Key result
Higher rheumatoid arthritis activity is linked to ~39% greater odds of diastolic dysfunction without heart failure.
Why the study?
Diastolic dysfunction is more prevalent in patients with rheumatoid arthritis, but its evolution over time and clinical predictors remain uncharacterized.
Cohort (n=158)
No
Effect estimate: OR 1.39 (95% CI 1.02-1.90)
p-value: p=0.034
Diastolic dysfunction is highly prevalent and progressive in rheumatoid arthritis patients without clinical heart failure, and its presence is driven by RA disease activity rather than subclinical atherosclerosis or myocardial inflammation.
May support vigilance for diastolic dysfunction in active RA; leaves open whether tighter control alters progression.
BACKGROUND: Diastolic dysfunction (DD) is more prevalent in patients with rheumatoid arthritis (RA) compared to the general population. However, its evolution over time and its significant clinical predictors remain uncharacterized. We report on baseline and prospective changes in diastolic function and its associated RA and cardiovascular (CV) predictors. METHODS: In this study, 158 RA patients without clinical CV disease (CVD) were enrolled and followed up at 4 to 6 years, undergoing baseline and follow-up echocardiography to assess for DD, as well as extensive characterization of RA disease activity and CV risk factors. Novel measures of myocardial inflammation and perfusion were obtained at baseline only. Using baseline and follow-up composite DD (E/e', Left Atrial Volume Index (LAVI) or peak tricuspid regurgitation (TR) velocity; ≥ 1 in top 25%) as the outcome, multivariable regression models were constructed to identify predictors of DD. RESULTS: DD was prevalent in RA patients without clinical heart failure (HF) (40.7% at baseline) and significantly progressed on follow-up (to 57.9%). Baseline composite DD was associated with baseline RA disease activity (Clinical Disease Activity Index; CDAI) (OR 1.39; 95% CI 1.02-1.90; p=0.034). Several individual diastolic parameters (baseline E/e' and LAVI) were associated with troponin-I and brain natriuretic peptide (BNP). Baseline and follow-up composite DD, however, were not associated with myocardial inflammation, myocardial microvascular dysfunction, or subclinical atherosclerosis. CONCLUSIONS: DD is prevalent in RA patients without clinical HF and increases to >50% over time. Higher RA disease activity at baseline predicted baseline composite DD. Future longitudinal studies should explore whether adverse changes in diastolic function lead to clinical HF and are attenuated by disease-modifying antirheumatic drugs (DMARDs).
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Park et al. (2022) conducted a cohort in Rheumatoid arthritis without clinical cardiovascular disease (n=158). Higher baseline rheumatoid arthritis disease activity (CDAI) was significantly associated with baseline composite diastolic dysfunction (OR 1.39) in patients without clinical heart failure.
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