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Tomas L'.,University of P.J. Šafarik | Lazurova I.,University of P.J. Šafarik | Pundova L.,University of P.J. Šafarik | Oetterova M.,University of P.J. Šafarik | And 3 more authors.
Clinical Rheumatology | Year: 2013

Tumor necrosis factor alpha (TNF-alpha) plays an important role in the pathogenesis of chronic inflammatory diseases, i.e., rheumatoid arthritis (RA), ankylosing spondylitis (AS), Crohn's disease (CD), and ulcerative colitis (UC). Anti-TNF-alpha strategies are successfully used in their treatment. However, their effect on heart function is still uncertain. The objectives of the study were to examine the acute and long-term effect of infliximab on the heart morphology and function in patients with chronic inflammatory disorders. Thirty-one patients (21 men and 10 women) were included. Ten percent of them were diagnosed with RA, 22.5% with AS, 22.5% with CD, and 45% with UC, respectively. Nterminal fragment of pro-brain natriuretic peptide (NTproBNP) was measured before and immediately after infliximab administration at the beginning of the study and in the sixth and 12th months. Echocardiography was performed at baseline and in the sixth and 12th months. There was a significant increase in NT-proBNP after the first infliximab infusion (88.40±14.09 vs. 95.24±14.28 pg/ml, p=0.0046) and similar response was detected after each infusion in the sixth and 12th months. Plasma NT-proBNP slightly but not significantly decreased (88.40±14.09 vs. 81.74±23.14 pg/ml, p=0.583, and 88.40±14.09 vs. 56.83±17.77 pg/ml, p=0.0576, in the sixth and 12th months, respectively). There were no significant changes in echocardiographic structural and functional parameters of the left ventricle during followup. Plasma NT-proBNP mildly but significantly increases immediately after infliximab infusion. However, long-term infliximab administration does not deteriorate both cardiac morphology and function. © Clinical Rheumatology 2012.

Tomas L.,University of P.J. Šafarik | Lazurova I.,University of P.J. Šafarik | Oetterova M.,University of P.J. Šafarik | Pundova L.,University of P.J. Šafarik | And 2 more authors.
Wiener Klinische Wochenschrift | Year: 2013

Objectives: Congestive heart failure (CHF) and inflammation are important contributors to the excess of overall morbidity and mortality in patients with rheumatoid arthritis (RA). CHF rather than ischaemic heart disease (IHD) appears to participate on the mortality in these patients. However, there are controversial results about significance of plasma N-terminal of pro-B type natriuretic peptide (NT-proBNP) and other inflammatory markers investigation for an early detection of heart dysfunction. The aim of this study was to examine the cardiac morphology and function in patients with RA in relation to the plasma NT-proBNP and to inflammatory markers. Subjects and methods: Sixty patients with RA (52 women and 8 men) and 30 gender and age matched controls were included in the study. Blood samples were analyzed for NT-proBNP, tumor necrosis factor alpha (TNF-alpha), interleukin 6 (IL-6), and C-reactive protein (CRP). Transthoracic echocardiography was performed on the same day in all subjects. Results: RA patients had significantly higher plasma NT-pro BNP as compared with controls (99.39 ± 8.98 vs. 66.90 ± 7.93 pg/ml, p < 0.05) and significantly higher levels of TNF-alpha, IL-6 and CRP (for all p < 0.01). In RA group higher levels of NT-proBNP were detected in rheumatoid factor (RF) posivite patients. Patients with RA had significantly worse left ventriclular (LV) systolic function (LV ejection fraction (LVEF) 64.6 ± 0.8 vs. 70.1 ± 1.3 %, p < 0.01) and diastolic function (E/A 1.11 ± 0.05 vs. 1.32 ± 0.07, p < 0.05). There were no correlations of NT-proBNP with paramaters of systolic and diastolic function, however, a negative correlation of TNF-alpha with these parameters was detected (TNF-alpha vs. LV mass index (LVM-i): r = - 0.34, p < 0.05), TNF-alpha vs. LVEF: r = - 0.30, p < 0.05 and TNF-alpha vs. E/A: r = - 0.30, p < 0.05). Conclusion: We conclude that TNF-alpha may be better marker of heart impairment caused by chronic inflammation in RA patients than NT-proBNP. © 2013 Springer-Verlag Wien.

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