PMID- 22045840 OWN - NLM STAT- MEDLINE DCOM- 20120501 LR - 20151119 IS - 1499-2752 (Electronic) IS - 0315-162X (Linking) VI - 39 IP - 1 DP - 2012 Jan TI - Biological drug treatment of rheumatoid arthritis and spondyloarthritis: effects on QT interval and QT dispersion. PG - 41-5 LID - 10.3899/jrheum.110158 [doi] AB - OBJECTIVE: Tumor necrosis factor-alpha (TNF-alpha) antagonists bring about significant improvement in chronic inflammatory diseases such as rheumatoid arthritis (RA) and spondyloarthritis (SpA). There is some evidence that they can also have negative myocardial effects, but to date this issue has not been clarified. We evaluated changes in electrocardiographic measures [QT interval, corrected, dispersion, and dispersion corrected (QT, QTc, QTd, QTdc, respectively)] in patients with RA or SpA treated with anti-TNF agents (infliximab and etanercept), those treated with other biological agents (rituximab), and with methotrexate. METHODS: We studied 38 consecutive patients with RA (21 patients) or SpA (19 patients) being treated with TNF-alpha antagonists, 8 patients with RA being treated with rituximab, and 13 patients (8 with RA and 5 with SpA) taking methotrexate. Electrocardiographs (ECG) were performed on all participants at baseline and 12 months after initiation of treatment, and the QT, QTc, and QTd were calculated with standard procedures. RESULTS: After 12 months of treatment, significant increases over baseline values were observed in the mean QT (p < 0.009), QTd (p < 0.0001), and QTdc (p < 0.0001) of the anti-TNF group, but no significant changes were observed in those taking rituximab. QT changes in the anti-TNF group were unrelated to the disease (RA vs SpA) or drug (infliximab vs etanercept), and none were associated with clinical manifestations of cardiac disease. CONCLUSION: In patients with RA and SpA, TNF-alpha antagonists seem to increase the QT and QTd measures. Although these changes were completely asymptomatic, ECG may be indicated in patients being considered for anti-TNF therapy to identify those at risk for cardiac complications. FAU - DI Franco, Manuela AU - DI Franco M AD - Cattedra di Reumatologia, Dipartimento di Medicina Interna e Specialita Mediche, Sapienza Universita di Roma, Viale del Policlinico 155, 00161 Rome, Italy. manuela.difranco@uniroma1.it FAU - Paradiso, Michele AU - Paradiso M FAU - Ceccarelli, Fulvia AU - Ceccarelli F FAU - Scrivo, Rossana AU - Scrivo R FAU - Spinelli, Francesca Romana AU - Spinelli FR FAU - Iannuccelli, Cristina AU - Iannuccelli C FAU - Valesini, Guido AU - Valesini G LA - eng PT - Journal Article DEP - 20111101 PL - Canada TA - J Rheumatol JT - The Journal of rheumatology JID - 7501984 RN - 0 (Antibodies, Monoclonal) RN - 0 (Antibodies, Monoclonal, Murine-Derived) RN - 0 (Antirheumatic Agents) RN - 0 (Immunoglobulin G) RN - 0 (Receptors, Tumor Necrosis Factor) RN - 0 (Tumor Necrosis Factor-alpha) RN - 4F4X42SYQ6 (Rituximab) RN - B72HH48FLU (Infliximab) RN - OP401G7OJC (Etanercept) RN - YL5FZ2Y5U1 (Methotrexate) SB - IM MH - Antibodies, Monoclonal/pharmacology/therapeutic use MH - Antibodies, Monoclonal, Murine-Derived/pharmacology/therapeutic use MH - Antirheumatic Agents/*pharmacology/*therapeutic use MH - Arthritis, Rheumatoid/*drug therapy/*physiopathology MH - Electrocardiography MH - Etanercept MH - Humans MH - Immunoglobulin G/pharmacology/therapeutic use MH - Infliximab MH - Methotrexate/pharmacology/therapeutic use MH - Myocardial Contraction/*drug effects MH - Receptors, Tumor Necrosis Factor/therapeutic use MH - Retrospective Studies MH - Rituximab MH - Spondylarthritis/*drug therapy/*physiopathology MH - Tumor Necrosis Factor-alpha/antagonists & inhibitors EDAT- 2011/11/03 06:00 MHDA- 2012/05/02 06:00 CRDT- 2011/11/03 06:00 PHST- 2011/11/03 06:00 [entrez] PHST- 2011/11/03 06:00 [pubmed] PHST- 2012/05/02 06:00 [medline] AID - jrheum.110158 [pii] AID - 10.3899/jrheum.110158 [doi] PST - ppublish SO - J Rheumatol. 2012 Jan;39(1):41-5. doi: 10.3899/jrheum.110158. Epub 2011 Nov 1.