medwireNews: People with rheumatoid arthritis (RA) still have a substantial excess risk for acute myocardial infarction (AMI) relative to the general population even though rates have fallen in both groups in recent years, Canadian research shows.
Diane Lacaille (Arthritis Research Canada, Richmond, British Columbia) and colleagues say: “Despite changes in treatment recommendations aiming at early treatment and eradication of inflammation, and cardiovascular risk management, the risk of AMI remains higher in RA than in the general population and the excess risk has not improved over time.”
They therefore believe that “[t]here is a need for tailoring cardiovascular risk management strategies specifically at RA patients, in addition to ensuring control of RA inflammation, to reduce the excess risk of AMI.”
The researchers studied data for 23,237 people (mean age 58 years, 66% women) who were diagnosed with RA in British Columbia between 1997 and 2004, and 46,474 general population controls with no history of inflammatory arthritis who were matched by age and sex.
During a mean 8.9 years of follow-up, there were 1133 incident AMI events in the people with RA and 1606 events among the controls, of which 60 and 13 events, respectively, were fatal.
Lacaille and co-authors report in Seminars in Arthritis and Rheumatism that the crude 10-year incidence of AMI decreased from 6.06 per 1000 person–years in people diagnosed with RA in 1997 to 4.42 per 1000 person–years among people with RA onset in 2004.
They also note that the decline was not linear, with an unexplained peak in incidence at 7.11 per 1000 person–years among people diagnosed with RA in 1999 followed by a subsequent drop to 4.94 per 1000 person–years among those diagnosed in 2000.
In the general population, there was a linear decline, with the crude 10-year incidence of AMI falling from 4.80 per 1000 person–years in 1997 to 2.88 per 1000 person–years in 2004.
After adjustment for potential confounders, the investigators found that the risk for AMI fell by a significant 6% per year among the people with RA and by a significant 7% per year among the general population, with no significant difference in the rate of decline between the two groups.
This meant that overall, RA patients had a significant 21% higher risk for AMI than the general population controls.
Lacaille and team had hypothesized that the excess risk for AMI in RA relative to the general population would have reduced with time as a result of “better control of inflammation in recent years from earlier and more aggressive RA treatment recommendations, aimed at achieving remission, or low disease activity, as well as with the advent of more effective RA therapies, such as biologic agents.”
They suggest that the reasons this was not the case may be that “the improvements in RA inflammation achieved in recent years are not sufficient to reduce the excess risk of AMI” or that “a significant portion of the RA population are not receiving treatment according to the treat-to-target approach, and/or the targeted remission or low disease activity states are not achieved.”
The authors also note that the study was carried out in the early era of biologic availability and more recent incident cohorts may yield different results.
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