{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,8]],"date-time":"2026-09-08T16:09:25Z","timestamp":1788883765141,"version":"build-2803163510"},"reference-count":51,"publisher":"The Journal of Rheumatology","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J Rheumatol"],"published-print":{"date-parts":[[2015,3]]},"abstract":"<jats:sec><jats:title>Objective.<\/jats:title><jats:p>Corrected QT (QTc) interval predicts all-cause and cardiovascular mortality and may contribute to the increased mortality risk in rheumatoid arthritis (RA). Animal experiments have shown that proinflammatory cytokines [tumor necrosis factor (TNF)-\u03b1 and interleukin 1 (IL-1)] can prolong cardiomyocyte action potential. We sought to determine whether elevations in circulating inflammatory cytokines were independently associated with QTc prolongation in patients with RA.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods.<\/jats:title><jats:p>One hundred twelve patients [median age 62 (interquartile range 17) yrs; 80 women (71%)] from a well-characterized RA cohort underwent baseline 12-lead electrocardiograms for QT interval measurement and contemporary blood sampling to assess concentrations of inflammatory markers including C-reactive protein (CRP), TNF-\u03b1, and interleukins (IL-1\u03b1, IL-1\u03b2, IL-6, IL-10). QTc was calculated using the Bazett (QT<jats:sub>BAZ<\/jats:sub>= QT \u00f7 \u221aRR) and Framingham Heart Study (QT<jats:sub>FHS<\/jats:sub>= QT + 0.154 \u00d7 [1 \u2013 RR]) heart rate correction formulas.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results.<\/jats:title><jats:p>Inflammatory cytokines (TNF-\u03b1, IL-1\u03b2, IL-6, IL-10) were positively correlated with QT<jats:sub>BAZ<\/jats:sub>(Spearman rank correlation coefficient rho = 0.199, 0.210, 0.222, 0.333; all p &lt; 0.05). In multivariable regression analysis, these associations were all confounded by age except IL-10, where higher tertile groups were independently and positively associated with QT<jats:sub>BAZ<\/jats:sub>(\u03b2 = 0.202, p = 0.023) and QT<jats:sub>FHS<\/jats:sub>(\u03b2 = 0.223, p = 0.009) when compared to the lower tertile. CRP (per unit increase) was independently associated with QT<jats:sub>BAZ<\/jats:sub>(\u03b2 = 0.278, p = 0.001), but not QT<jats:sub>FHS<\/jats:sub>.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion.<\/jats:title><jats:p>To our knowledge, ours is the first study demonstrating a contemporary link between inflammatory cytokines and QT interval in humans. Our results suggest that a lower inflammatory burden may protect against QTc prolongation in patients with RA. However, further studies are required to confirm the effects of pro- and antiinflammatory cytokines on QTc interval.<\/jats:p><\/jats:sec>","DOI":"10.3899\/jrheum.140861","type":"journal-article","created":{"date-parts":[[2015,1,16]],"date-time":"2015-01-16T03:16:23Z","timestamp":1421378183000},"page":"421-428","source":"Crossref","is-referenced-by-count":68,"title":["Association Between Corrected QT Interval and Inflammatory Cytokines in Rheumatoid Arthritis"],"prefix":"10.3899","volume":"42","author":[{"given":"Ahmed M.","family":"Adlan","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Vasileios F.","family":"Panoulas","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jacqueline P.","family":"Smith","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"James 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