Inmaculada del Rincón1, Joseph F Polak2, Daniel H O'Leary2, Daniel F Battafarano3, John M Erikson4, Jose F Restrepo1, Emily Molina1, Agustín Escalante1. 1. Division of Rheumatology and Clinical Immunology, Department of Medicine, The University of Texas Health Science Center at San Antonio, Texas, USA. 2. Ultrasound Reading Center, Tufts Medical Center, Boston, Massachusetts, USA. 3. Brooke Army Medical Center, Fort Sam Houston, Texas, USA. 4. Division of Cardiology, Department of Medicine, The University of Texas Health Science Center at San Antonio, Texas, USA.
Abstract
OBJECTIVE: To estimate atherosclerosis progression and identify influencing factors in rheumatoid arthritis (RA). METHODS: We used carotid ultrasound to measure intima-media thickness (IMT) in RA patients, and ascertained cardiovascular (CV) risk factors, inflammation markers and medications. A second ultrasound was performed approximately 3 years later. We calculated the progression rate by subtracting the baseline from the follow-up IMT, divided by the time between the two scans. We used logistic regression to identify baseline factors predictive of rapid progression. We tested for interactions of erythrocyte sedimentation rate (ESR) with CV risk factors and medication use. RESULTS: Results were available for 487 RA patients. The mean (SD) common carotid IMT at baseline was 0.571 mm (0.151). After a mean of 2.8 years, the IMT increased by 0.050 mm (0.055), p≤0.001, a progression rate of 0.018 mm/year (95% CI 0.016 to 0.020). Baseline factors associated with rapid progression included the number of CV risk factors (OR 1.27 per risk factor, 95% CI 1.01 to 1.61), and the ESR (OR 1.12 per 10 mm/h, 95% CI 1.02 to 1.23). The ESR×CV risk factor and ESR×medication product terms were significant, suggesting these variables modify the association between the ESR and IMT progression. CONCLUSIONS: Systemic inflammation and CV risk factors were associated with rapid IMT progression. CV risk factors may modify the role of systemic inflammation in determining IMT progression over time. Methotrexate and antitumour necrosis factor agents may influence IMT progression by reducing the effect of the systemic inflammation on the IMT. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.
OBJECTIVE: To estimate atherosclerosis progression and identify influencing factors in rheumatoid arthritis (RA). METHODS: We used carotid ultrasound to measure intima-media thickness (IMT) in RApatients, and ascertained cardiovascular (CV) risk factors, inflammation markers and medications. A second ultrasound was performed approximately 3 years later. We calculated the progression rate by subtracting the baseline from the follow-up IMT, divided by the time between the two scans. We used logistic regression to identify baseline factors predictive of rapid progression. We tested for interactions of erythrocyte sedimentation rate (ESR) with CV risk factors and medication use. RESULTS: Results were available for 487 RApatients. The mean (SD) common carotid IMT at baseline was 0.571 mm (0.151). After a mean of 2.8 years, the IMT increased by 0.050 mm (0.055), p≤0.001, a progression rate of 0.018 mm/year (95% CI 0.016 to 0.020). Baseline factors associated with rapid progression included the number of CV risk factors (OR 1.27 per risk factor, 95% CI 1.01 to 1.61), and the ESR (OR 1.12 per 10 mm/h, 95% CI 1.02 to 1.23). The ESR×CV risk factor and ESR×medication product terms were significant, suggesting these variables modify the association between the ESR and IMT progression. CONCLUSIONS:Systemic inflammation and CV risk factors were associated with rapid IMT progression. CV risk factors may modify the role of systemic inflammation in determining IMT progression over time. Methotrexate and antitumour necrosis factor agents may influence IMT progression by reducing the effect of the systemic inflammation on the IMT. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.
Authors: H G Raterman; A E Voskuyl; S Simsek; M W J Schreurs; I M W van Hoogstraten; M J L Peters; V P van Halm; B A C Dijkmans; P Lips; W F Lems; M T Nurmohamed Journal: Eur J Endocrinol Date: 2013-10-21 Impact factor: 6.664
Authors: Alfonso Corrales; José A Parra; Carlos González-Juanatey; Javier Rueda-Gotor; Ricardo Blanco; Javier Llorca; Miguel A González-Gay Journal: Ann Rheum Dis Date: 2013-07-13 Impact factor: 19.103
Authors: Inmaculada Del Rincón; Ken Williams; Michael P Stern; Gregory L Freeman; Daniel H O'Leary; Agustín Escalante Journal: Arthritis Rheum Date: 2003-07
Authors: Alfonso Corrales; Carlos González-Juanatey; María E Peiró; Ricardo Blanco; Javier Llorca; Miguel A González-Gay Journal: Ann Rheum Dis Date: 2013-03-16 Impact factor: 19.103
Authors: Diane E Bild; David A Bluemke; Gregory L Burke; Robert Detrano; Ana V Diez Roux; Aaron R Folsom; Philip Greenland; David R Jacob; Richard Kronmal; Kiang Liu; Jennifer Clark Nelson; Daniel O'Leary; Mohammed F Saad; Steven Shea; Moyses Szklo; Russell P Tracy Journal: Am J Epidemiol Date: 2002-11-01 Impact factor: 4.897
Authors: Martin I Wah-Suarez; Dionicio A Galarza-Delgado; Jose R Azpiri-Lopez; Iris J Colunga-Pedraza; Jesus Alberto Cardenas-de la Garza; Raymundo Vera-Pineda; Rosa I Arvizu-Rivera; Adrian Martinez-Moreno; Ray E Ramos-Cazares; Elizabeth E Abundis-Marquez; Andres H Guillen-Lozoya; Jose A Davila-Jimenez; Cinthia Y Guillen-Gutierrez; Guillermo Elizondo-Riojas Journal: Clin Rheumatol Date: 2018-07-02 Impact factor: 2.980