Background The increase in Rheumatoid arthritis (RA) associated mortality is predominantly due to accelerated coronary artery and cerebrovascular atherosclerosis with increased risk of ischemic heart disease about 50% in patients RA compared to controls1.
Objectives To study the pathogenesis of ischemic heart disease in RA, role of inflammatory cytokine interplay, disease activity and rheumatoid factor positivity.
Methods Eighty RA patients and 44 healthy controls were included. All subjects were younger than 45 years for females and 55 years for males with exclusion of all traditional risk factors for atherosclerosis. Interleukin (IL) 1,6 and 18 were assessed in all subjects. RA patients fulfilled ACR/EULAR 2010 criteria2 and were subjected to Dobutamine-stress-echocardiography, diseases activity assessement by DAS-283, X-ray hands for Larcen score4 and function assessment by HAQ5.
Results RA patients had significantly higher serum IL 1,6 and 18 than controls (p=0.00 in all). Thirty four (42.5%) patients had hypertensive reaction on Dobutamine-stress-echocardiography, four of them had ischemic change, and 46 (57.5%) had normal reaction. All patients with hypertensive reaction had positive RF (p=0.00), 10 had DAS-28>5.1, 20 had DAS-28 from 3.2 to5.1 and 4 were in remission (p=0.001). CRP was higher in patients with hypertensive reaction (p=0.003) while serum levels of IL1,6 and 18 showed no significant difference. In all patients, serum levels of IL1,6 and 18 showed significant positive correlation with VAS, HAQ and DAS-28 (p<0.001 in all). Only IL18 showed significant positive correlation with X-ray score in all patients.
Conclusions Disease activity and RF positivity play an important risk factor for ischemic heart disease in RA. Serum levels of IL1,6 and 18 did not help much in detecting patients at risk of ischemic heart disease. Better control of RA disease activity with early remission helps in preventing cardiac complications. More studies on larger number of patients are needed for better understanding of mechanism of ischemic heart disease in RA.
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Disclosure of Interest None declared