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N-Terminal Pro-Brain Natriuretic Peptide in Systemic Lupus Erythematosus: Relationship with Inflammation, Augmentation Index, and Coronary Calcification

CECILIA P. CHUNG, JOSEPH F. SOLUS, ANNETTE OESER, INGRID AVALOS, DANIEL KURNIK, PAOLO RAGGI, and C. MICHAEL STEIN

ABSTRACT.

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-α, interleukin 6, coronary calcium score, or augmentation index (all p ≥ 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. (First Release June 1 2008; J Rheumatol 2008;35:1314-9)

Key Indexing Terms:

SYSTEMIC LUPUS ERYTHEMATOSUS
ATHEROSCLEROSIS
N-TERMINAL PRO-BRAIN NATRIURETIC PEPTIDE


From the Departments of Medicine, Pharmacology, and Molecular Physiology, Vanderbilt University, Nashville, Tennessee; and the Department of Medicine, Division of Cardiology, Emory University, Atlanta, Georgia, USA.

Supported by grants HL04012, HL65082, and GM5M01-RR00095 from the National Institutes of Health and by grants from the Lupus Foundation of America, Nashville Chapter, and the Lupus Clinical Trials Consortium. Dr. Avalos is supported in part by a grant from the American College of Rheumatology.

C.P. Chung, MD, MPH; A. Oeser, BS; D. Kurnik, MD; C.M. Stein, MD, Departments of Medicine and Pharmacology; I. Avalos, MD, Department of Medicine; J.F. Solus, PhD, Department of Molecular Physiology, Vanderbilt University; P. Raggi, MD, Department of Medicine, Division of Cardiology, Emory University.

Address reprint requests to Dr. C.P. Chung, Divisions of Rheumatology and Clinical Pharmacology, Vanderbilt University School of Medicine, T-3219 MCN 1161 21st Ave. South, Nashville, TN 37232-6248. E-mail: c.chung@vanderbilt.edu

Accepted for publication February 7, 2008.




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