Key result
Higher levels of C-reactive protein and classical cardiovascular risk factors were significantly associated with a reduction in the subendocardial viability ratio in patients with rheumatoid arthritis.
Why the study?
Does anti-TNFα treatment improve subendocardial viability ratio in patients with rheumatoid arthritis?
Observational (n=347)
Yes
Does anti-TNFα treatment improve subendocardial viability ratio in patients with rheumatoid arthritis?
Effect estimate: β -0.031 (95% CI -0.059 to -0.004)
p-value: p=0.02
In patients with rheumatoid arthritis, subendocardial viability ratio is associated with markers of disease activity and classical cardiovascular risk factors, and is negatively impacted by increasing systemic inflammation.
Supports link between inflammation and reduced SEVR in RA; leaves open whether anti-TNFα improves myocardial viability.
INTRODUCTION: Evidence indicates that rheumatoid arthritis (RA) patients have increased susceptibility to myocardial ischaemia that contributes to myocardial infarction. The subendocardial viability ratio (SEVR) can be measured using pulse wave analysis and reflects myocardial oxygen supply and demand. The objective of the present study was to examine specific predictors of SEVR in RA patients, with a specific focus on inflammation and classical cardiovascular disease (CVD) risk factors. METHODS: Two patient cohorts were included in the study; a primary cohort consisting of 220 RA patients and a validation cohort of 127 RA patients. All patients underwent assessment of SEVR using pulse wave analysis. Thirty-one patients from the primary cohort who were about to start anti-inflammatory treatment were prospectively examined for SEVR at pretreatment baseline and 2 weeks, 3 months and 1 year following treatment. Systemic markers of disease activity and classical CVD risk factors were assessed in all patients. RESULTS: The SEVR (mean ± standard deviation) for RA in the primary cohort was 148 ± 27 and in the validation cohort was 142 ± 25. Regression analyses revealed that all parameters of RA disease activity were associated with SEVR, along with gender, blood pressure and heart rate. These findings were the same in the validation cohort. Analysis of longitudinal data showed that C-reactive protein (P < 0.001), erythrocyte sedimentation rate (P < 0.005), Disease Activity Score in 28 joints (P < 0.001), mean blood pressure (P < 0.005) and augmentation index (P < 0.001) were significantly reduced after commencing anti-TNFα treatment. Increasing C-reactive protein was found to be associated with a reduction in SEVR (P = 0.02) and an increase in augmentation index (P = 0.001). CONCLUSION: The present findings reveal that the SEVR is associated with markers of disease activity as well as highly prevalent classical CVD risk factors in RA, such as high blood pressure and diabetes. Further prospective studies are required to determine whether the SEVR predicts future cardiac events in RA.
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Sandoo et al. (2012) conducted an observational in Rheumatoid arthritis (n=347). Systemic inflammation (C-reactive protein) vs. Lower levels of inflammation was evaluated on Subendocardial viability ratio (SEVR) (β -0.031, 95% CI -0.059 to -0.004, p=0.02). Higher levels of C-reactive protein and classical cardiovascular risk factors were significantly associated with a reduction in the subendocardial viability ratio in patients with rheumatoid arthritis.
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