Background High-frequency of traditional risk factors of AS development is well-proven for patients (pts) with SLE. Significance of immunological and inflammatory factors, character of treatment and other factors were also reported. However, SLE pts with AS are usually considerably older, had longer disease duration and were treated with glucocorticoid (GC) for longer period vs pts without AS, which makes impossible exact estimation of these factors’ significance in accelerated AS development.

Objectives To determine independent risk factors of ED and AS development in pts with SLE.

Methods 100 pts with SLE (90 women and 10 men, the mean age–40,9±1,4 years, the disease duration–9.93±0.88 years) with mild and moderate disease activity and GC therapy that lasted not less than 1 year were studied endothelial dependent dilation (EDD) through ultrasound (US) of brachial artery during reactive hyperemia. The control group consisted of 32 apparently healthy pts. Coronary arteries AS was discovered through Ca-scoring; as for AS of carotid, vertebral arteries, abdominal aorta, iliac, femoral, popliteal and tibial arteries–through duplex scanning US (intima-media thickness ≥0,8 mm or presence of plaques). For detection of independent risk factors of ED as a substitute for AS marker we used multiple linear regression, for AS – method of binary logictic regression. Analysis of probable prognostic factors included: 1) traditional factors (17 variables for EDD and AS, including absolute values in serum cholesterol (CS), triglycerides, low- and high-density lipoprotein CS and presence/absence of their proatherogenic changes; for AS – also absolute values and presence/absence of impaired EDD); 2) SLE-related potential factors of AS development (30 variables, including pts’ age at the onset of the disease and SLE duration, duration of GC treatment and other drugs, clinical symptoms, immunological indexes, SLEDAI and SLICC).

Results EDD was impaired in 89% of pts with SLE, mean by 31,5% vs healthy subjects. Independent determinants which significantly influence EDD value are age (p<0,001), presence of nephritis (regardless of its severity) (p=0,001), polyarthritis (p=0,019) and Raynaud’s syndrome (p=0,045).

Expected EDD (%) = 19,53 – 0,13 × age – 3,05 (if nephritis is present) – 4,73 (if polyarthritis is present) – 1,89 (if Raynaud’s syndrome is present).

AS of any localization was discovered total in 66% pts. Independent risk determinants of AS development in pts with SLE are age (p<0,001), body mass index (BMI) (p=0,001), increased antibodies titre to ds-DNA (AB-dsDNA) (p=0,023), EDD value (p=0,017), and presence of “butterfly rash” (p=0,020).

Coefficient Z = –16,74 + 0,17 × age + 0,50 × BMI + 2,03 (if elevated AB-dsDNA) – 0,20 × EDD-2,04 (if “butterfly rash” is present)

Probability of AS development in pts with SLE to be calculated by formula:

p=1/1 + e – z,

where p = probability of event occurrence, e = mathematical constant (e=2,72).

If p<0,5, with a predict accuracy 79,4% it is supposed that an event will not occur, if p≥0,5 – AS development is probable with a predict exactness 92,4%.

Conclusions Calculation formula of probability of AS development in pts with SLE may be used to select the pts who are recommended to undergo full complex of anti-AS treatment, as well as regular monitoring for early AS diagnosis.

Disclosure of Interest None Declared