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. 2018 Feb 23;77(6):926–934. doi: 10.1136/annrheumdis-2017-212597

Figure 1.

Figure 1

Tg197 arthritis model develops tumour necrosis factor (TNF)-dependent left-sided heart valve disease which leads to left ventricle (LV) dysfunction. (A, B) Representative images of H&E and Masson’s trichrome-stained transverse heart sections showing the aortic valve (AV) (A) and the mitral valve (MV) (B) leaflets of Tg197 and WT littermate animals at 12 weeks old of age; (scale bar, 400 μm) (C) Comparison of the AoV and MV thickness between WT, Tg197 and Tg197 treated with anti-TNF infliximab (Remicade) animals at 11–12 weeks of age (data are presented as individual values, with mean±SEM; *P<0.02; **P<0.01). (D) Blood aortic (AoV) and mitral velocities (MV E and A) acquired by Doppler analysis of Tg197 mice and WT littermates at their 12 weeks of age (left and right panels, respectively; data are presented as individual values, with mean±SEM; ***P<0.0001). (E) Ejection fraction (EF%) of Tg197 mice and WT littermates at their 12 weeks of age, calculated by the modified Simpson equation, using 2D images in echocardiography analysis (data are presented as individual values, with mean±SEM; ***P<0.0001). (F) Representative ECGs of Tg197 animals with few minutes interval (four consecutive time points with ~1 min interval, starting from the upper panel), at their 12 weeks of age. AVR, aortic valve root; WT, wild type.