Atherogenic Profile Worsens With Polyarthritis Treatment
BIRMINGHAM, ENGLAND — Successful reduction of early inflammatory polyarthritis disease measures is accompanied by deterioration of the atherogenic profile, which potentially signals an increased risk of cardiovascular disease in an already at-risk population, judging from findings presented at the annual meeting of the British Society of Rheumatology.
Results from a cardiovascular disease (CVD) subset analysis of data from the Norfolk Arthritis Register (NOAR) suggest that lipid parameters should be assessed and managed carefully in all patients with early arthritic disease. Such assessment and management should be done regardless of any ongoing inflammatory polyarthritis treatment.
“When we look at the HAQ [Health Assessment Questionnaire] scores, patients' disability and the disease severity are improving significantly over the first 2 years, but at the same time we see an overall worsening in their lipid profile,” said clinical research fellow Dr. Hoda Mirjafari of the Arthritis Research UK Epidemiology Unit at the University of Manchester (England).
In her discussion of 2-year follow-up data on 223 patients, Dr. Mirjafari noted that although lipid levels initially seem to decrease in patients with early inflammatory polyarthritis, they creep back to normal levels over time.
“This is worrying on two counts,” Dr. Mirjafari explained. “One is that when you first meet your patient and you are reassured that their lipid levels are low, that is false reassurance. Their true lipids, once their inflammatory disease is sorted out, are actually higher.”
In addition, she said, conventional CV risk factor markers such as LDL and HDL cholesterol measures may not be good enough to track the worsening atherogenic profile and subsequent risk of atherosclerosis. A better measure is the atherogenic index, specifically the ratio of apolipoprotein B to apolipoprotein A-I. This is the only measure that can predict the likelihood of an atherosclerotic plaque's being present upon imaging of the carotid arteries.
Patients were recruited into the NOAR CVD substudy in 2004-2008 if they had evidence of early inflammatory polyarthritis and a disease duration shorter than 2 years. Information was collated at baseline and reassessed at 2 years on conventional CV risk factors (blood pressure, lipids, fasting glucose, height, and weight) and inflammatory polyarthritis risk factors (rheumatoid factor, HAQ, swollen and tender joint counts, and disease-modifying antirheumatic drug and steroid therapy).
Two-thirds (68%) of patients were female; the median age was 50 years, and the median symptom duration was 7 months. The median 28-joint count disease activity score based on C-reactive protein measures (DAS28-CRP) at baseline was 3.8. In all, 44% patients met American College of Rheumatology criteria for early inflammatory polyarthritis, and 48% were positive for rheumatoid factor. Only 5% of patients were receiving statin therapy; 23% were smokers, and 9% had a Framingham risk of CVD event greater than 20% at 10 years. One-fifth (22%) of patients had been exposed to steroids at baseline and 32% at 2 years, whereas 53% and 82%, respectively, had been treated with DMARDs.
Mean HAQ scores at baseline and at 2 years were 0.95 and 0.81, respectively. Mean swollen and tender joint counts were 3.73 at baseline, but decreased to 2.00 at 2 years. Although there was no great change in total cholesterol levels, LDL levels rose slightly and HDL levels decreased, and the atherogenic index increased substantially from a baseline value of 2.38 to 2.60 at 2 years.
Disclosures: The NOAR is supported by a grant from Arthritis Research UK. Dr. Mirjafari reported no conflicts of interest.
'When you first meet your patient and you are reassured that their lipid levels are low, that is false reassurance.'
Source DR. MIRJAFARI
My Take
Questions Remain About Statin Use in RA
Cardiovascular morbidity and mortality are obviously increasingly important in diseases like rheumatoid arthritis. Dr. Mirjafari made some interesting observations from some of the data from the Norfolk Arthritis Register. The findings so far leave a slightly counterintuitive impression. Here, evidence shows that the better we treat RA, not only the better the articular outcomes, but also the better the comorbidity outcomes. Yet the lipid profile seems to be deteriorating despite improvement in the disease.
What is a bit alarming is that this was a cohort of patients with relatively mild disease (only 48% were RF positive). It makes TRACE RA (Trial of Atorvastatin for the Primary Prevention of Cardiovascular Events in Rheumatoid Arthritis) even more important as a study, so we can try and work out when it's the most appropriate time to use statins—not just with RA, but with a persistent inflammatory arthritis, even if it doesn't fulfill the American College of Rheumatology criteria.