Left ventricular morphology and function in patients with rheumatoid arthritis

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. 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. 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 = -aEuro parts per thousand 0.34, p < 0.05), TNF-alpha vs. LVEF: r = -aEuro parts per thousand 0.30, p < 0.05 and TNF-alpha vs. E/A: r = -aEuro parts per thousand 0.30, p < 0.05). We conclude that TNF-alpha may be better marker of heart impairment caused by chronic inflammation in RA patients than NT-proBNP.