Key result
TNF-α inhibition protected against inflammation-induced LV concentric remodelling (relative wall thickness similar to controls, p=0.55) but did not improve diastolic dysfunction.
Why the study?
To determine the effects of biologic disease-modifying anti-rheumatic drugs on inflammation-induced changes in cardiac geometry and function.
Does TNF-α or IL-6 inhibition prevent inflammation-induced adverse cardiac remodeling and diastolic dysfunction in a rat model of collagen-induced arthritis?
Does TNF-α or IL-6 inhibition prevent inflammation-induced adverse cardiac remodeling and diastolic dysfunction in a rat model of collagen-induced arthritis?
p-value: p=0.55
In a rat model of collagen-induced arthritis, TNF-α inhibition prevented inflammation-induced concentric remodeling but did not improve diastolic dysfunction.
Does not support TNF-α inhibition for diastolic dysfunction; leaves open its role in preventing concentric remodeling in human inflammatory disease.
OBJECTIVES: To determine biologic disease-modifying anti-rheumatic drug effects on inflammation-induced cardiac geometry and function changes. METHODS: Male and female Sprague-Dawley rats (n=92) were divided into four groups: control group, collagen-induced arthritis (CIA) group, anti-TNF-α group and anti-IL-6 group. Inflammation was induced by injecting bovine type-II collagen emulsified in incomplete Freund's adjuvant at the base of the tail, in all groups except the control group. Following the onset of arthritis, the anti-TNF-α group received etanercept, and the anti-IL-6 group received tocilizumab, for six weeks. Left ventricular (LV) geometry and function were assessed with echocardiography and circulating inflammatory markers were measured with ELISA. RESULTS: Relative wall thickness in the CIA and anti-IL-6 groups were increased compared to controls (p<0.001 and p=0.02, respectively). TNF-α inhibition protected against inflammation-induced LV concentric remodelling, as relative wall thickness in the anti-TNF-α group was similar to controls (p=0.55). Systolic function variables were not different between the groups. In all groups inoculated with collagen, myocardial relaxation (lateral e') were impaired compared to controls (all p<0.001). LV filling pressures (E/e') were increased in the CIA, anti-TNF-α and anti-IL-6 groups compared to controls (p<0.001, p<0.001 and p=0.05, respectively). Independent of concentric remodelling, circulating CRP concentrations were associated with decreased e' and increased E/e', while TNF-α concentrations were associated with E/A. CONCLUSIONS: TNF-α inhibition protected against inflammation-induced adverse cardiac remodelling, but not diastolic dysfunction. IL-6 receptors blocker effects on inflammation-induced cardiac changes were inconclusive. Systemic inflammation likely impacts LV concentric remodelling and diastolic dysfunction through distinct pathways.
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Roux et al. (2022) studied Collagen-induced arthritis (n=92). Etanercept (anti-TNF-α) and Tocilizumab (anti-IL-6) vs. Control group and untreated collagen-induced arthritis group was evaluated on Left ventricular geometry (relative wall thickness) and function (p=0.55). TNF-α inhibition protected against inflammation-induced LV concentric remodelling (relative wall thickness similar to controls, p=0.55) but did not improve diastolic dysfunction.
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