OBJECTIVE: Cardiovascular mortality is increased in systemic lupus erythematosus (SLE). Increased plasma concentrations of N-terminal pro-brain natriuretic peptide (NT-proBNP) are associated with cardiovascular morbidity and mortality in the general population. We examined the hypothesis that NT-proBNP concentrations are higher in patients with SLE, and are related to inflammation, augmentation index, coronary atherosclerosis, and cardiovascular risk factors. METHODS: Serum concentrations of NT-proBNP were measured in 113 patients with SLE and in 80 control subjects. Coronary calcification and augmentation index were measured by electron beam computed tomography and noninvasive pulse wave analysis, respectively. RESULTS: Patients with SLE had higher concentrations of NT-proBNP [median 38.6 (interquartile range 2.5-126.9) pg/ml] than controls [11.7 (1.6-47.9) pg/ml] (p = 0.002). Augmentation index was higher in patients with SLE [25.0% (20.5%-31.5%)] than controls [20.5% (12.0%-29.0%)] (p = 0.04). In patients with SLE, NT-proBNP concentrations were associated with disease damage (rho = 0.31, p < 0.001) and duration (rho = 0.21, p = 0.02) but not with disease activity, C-reactive protein, erythrocyte sedimentation rate, tumor necrosis factor-alpha, interleukin 6, coronary calcium score, or augmentation index (all p > or = 0.18). CONCLUSION: Patients with SLE have increased concentrations of NT-proBNP, but this is not explained by atherosclerotic burden, augmentation index, or inflammatory state.
OBJECTIVE: Cardiovascular mortality is increased in systemic lupus erythematosus (SLE). Increased plasma concentrations of N-terminal pro-brain natriuretic peptide (NT-proBNP) are associated with cardiovascular morbidity and mortality in the general population. We examined the hypothesis that NT-proBNP concentrations are higher in patients with SLE, and are related to inflammation, augmentation index, coronary atherosclerosis, and cardiovascular risk factors. METHODS: Serum concentrations of NT-proBNP were measured in 113 patients with SLE and in 80 control subjects. Coronary calcification and augmentation index were measured by electron beam computed tomography and noninvasive pulse wave analysis, respectively. RESULTS:Patients with SLE had higher concentrations of NT-proBNP [median 38.6 (interquartile range 2.5-126.9) pg/ml] than controls [11.7 (1.6-47.9) pg/ml] (p = 0.002). Augmentation index was higher in patients with SLE [25.0% (20.5%-31.5%)] than controls [20.5% (12.0%-29.0%)] (p = 0.04). In patients with SLE, NT-proBNP concentrations were associated with disease damage (rho = 0.31, p < 0.001) and duration (rho = 0.21, p = 0.02) but not with disease activity, C-reactive protein, erythrocyte sedimentation rate, tumor necrosis factor-alpha, interleukin 6, coronary calcium score, or augmentation index (all p > or = 0.18). CONCLUSION:Patients with SLE have increased concentrations of NT-proBNP, but this is not explained by atherosclerotic burden, augmentation index, or inflammatory state.
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