Analysis of laboratory indicators of inflammation, infection and indicators of subclinical atherosclerosis in patients with systemic lupus erythematosus and myocardial infarction

Objective of the study: to investigate the correlation between inflammation activity, infectious components, platelet function, dyslipidemia, and the development of subclinical atherosclerosis in patients with systemic lupus erythematosus (SLE) and ischemic heart disease. Materials and methods. The study involved the measurement of C-reactive protein (CRP), interleukin 6, IgG antibodies to Chlamydia pneumonia, antibodies to toll-like receptors (TLR2), platelet factor 4 (PF4), platelet aggregation parameters, lipid profile, concentration of antibodies to oxidized low-density lipoproteins (oxLDL), and the thickness of the intima-media complex (IMT) of the common carotid arteries. Results. The study included 50 women with SLE and 31 with myocardial infarction (MI), with a control group of 21 healthy women. Patients with SLE showed a significant increase in IMT of the common carotid artery (1.00 [0.80–1.10] > 0.80 [0.70–0.90], p = 0.01) and bifurcation of the carotid artery (1.10 [1.00–1.20] > 0.80 [0.70–1.10], p = 0.01) compared to the control group. Similarly, patients with MI had significantly different IMT values for both the common carotid artery (0.90 [0.80–1.10] > 0.80 [0.70–0.90], p = 0.01) and bifurcation (1.20 [1.10–1.40] > 0.80 [0.70–1.10], p = 0.01) compared to controls. There was pronounced activation of inflammation in SLE patients, evidenced by increased levels of CRP (3.67 [2.17–5.92] > 0.74 [0.30–1.26], p = 0.01), interleukin 6 (1.72 [1.39–2.68] > 0.60 [0.22–0.75], p = 0.01), and ESR (21.0 [18.0–26.0] > 10.0 [7.0–14.0], p = 0.01). These markers were also elevated in MI patients compared to controls: CRP (3.36 [1.44–5.90] > 0.74 [0.30–1.26], p = 0.01), interleukin 6 (1.1 [0.69–1.82] > 0.60 [0.22–0.75], p = 0.01), and ESR (19.0 [10.0–28.0] > 10.0 [7.0–14.0], p = 0.01). A significant activation of platelets was noted, with a marked increase in PF4 levels in SLE patients (21.5 [19.80–23.28] > 18.30 [13.88–20.46], p = 0.01) and MI patients (20.76 [19.00–23.50] > 18.30 [13.88–20.46], p = 0.01). SLE patients exhibited pronounced dyslipidemia, characterized by elevated levels of oxLDL antibodies (3.16 [1.45–4.60] > 1.39 [1.26–2,04], p = 0,01). In contrast, MI patients showed significant differences only in low-density lipoproteins (1.05 [0.88–1.21] < 1.32 [1.24–1.37], p = 0,01). The concentration of IgG antibodies to Chlamydia pneumonia in SLE patients (0,062 [0,035-0,124] > 0,0415 [0,022-0,071], p = 0,11) and TLR2 levels showed no significant diferences from controls (635,71 [357,14 –978,5] > 451,54 [352,05–775,0], p = 0,39). In MI patients, TLR2 levels did not differ from controls (448,98 [308,67–964,14] < 451,54 [352,05–775,0], p = 0,854). However, IgG antibodies to Chlamydia pneumonia were significantly higher in MI patients (0,067 [0,05–0,11] > 0,0415 [0,022–0,071], p = 0,026) compared to controls. Conclusion. In addition to traditional risk factors for cardiovascular diseases, both SLE patients and those with myocardial infarction exhibit common mechanisms of autoinflammation as a form of ischemic heart disease. The inflammatory component was more pronounced in the SLE group, particularly reflected in significantly elevated concentrations of IL-6 and CRP levels. The role of the infectious component requires further investigation.