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Exploring a comprehensive cardiovascular risk factor profile as well as an overall 10-year risk estimation of cardiovascular events in a large cohort of patients at-risk for RA enabled us to study the presence and extent of CVD risk prior to RA diagnosis. To calculate the 10-year CVD risk, the European Guidelines on Cardiovascular Disease prevention in clinical practice recommend using the SCORE (Systematic Coronary Risk Evaluation) in which the risk score is multiplied by 1.5 for RA patients . Additionally, the QRISK system is widely used in clinical practice in RA patients since its algorithm includes RA as an independent risk factor . The distribution of SCORE has previously been described in different populations of RA patients, where 14% to 20% of patients were classified as high or very high risk [16, 17]. A study using the QRISK3 score in RA patients, with a mean disease duration of 11.4 years, classified 30% of patients as high risk . The distribution of SCORE and QRISK3 in a population at-risk for RA has thus far not been reported.
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At baseline, demographics, medical history, medication use and presence of comorbidities were collected. Blood parameters, including autoantibodies and lipid profile, were determined. Lipid profile contained total cholesterol (TC, mmol/L), high density lipoprotein (HDL, mmol/L), low density lipoprotein (LDL, mmol/L), TC/HDL ratio, triglycerides (mmol/L), apolipoprotein A1 (ApoA, g/L) and apolipoprotein B (ApoB, g/L). In a subset of patients, those included from August 2012 onwards (n = 211), blood pressure (BP; using an automatic BP monitor) and heart rate (in beats per minute (bpm) either from an automatic BP monitor or a 12 lead ECG) were measured according to the standard hospital procedures. A physician performed the physical examination to confirm absence of arthritis. Following baseline assessment, all patients were reassessed at 12-month intervals during 5 years with a focus on development of clinical arthritis. In case of arthritis development, an extra visit was scheduled.
Seventy-one seronegative controls were matched in a 1:1 ratio for sex and age to seropositive arthralgia patients, those with the closest match were selected. The selected arthralgia patients did not differ from the unselected patients regarding sex, age and percentage of ACPA positivity, but less patients developed arthritis (21% vs 36%, p = 0.015). Compared to the seronegative controls, more people smoked (25% vs 7%, p = 0.005) and used antihypertensive drugs (24% vs 7%, p = 0.010) in the seropositive arthralgia group. Of all antihypertensive drugs used, 37% could increase serum lipid levels (hydrochlorothiazide, n = 6; sotalol, n = 1). Lipid profile and cardiovascular risk scores are shown in Table 3. In seropositive arthralgia patients, HDL was lower while TC, TC/HDL ratio, triglycerides, ApoB, SCORE and QRISK3 were overall higher compared to the seronegative controls.
Our results suggest that changes in serum lipid profile and heartrate commence prior to RA diagnosis and that ACPAs might be involved in the link between immune mechanisms, inflammation and lipid metabolism changes. These changes do not result in different 10-year CVD risk scores. Our findings encourage further research into CVD in persons at risk of RA. We suggest research into identifying more sensitive screening tools than clinical risk scores to display early cardiovascular changes that are not solely a result of traditional CVD risk factors, for example subclinical atherosclerosis and arterial stiffness as measured by carotid IMT, PWV and MRI. Additionally, the interplay between ACPAs, lipids and CVD is an important item for the research agenda. Finally, prospective collection of cardiovascular event data is needed.