Key result
Rheumatoid arthritis is linked to ~29% higher cIMT, indicating increased subclinical atherosclerosis.
Why the study?
Patients with RA have an increased risk of CVD driven by inflammation, prompting this evaluation of cIMT, TNF-α, and hs-cTnI to refine CV risk assessment.
Do TNF-α and hs-cTnI levels correlate with subclinical atherosclerosis (cIMT) and disease activity in patients with rheumatoid arthritis?
Case-Control (n=160)
Do TNF-α and hs-cTnI levels correlate with subclinical atherosclerosis (cIMT) and disease activity in patients with rheumatoid arthritis?
Absolute Event Rate: 0.9% vs 0.7%
p-value: p=0.001
Elevated TNF-α and hs-cTnI levels in rheumatoid arthritis patients correlate with increased carotid intima-media thickness, highlighting their potential as early markers for subclinical atherosclerosis.
Patients with rheumatoid arthritis (RA) have a higher risk of cardiovascular disease (CVD) compared to the general population, which leads to increased morbidity and mortality. Inflammation is the key in RA and CVD. Our study aimed to refine cardiovascular (CV) risk assessment in RA patients by using carotid intima-media thickness (cIMT) as a marker of subclinical atherosclerosis. We also explored whether proinflammatory cytokines represented by tumor necrosis factor-alpha (TNF-α) and high-sensitivity cardiac troponin I (hs-cTnI), a biomarker of myocardial injury, could be correlated in RA patients. The study included 80 RA patients and 80 control subjects. TNF-α and hs-cTnI levels were measured. Subclinical atherosclerosis was evaluated by cIMT by means of carotid ultrasound. Disease activity score 28 (DAS28) was used to evaluate disease activity. hs-cTnI and TNF-α serum levels were higher in RA patients compared to controls (p=0.001). There was a significant difference in the median of cIMT between cases and controls (median (IQR) 0.9 (0.2) for cases, 0.7 (0.1) for controls, (p=0.001). A significant correlation was found between the level of TNF-α and hs-cTnI (p=0.002). Also, there was a significant correlation between the cIMT level and TNF-α and hs-cTnI (p=0.003 and p=0.002, respectively). Significant correlation was found between cIMT, TNF-α, and hs-cTnI in relation to the DAS28 score (p < 0.001, p < 0.001, and p=0.001, respectively). In conclusion, patients with RA are more likely to develop subclinical atherosclerosis, as reflected in increased cIMT. Higher levels of hs-cTnI in RA patients may correlate with the presence of occult cardiovascular disease. TNF-α and hs-cTnI correlations can reveal the interplay between disease activity and CVD. Thus, inflammation must be the primary target of various therapeutic approaches.
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Ibrahem et al. (2023) conducted a case-control in Rheumatoid arthritis (n=160). Rheumatoid arthritis vs. Control subjects was evaluated on Carotid intima-media thickness (cIMT) (p=0.001). Rheumatoid arthritis patients had significantly higher median carotid intima-media thickness compared to controls (0.9 vs 0.7, p=0.001), indicating increased subclinical atherosclerosis.
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