title: Cardiac valvular abnormalities are frequent in systemic lupus erythematosus patients with manifest arterial disease.
abstract: The objective of this study was to study cardiac valve morphology and function and ventricular function in systemic lupus erythematosus (SLE) patients with and without co-existing cardiovascular disease (CVD) and in population controls. Twenty-six women (52 +/- 8.2 years) with SLE (SLE cases) and a history of CVD (angina pectoris, myocardial infarction, cerebral infarction or intermittent claudication) were compared with 26age-matched women with SLE but without manifest CVD (SLE controls) and 26 age-matched control women (population controls). Echocardiographywas performed to assess valvular abnormalities and manifestations of ischaemic heart disease. Thirteen of the 26 SLE cases but only one of the SLE controls and one of the population controls had cardiac valvular abnormalities. Three of the SLE cases had already undergone valve replacement and another had significant aortic insufficiency; the other nine had thickening of mainly mitral leaflets without hemodynamic significance. Among SLE cases, patients with valvular abnormalities had higher homocysteine (P < 0.001) and triglyceride (P = 0.02) concentrations than patients without valvular disease. In contrast atherosclerosis as determined by IMT, oxidized LDL as measured by the monoclonal antibody E06, autoantibodies against epitopes of OxLDL (aOxLDL) or phospholipids (aPL), disease duration or activity, or acute phase reactants did not differ between SLE cases with or without valvular abnormalities. Valvular abnormalities were not more common in SLE cases with stroke as compared to those with myocardial infarction, angina or claudication. In conclusion, valvular abnormalities are strongly associated with CVD in SLE. Raised levels of homocysteine and triglycerides characterize patients with cardiac valve abnormalities.
authors.affiliation: Cardiovascular Laboratory, Department of Medicine, Karolinska Institute at Karolinska Hospital, Stockholm, Sweden. kerstinju@telia.com
authors.forename: K
authors.initials: K
authors.lastname: Jensen-Urstad
authors.forename: E
authors.initials: E
authors.lastname: Svenungsson
authors.forename: U
authors.initials: U
authors.lastname: de Faire
authors.forename: A
authors.initials: A
authors.lastname: Silveira
authors.forename: J L
authors.initials: JL
authors.lastname: Witztum
authors.forename: A
authors.initials: A
authors.lastname: Hamsten
authors.forename: J
authors.initials: J
authors.lastname: Frostegård
mesh_terms: D000210:Acute-Phase Reaction; D000328:Adult; D001161:Arteriosclerosis / Q000453:epidemiology* / Q000473:pathology; D001323:Autoantibodies; D002784:Cholesterol / Q000097:blood; D015331:Cohort Studies; D004452:Echocardiography; D005260:Female; D006349:Heart Valve Diseases / Q000000981:diagnostic imaging / Q000453:epidemiology* / Q000473:pathology; D006710:Homocysteine / Q000097:blood; D006801:Humans; D006976:Hypertension, Pulmonary / Q000453:epidemiology / Q000473:pathology; D008077:Lipoproteins, LDL / Q000097:blood / Q000276:immunology; D008180:Lupus Erythematosus, Systemic / Q000453:epidemiology* / Q000473:pathology; D008875:Middle Aged; D012307:Risk Factors; D014280:Triglycerides / Q000097:blood; D018487:Ventricular Dysfunction, Left / Q000000981:diagnostic imaging / Q000453:epidemiology / Q000473:pathology; D018497:Ventricular Dysfunction, Right / Q000000981:diagnostic imaging / Q000453:epidemiology / Q000473:pathology
chemical_list: D001323:Autoantibodies; D008077:Lipoproteins, LDL; D014280:Triglycerides; C099252:oxidized low density lipoprotein; D006710:Homocysteine; D002784:Cholesterol