Background In our previous study, we identified that cumulative inflammatory burdern contributes to the development of carotid atherosclerosis through a synergistic interaction with conventional cardiovascular (CV) risk factors in patients with rheumatoid arthritis (RA). However, it is controversial whether the presence of joint destruction which result from inflammatory burden may be a risk factor for carotid atherosclerosis.
Objectives To investigate whether intima-media thickness (IMT) and plaques of carotid artery are influenced by radiographic joint destruction in patients with RA.
Methods A total of 186 patients with RA were included in the present study. Plain X-ray of joints were used to assess the severity of joint destruction. We developed a new radiographic scoring system, named Rheumatoid Arthritis-Radiographic Severity Score (RA-RSS), which scores 21 joint groups with the modified Steinbrocker method. The following joint groups were included: 2 proximal interphalangeal (PIP) joint group, 2 metacarpophalangeal (MCP) joint group, 2 wrist joint group, 2 elbow joint group, 2 shoulder joint group, 1 atlantoaxial joint group, 2 hip joint group, 2 knee joint group, 2 ankle joint group, 2 tarsometatarsal (TMT) joint group, and 2 metatarsophalangeal (MTP) joint group. The grade was determined by the worst changes in each joint group of PIP, MCP, TMT, and MTP joints. RA-RSS grades are assigned as follows: 0 = No radiographic changes; 1 = mild destruction of bone and cartilage; 2 = moderate destruction of bone and cartilage or joint deformities; 3 = Severe destruction of bone and cartilage or bony ankylosis (Score ranges from 0–63). We performed carotid ultrasound to detect the presence of carotid atherosclerosis.
Results Among 186 patients who were graded using RA-RSS, 110 patients had carotid plaques (59.1%). RA-RSS was significantly higher in patients with plaques compared to patients without plaques (11.2±8.79 vs. 7.6±7.72, p=0.004). Patients were divided into two groups by the cut-off value of plaque development as determined using receiver operating characteristic (ROC) curves: 115 (61.8%) patients with RA-RSS <10 and 71 (38.2%) with RA-RSS ≥10. There was a significant difference between the groups with respect to the presence of plaques (48.7% vs. 76.1%, p<0.001), while there was no difference in mean carotid IMT (0.87±0.19 vs. 0.88±0.14, p=0.684). The mean age, the presence of conventional CV risk factors, Korean version of the modified HAQ (mKHAQ), DAS28-ESR, and RA-RSS ≥10 were significantly associated with plaque development. Multivariate logistic regression analysis showed that RA-RSS ≥10 (OR 2.94 [95% CI 1.48–5.84]) and the presence of conventional CV risk factors (OR 2.30 [95% CI 1.21–4.35]) were independent risk factors for plaque development.
Conclusions The present study shows that radiographic destruction over peripheral joints, which directly reflects cumulative inflammatory burden, is a strong independent risk factor for plaque development that is associated with CV events and mortality.
Churl Hyun Im, et al. Inflammatory burden interacts with conventional cardiovascular risk factors for carotid plaque formation in rheumatoid arthritis. Rheumatology (Oxford). 2015 May;54(5):808–15.
Disclosure of Interest None declared
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