35 patients examined by 2-D transthoracal Doppler and transesophageal echocardiography. Results : Mitral and aortic valve abnormalities were seen in 12 patients (34%) respectively, and occurred altogether in 16 patients (46%). They were in general significantly associated with longer disease duration, but not with anticardiolipin antibodies (aCL), disease activity, or any other variable, except for time on corticosteroids, which was significantly longer in patients with aortic valve calcifications. Conclusion : Valve masses and valve thickening - often in combination - are the most frequent structural findings in SLE, occurring more often on the aortic than on the mitral valves. Factors other than antiphospholipid antibodies, medication, hypertension, or coronary heart disease seem to be responsible for this phenomenon. Drugs that modulate inflammation in endo- and pericardial tissue may, at least in part, be responsible for the observed mitral valve calcifications and pericardial fibrosis.