Abstract 1997: Systemic Lupus Erythematosus Increases Left Ventricular Mass Independent of Traditional Stimuli to Hypertrophy
INTRODUCTION: Systemic lupus erythematosus (SLE) is associated with premature atherosclerosis and vascular stiffening, however whether SLE alters left ventricular (LV) structure and function independent of valvular and clinical coronary disease is unknown.
HYPOTHESIS: SLE leads to LV hypertrophy due to preclinical atherosclerosis and/or vascular stiffening.
METHODS: Patients with SLE without clinical or echocardiographic evidence of coronary or significant valvular disease (n = 173) were age and gender matched to 173 control subjects. All subjects underwent echocardiography to quantify LV structure and function, carotid ultrasonography to detect atherosclerosis, and radial applanation tonometry to measure arterial stiffness. Disease aspects (serologic markers, clinical features, inflammatory mediators, treatment) were evaluated.
RESULTS: SLE patients and controls were similar in body size, hypertension and diabetes status, smoking, and cholesterol. Mean septal wall thickness (.88 vs. .85 cm), end-diastolic diameter (5.0 vs. 4.7 cm), LV mass (144 vs. 124 gm or 38.3 vs. 32.8 gm/m2.7), ejection fraction (71 vs. 67%), and prevalence of LV hypertrophy (20 vs. 10%) were higher in SLE patients than in controls (all p < 0.01). LV mass in normotensive SLE patients and hypertensive controls was comparable; the combination of SLE and hypertension further increased LV mass. In multivariate analysis, disease status (SLE vs. control, p < 0.001) was an important correlate of LV mass, independent of age, BMI, diabetes and hypertension. Among SLE patients, arterial stiffness index (p = 0.017) was independently related to LV mass, in addition to other known stimuli to hypertrophy (diabetes, hypertension, BMI, all p < 0.01). Carotid atherosclerosis, SLE duration, SLE damage index, creatinine and homocysteine were significantly related to LV mass in univariate but not multivariate analyses with relevant covariates.
CONCLUSIONS: LV systolic function is preserved in SLE patients without concom-mitant coronary or valvular disease. In contrast, LV mass is increased in SLE independent of traditional stimuli to hypertrophy (possibly due to inflammation-related arterial stiffening) but these stimuli provoke even greater LV hypertrophy in the presence of SLE.