Significance of inflammation markers in patients with coronary microvascular dysfunction and non-obstructive coronary artery disease

Abstract

Aim. To study the relationship of coronary microvascular dysfunction (CMD) with the levels of pro- and anti-inflammatory biomarkers in patients with preserved ejection fraction (LVEF) and non-obstructive coronary artery disease (CAD).Material and methods. The study included 118 patients (70 men, mean age, 62,0 [58,0; 69,0] years) with preserved LVEF (62 [59; 64] %) and non-obstructive CAD. Serum levels of N-terminal pro-brain natriuretic peptide (NT-proBNP), high-sensitivity C-reactive protein (hsCRP), interleukin-1β, 6, and 10 were assessed initially by enzyme immunoassay. Coronary flow reserve (CFR) was assessed by dynamic single photon emission computed tomography. CFR ≤2 was a CMD marker.Results. Patients were divided into groups depending on CMD presence: group 1 included patients with CMD (n=45), and group 2 was the control group and included patients without CMD (n=73). HsCRP concentrations were 1,8 times higher (p=0,011) in group 1 compared to group 2. Interleukin-6 levels did not differ significantly between groups (p=0,842), while interleukin-10 concentrations were lower by 21,7 % (p=0,048), and interleukin-1β was 2,7 times higher (p=0,046) in group 1 compared to group 2. According to ROC analysis, hsCRP concentration ≥4,8 g/l (AUC=0,655; p=0,012), and NT-proBNP ≥950,6 pg/ml (AUC=0,792; p<0,001) were identified as markers associated with CMD in patients with non-obstructive CAD, while levels of interleukin-1β, 6 and 10 showed no diagnostic significance. Multivariate regression analysis showed that diastolic dysfunction (odds ratio, 3,27; 95% confidence interval, 2,26-5,64; p<0,001) and NT-proBNP ≥950,6 pg/ml (odds ratio, 2,07; 95% confidence interval, 1,56-4,12; p=0,023) were independent factors associated with CMD.Conclusion. We established that in patients with non-obstructive CAD, the pre­sence of CMD is associated with a higher expression of pro-inflammatory markers and a decrease in the expression of an anti-inflammatory marker, which may confirm the fact that chronic inflammation is one of CMD pathogenesis links.