Etanercept normalises left ventricular mass in patients with rheumatoid arthritis. Issue 6 (7th August 2012)

• Record Type: Journal Article
• Authors: Daïen, Claire Immediato; Fesler, Pierre; du Cailar, Guilhem; Daïen, Vincent; Mura, Thibault; Dupuy, Anne-Marie; Cristol, Jean-Paul; Ribstein, Jean; Combe, Bernard; Morel, Jacques
• Is Part Of: Annals of the rheumatic diseases. Volume 72:Issue 6(2013)
• Page Start: 881
• Page End: 887
• Publication Date: 2012-08-07
• Subjects: Rheumatism -- Periodicals; 616.723005
• DOI: 10.1136/annrheumdis-2012-201489
• Languages: English
• ISSNs: 0003-4967

Abstract

Abstract : Background: Cardiovascular mortality is increased in patients with rheumatoid arthritis (RA). RA is associated with an increased left ventricular mass index (LVMI), a strong marker of cardiovascular mortality, and vessel abnormalities. Experimental studies have suggested that tumour necrosis factor α (TNFα) may induce LV hypertrophy. Objective: To study the effect of medium-term (3- and 6-months) treatment with the TNFα inhibitor etanercept (ETN) and synthetic disease-modifying antirheumatic drugs (sDMARDs) on LV morphological features and arterial stiffness in patients with RA. Methods: Consecutive female patients with active RA requiring treatment with ETN (n=28) or sDMARDs (n=20) were included. Clinical and biological monitoring, echocardiography and pulse wave velocity (PWV) assessment were performed at inclusion and at 3 and 6 months after the start of treatment. Paired t tests and multivariate linear regression analysis were used. Results: Mean LVMI tended to be higher at baseline in the ETN group than in the sDMARD group (96.5±19.8 vs 84.3±26.8 g/m 2 ; p=0.11 for the ETN and sDMARD groups, respectively). In patients with ETN treatment, mean LVMI was significantly decreased at 3 and 6 months (−6.3±7.6 and −14.2±9.3 g/m 2 ; p<0.001), with no change from baseline for patients with sDMARD treatment (−2.2±10.9 and −2.7±10.2 g/m 2, respectively). Blood pressure (BP) and aortic PWV were not changed by either treatment. Conclusions: ETN induced a significant decrease in LVMI with medium-term treatment with no change in BP or PWV. TNFα may be an important factor of LV hypertrophy, which may explain the benefit of TNF inhibitors on cardiovascular morbidity and mortality in RA. These results need to be confirmed by larger studies and with other TNF inhibitors.