Background/Purpose: Cardiovascular disease plays a central role in morbidity and mortality in rheumatic patients. N-terminal pro-brain natriuretic peptide (NT-proBNP) is a strong marker of cardiovascular risk with recent evidence that inflammation may also influence its levels. The discrimination of this confounding variable is of particular interest in rheumatic diseases. Therefore, we evaluated NT-proBNP in ankylosing spondylitis (AS) patients pre- and post-TNF blockage therapy to determine the possible association between NT-proBNP levels and inflammatory parameters.

Methods: Forty-five consecutive AS patients without previous/current cardiovascular disease or systolic myocardial dysfunction, who were eligible to anti-TNF therapy, were prospectively enrolled. All patients received TNF blockers (infliximab, adalimumab and etanercept in their regular schedule) and they were evaluated for circulating NT-proBNP levels, clinical and laboratory parameters of disease activity including BASDAI, ASDAS, ESR and CRP, traditional cardiovascular risk factors including blood pressure, body mass index, waist circumference and dyslipidemia; conventional and tissue Doppler imaging echocardiography and treatment data at baseline (BL) and six months after (6M). Statistical analysis included: Spearman rank order correlation, Mann-Whitney test or t-test to observe differences between patients with high or normal NT-proBNP levels at BL; paired-sample t tests or the Wilcoxon signed-rank test to observe differences between measurements at BL and 6M; Fisher exact test to compare categorical variables and multivariable linear regression analysis. All analyses used a two-sided significance level of 0.05.

Results: At BL, all patients had active AS, NT-proBNP levels had a median of 36 (20-72)pg/ml and 11% were high in spite of no systolic alteration. Multiple linear regression analysis revealed that this peptide, at BL, was independently correlated with ESR (p<0.001), age (p=0.01) and pulse pressure (p=0.01). After 6M, all disease parameters improved and NT-proBNP levels were significantly reduced [24 (16-47) pg/mL, p=0.037] compared to BL. Changes in NT-proBNP were positively correlated with ESR changes (r=0.41, p=0.006). Cardiovascular risk factors remained stable during follow-up.

Conclusion: Elevations of NT-proBNP should be interpreted with caution in active AS patients with no evidence of cardiovascular disease. The short-term reduction of NT-proBNP levels in these patients treated with anti-TNF therapy appears to reflect an improvement in inflammatory status. (ClinicalTrials.govnumber:NCT01072058).

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ACR Meeting Abstracts - https://acrabstracts.org/abstract/nt-probnp-and-inflammation-in-active-ankylosing-spondylitis-receiving-tnf-blockers-is-there-a-link/