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Background There is increasing evidence that environmental air pollution is associated with the development of chronic inflammatory arthritides (CIA). The role of air pollutants on the biological treatment (biological disease‐modifying antirheumatic drugs [bDMARDs]) response of CIA is still unclear. Methods We retrieved longitudinal data on patients affected by CIA on biological therapies and on the daily concentration of air pollutants in the Verona area. We designed a case‐crossover study to compare the exposure to pollutants in the 60‐day period preceding a drug switch or swap due to disease progression referent to the 60‐day period preceding a visit with stable treatment for at least 6 months. Results A total of 1257 patients with CIA (863 with rheumatoid arthritis, 256 with psoriatic arthritis, and 138 with ankylosing spondylitis) with 5454 follow‐up visits were included in the study (median follow‐up 2.09 years [interquartile range: 0.82‐2.58 years]). A total of 282 patients were included in the case‐crossover study. We retrieved 13 636 daily air pollution records. We found that air pollutants’ concentrations were higher in the 60‐day period before a failure of bDMARD response and prior to a switch or swap compared with the period preceding a visit with stable bDMARD therapy for at least 6 months. Conclusion We found that environmental air pollution was a determinant of poor response to bDMARDs in a cohort of patients with CIA followed over a 5‐year period. An intervention aimed at decreasing fossil combustion emissions might have beneficial effects on biologic persistence rates of patients with CIA and economic expenditures related to switches and swaps.

Objective This prospective study was designed to analyze the incidence and the factors associated with impairment in left ventricular systolic function (LVSF) overtime in patients with rheumatoid arthritis (RA) without overt cardiac disease. In particular, we verified the hypothesis that a relationship between worsening of LVSF and markers of RA disease activity exists. Methods One hundred forty outpatients with RA without overt heart disease underwent clinical, laboratory, and echocardiographic evaluation at baseline and after 35 (interquartile range [IQR] 23‐47) months of follow‐up. A clinical Disease Activity Index (CDAI) score greater than 10 indicated the presence of moderate‐high RA disease activity; data on anticitrullinated peptide antibody (ACPA) positivity were recorded at baseline. Stress‐corrected midwall fractional shortening (sc‐MFS) was used as a measure of LVSF and was considered impaired if less than 86.5%. Results At 36 (IQR 23‐47) months follow‐up, impaired sc‐MFS was detected in 60 of 140 (43%) patients, compared with 80 patients with normal sc‐MFS. Disease duration and activity, ACPA positivity, inflammatory markers, cardiovascular and antirheumatic therapies, and sc‐MFS were similar between the two groups at baseline. A multiple logistic regression analysis showed ACPA positivity, moderate‐high disease activity (CDAI greater than 10), and disease duration as independent predictors of impaired sc‐MFS at follow‐up. Finally, a simple clinical score to predict worsening of LVSF at midterm was built (area under the curve of 0.80, with a sensibility and specificity of 78% and 82%, respectively). Conclusion Disease duration, ACPA positivity, and moderate‐high disease activity are independent prognosticators of LVSF impairment in RA. Adverse changes in heart function could be prevented by good control of inflammation and modulation of autoimmunity.