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Initiation and adherence to secondary prevention pharmacotherapy after myocardial infarction in patients with rheumatoid arthritis: a nationwide cohort study.
Annals of the rheumatic diseases 2012 Mar 8; In press
Lindhardsen J, Ahlehoff O, Gislason GH, Madsen OR, Olesen JB, Torp-Pedersen C, Hansen PR
1Department of Cardiology, Gentofte University Hospital, Copenhagen, Denmark.
OBJECTIVES: To examine whether rheumatoid arthritis (RA) is associated with less optimal secondary prevention pharmacotherapy after first-time myocardial infarction (MI).METHODS: The authors identified all patients with first-time MI in the Danish National Patient Register from 2002 to 2009 and gathered individual level information including pharmacy records from nationwide registers. Initiation of standard care post-MI secondary prevention drugs, that is, aspirin, β-blockers, clopidogrel, renin angiotensin system (RAS) blockers and statins, was determined after discharge. In addition, adherence to each drug was evaluated as the proportion of patients on treatment during follow-up and time to first treatment gap.RESULTS: A total of 66 107 MI patients (37% women) were discharged alive; 877 were identified as RA patients (59% women). Thirty days after discharge, RA was associated with significantly lower initiation of aspirin (OR 0.80 (0.67-0.96)), β-blockers (0.77 (0.65-0.92)) and statins (0.69 (0.58-0.82)), while initiation of RAS blockers (0.80 (0.57-1.11)) and clopidogrel (0.88 (0.75-1.02)) was non-significantly reduced. These estimates were virtually unchanged at day 180 and the results were corroborated by Cox regression analyses. Adherence to statins was lower in RA patients relative to non-RA patients (HR for treatment gap of 90 days: 1.26 (1.07-1.48)), while no significant differences were found in adherence to the other drugs.CONCLUSIONS: In this nationwide study of unselected patients with first-time MI, a reduced initiation of secondary prevention pharmacotherapy was observed in RA patients. This undertreatment may contribute to the increased cardiovascular disease burden in RA and the underlying mechanisms warrant further study.