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.
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.
Authors: Carlos A Roldan; Wilmer L Sibbitt; Clifford R Qualls; Rex E Jung; Ernest R Greene; Charles M Gasparovic; Reyaad A Hayek; Gerald A Charlton; Kendall Crookston Journal: JACC Cardiovasc Imaging Date: 2013-09