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January 11, 2017Annals of the Rheumatic Diseases160 citationsOpen Access

Relationship between exposure to tumour necrosis factor inhibitor therapy and incidence and severity of myocardial infarction in patients with rheumatoid arthritis

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ALA. LowDSDeborah SymmonsMLMark Lunt

Key Result

Tumour necrosis factor inhibitors decreased the risk of first myocardial infarction compared with synthetic DMARDs in patients with rheumatoid arthritis (HR 0.61; 95% CI 0.41 to 0.89).

Study Design

Type

Cohort (n=14,258)

Multicenter

Yes

Structured PICO

Does tumour necrosis factor inhibitor therapy reduce the risk of first myocardial infarction in patients with rheumatoid arthritis compared to synthetic disease-modifying antirheumatic drugs?

P
Population
14,258 patients with rheumatoid arthritis (RA) recruited from 2001 to 2009 to the British Society for Rheumatology Biologics Register for Rheumatoid Arthritis
I
Intervention
Tumour necrosis factor inhibitors (TNFi) (etanercept, infliximab, or adalimumab)
C
Comparator
Biologic-naïve comparator cohort receiving synthetic disease-modifying antirheumatic drugs (sDMARDs)
O
Outcome
Risk of first verified myocardial infarction (MI)hard clinical

In patients with rheumatoid arthritis, TNFi therapy is associated with a 39% reduced risk of first myocardial infarction compared to sDMARDs, with no significant differences in MI severity or post-MI mortality.

Main Result

Effect estimate: HR 0.61 (95% CI 0.41 to 0.89)

Absolute Event Rate: 1.7% vs 1.9%

Abstract

OBJECTIVES: Patients with rheumatoid arthritis (RA) are at increased risk of myocardial infarction (MI) compared with subjects without RA, with the increased risk driven potentially by inflammation. Tumour necrosis factor inhibitors (TNFi) may modulate the risk and severity of MI. We compared the risk and severity of MI in patients treated with TNFi with that in those receiving synthetic disease-modifying antirheumatic drugs (sDMARDs). METHODS: This analysis included patients with RA recruited from 2001 to 2009 to the British Society for Rheumatology Biologics Register for Rheumatoid Arthritis starting TNFi (etanercept/infliximab/adalimumab) and a biologic-naïve comparator cohort receiving sDMARD. All patients were followed via physician and patient questionnaires and national death register linkage. Additionally, all patients were linked to the Myocardial Ischaemia National Audit Project, a national registry of hospitalisations for MI. Patients were censored at first verified MI, death, 90 days following TNFi discontinuation, last physician follow-up or 20 April 2010, whichever came first. The risk of first MI was compared between cohorts using COX regression, adjusted with propensity score deciles (PD). MI phenotype and severity were compared using descriptive statistics. 6-month mortality post MI was compared using logistic regression. RESULTS: 252 verified first MIs were analysed: 58 in 3058 patients receiving sDMARD and 194 in 11 200 patients receiving TNFi (median follow-up per person 3.5 years and 5.3 years, respectively). The PD-adjusted HR of MI in TNFi referent to sDMARD was 0.61 (95% CI 0.41 to 0.89). No statistically significant differences in MI severity or mortality were observed between treatment groups. CONCLUSIONS: Patients with RA receiving TNFi had a decreased risk of MI compared with patients with RA receiving sDMARD therapy over the medium term. This might be attributed to a direct action of TNFi on the atherosclerotic process or better overall disease control.

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Cite This Study

Low et al. (2017) conducted a cohort in Rheumatoid arthritis (n=14,258). Tumour necrosis factor inhibitors (TNFi) vs. Synthetic disease-modifying antirheumatic drugs (sDMARDs) was evaluated on First myocardial infarction (HR 0.61, 95% CI 0.41 to 0.89). Tumour necrosis factor inhibitors decreased the risk of first myocardial infarction compared with synthetic DMARDs in patients with rheumatoid arthritis (HR 0.61; 95% CI 0.41 to 0.89).

synapsesocial.com/papers/6a1ac52ca020f538e6858a0chttps://doi.org/10.1136/annrheumdis-2016-209784
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Also Consider

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