medwireNews: People with rheumatoid arthritis (RA) have a significantly increased risk for acute coronary syndrome (ACS) that generally does not vary according to which biologic DMARD they are taking, show data from four Nordic countries.
“Comparing the [biologics] to each other, we noted little differences in ACS rates in the short and intermediate terms,” write Benedicte Delcoigne (Karolinska Institute, Stockholm, Sweden) and co-authors in the Annals of the Rheumatic Diseases.
“In the longer term, initiation of abatacept, infliximab and rituximab was associated with a moderately increased rate of ACS, a finding which remained when patients with previous [cardiovascular disease] were excluded, but was largely confined to patients starting their third or later [treatment],” they add.
Using registry data, the researchers identified 24,083 people with RA (mean age 56 years, 75% women) who received 40,850 biologic treatment courses in Denmark, Finland, Norway, or Sweden between 2008 and 2017.
Etanercept was the most commonly initiated treatment (27%), followed by adalimumab (14%), infliximab (13%), rituximab (12%), tocilizumab (10%), certolizumab pegol (9%), abatacept (9%), golimumab (6%), and baricitinib and tofacitinib (<1% each).
The researchers report that during 5 years of follow-up there were 780 ACS events, corresponding to a crude incidence rate of 5.5 cases per 1000 person–years.
Compared with the general population in Denmark and Sweden, individuals with RA in these two countries had a significant 80% higher risk for ACS, with crude incidence rates of 4.5 versus 2.4 per 1000 person–years and 4.4 versus 3.6 per 1000 person–years, respectively.
At 1 year from treatment initiation, the risk for ACS did not differ significantly by treatment type, but the team found that the hazard ratios (HRs) increased with time relative to etanercept treatment.
By 5 years, the risk for ACS was a significant 26% higher with rituximab than with etanercept after adjustment for potential confounders, but there were no other significant differences among the treatments.
In an analysis that focused on time on treatment rather than time since treatment initiation, 5 years of infliximab use was associated with a 49% higher risk for ACS than 5 years of etanercept use. There was also a trend for an increased risk for ACS with abatacept and rituximab versus etanercept.
However, when the analysis was repeated according to the number of prior treatments, there was no significantly increased ACS risk with the majority of biologics in people who were treatment naïve or who had received one previous biologic or conventional DMARD. The only exception was abatacept where the risk was a significant 2.17 times higher versus etanercept in people who were treatment-naïve.
For those who had received two or more prior treatments, infliximab and certolizumab were associated with significantly increased ACS risk in the on-treatment analysis (HR=3.47 and 2.92, respectively), while abatacept, infliximab, and rituximab had a borderline or statistically significant increased ACS risk in the time since treatment analysis (HRs=1.83–2.18).
“The observed increased risk for abatacept, infliximab and rituximab in our study might be explained by residual confounding or confounding by indication,” Delcoigne et al suggest.
They add: “Patients on abatacept and rituximab had more comorbidities and longer disease duration with potentially longer exposure to inflammation, which is associated with CV risk.”
The authors conclude that their “results suggest that in RA treated with [biologics], the [biologic] used does not seem to matter for the risk of ACS.”
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