INTRODUCTION: We evaluated the impact of tumor necrosis factor alpha (TNF-α) inhibition on left ventricular torsion (LVtor) in patients with rheumatoid arthritis (RA) using speckle-tracking echocardiography (STE). METHODS: Thirty-eight RA patients without cardiovascular disease and 30 healthy subjects were enrolled in the study. Twenty patients received infliximab, a monoclonal antibody against TNF-α, and 18 patients received increasing doses of prednisolone for 180 days. Global systolic longitudinal strain (G-LS), global systolic radial strain (G-RS) and global systolic circumferential strain (G-CS) were determined by STE. LV basal and apical rotations from the base and apex were obtained and used for calculation of LVtor. Pre-treatment LVtor levels were compared with LVtor levels after therapy in both treatment groups. RESULTS: RA patients had lower G-LS (-16.5 ± 2.9; p<0.01), G-RS (37.6 ± 1.5; p<0.01) and higher GCS (-23.6 ± 3.5; p=0.04) compared with control subjects (-20.0 ± 2.8, 40.7 ± 4.8, -22.4 ± 2.5, respectively; p<0.01). LVtor levels were significantly higher in RA patients compared to controls (16.4 ± 2.7 vs. 15.1 ± 2.5; p=0.04), which might be attributed to higher values of apical rotation (9.7 ± 2.4 vs. 8.8 ± 2.3; p=0.01). Patients treated with infliximab experienced a significant decrease in LVtor (p=0.04), and a significant increase in G-LS (p<0.01) and G-RS (p<0.01). No significant changes were observed among patients treated with prednisolone. Percentage changes in LVtor were correlated with percent changes in C-reactive protein CRP (r=0.58; p<0.01), disease activity score (r=0.78; p<0.01), and G-LS (r=-0.40; p=0.04) in patients treated with infliximab. CONCLUSIONS: RA is characterized by increased LVtor. Long term TNF-α inhibition improves LV longitudinal and radial systolic deformation and decreases LVtor.
INTRODUCTION: We evaluated the impact of tumor necrosis factor alpha (TNF-α) inhibition on left ventricular torsion (LVtor) in patients with rheumatoid arthritis (RA) using speckle-tracking echocardiography (STE). METHODS: Thirty-eight RApatients without cardiovascular disease and 30 healthy subjects were enrolled in the study. Twenty patients received infliximab, a monoclonal antibody against TNF-α, and 18 patients received increasing doses of prednisolone for 180 days. Global systolic longitudinal strain (G-LS), global systolic radial strain (G-RS) and global systolic circumferential strain (G-CS) were determined by STE. LV basal and apical rotations from the base and apex were obtained and used for calculation of LVtor. Pre-treatment LVtor levels were compared with LVtor levels after therapy in both treatment groups. RESULTS:RApatients had lower G-LS (-16.5 ± 2.9; p<0.01), G-RS (37.6 ± 1.5; p<0.01) and higher GCS (-23.6 ± 3.5; p=0.04) compared with control subjects (-20.0 ± 2.8, 40.7 ± 4.8, -22.4 ± 2.5, respectively; p<0.01). LVtor levels were significantly higher in RApatients compared to controls (16.4 ± 2.7 vs. 15.1 ± 2.5; p=0.04), which might be attributed to higher values of apical rotation (9.7 ± 2.4 vs. 8.8 ± 2.3; p=0.01). Patients treated with infliximab experienced a significant decrease in LVtor (p=0.04), and a significant increase in G-LS (p<0.01) and G-RS (p<0.01). No significant changes were observed among patients treated with prednisolone. Percentage changes in LVtor were correlated with percent changes in C-reactive protein CRP (r=0.58; p<0.01), disease activity score (r=0.78; p<0.01), and G-LS (r=-0.40; p=0.04) in patients treated with infliximab. CONCLUSIONS:RA is characterized by increased LVtor. Long term TNF-α inhibition improves LV longitudinal and radial systolic deformation and decreases LVtor.