Disease Activity and Anticitrullinated Peptide Antibody Positivity Predict the Worsening of Ventricular Function in Rheumatoid Arthritis

ACR Open Rheumatol. 2020 Apr;2(4):232-241. doi: 10.1002/acr2.11119. Epub 2020 Apr 8.

Abstract

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.