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The results of a study presented at the Annual European Congress of Rheumatology (EULAR 2018) demonstrate an increased risk of acute coronary syndrome (ACS) in siblings of individuals with rheumatoid arthritis (RA), suggesting shared susceptibility between the two diseases.
Recent studies have demonstrated that severity of RA is associated with the risk of ACS, suggesting that it is the RA disease itself contributing to the excess risk.
A recently-published report demonstrated that despite more efficient control of inflammation in RA during recent years, the excess risk for ACS among patients with RA compared to the general population remains elevated. This suggests there may be a shared susceptibility between the two conditions.
To examine this, study authors investigated the risk of ACS in siblings of individuals with RA. If there were shared susceptibility between the two conditions, non-RA siblings would also have an increased risk of ACS due to their similar genetic set-up and background.
This Swedish Rheumatology Quality (SRQ) register is linked to the Swedish Multigeneration Register, Patient Register, the Cause of Death Register, and the Total Population Register. Through this, investigators identified 7,492 patients with RA from the SRQ (1996-2015) who had 10,671 full siblings; the patients with RA were matched for age and gender with 35,120 comparator subjects, along with their 47,137 full siblings.
Results showed that patients with early RA and their siblings were 44 per cent and 23 per cent more likely to suffer from an ACS event than matched comparator subjects from the general population. A direct comparison of patients with RA to their siblings demonstrated that those with RA had a 19 per cent higher risk of ACS than their siblings.
“Our results provide evidence of shared susceptibility between RA and ACS,” said study author Dr Helga Westerlind, Karolinska Institutet, Sweden. “Although the nature of this needs to be further investigated, we believe that to bring down the cardiovascular risk in patients with RA, cardio-preventive measures must go beyond optimised RA disease control.”
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