The aim – to study the activity of low-grade inflammation and determine an interaction of its parameters with characteristics of humoral systems of blood pressure regulation, hypertensive heart and kidney damage in patients with resistant arterial hypertension (AH).
Material and methods. The results of examination of 129 patients with AH (72 patients with controlled AH, 57 persons with resistant AH) were included into the analysis. All patients, besides routine clinical examination, underwent 24-hours’ blood pressure monitoring, evaluation of systemiс inflammation markers (C-reactive protein, fibrinogen, IL-6, TNF-α), MMP-12 activity, cystatin C, renin, aldosterone, citrulline blood concentration; 24-hours’ excretion of albumin and metanephrine.
Results. In the resistant AH, compared to the patients with controlled arterial hypertension, higher levels of inflammation active phase proteins (C-reactive proteins – by 17.3 %, fibrinogen – by 10.6 %) and proinflammatory cytokines (IL-6 by 21.8 % TNF-α by 13 %) were detected. The activation of low-grade inflammation in patients with resistant AH has been associated with higher renin-angiotensin-aldosterone system activity: the concentration of plasma aldosterone correlated with IL-6 level (r=0.334; Р=0.03) and matrix metalloproteinase 12 activity (r=0.326; Р=0.02); active renin blood contents – with IL-6 (r=0.416; Р=0.01) and TNF-α (r=0.323; Р=0.03) levels). In patients with resistant AH the increase of left ventricle myocardial mass index was accompanied by elevation of plasma IL-6, and decrease of glomerular filtration rate was associated with growth of plasma TNF-α blood level (r=0.318; Р=0.04). Correlation of MMP-12 activity with renal impairment markers – cystatin С (r=0.405; Р=0.01) and citrulline (r=0.338; Р=0.03) was detected. In resistant AH pts increase of LVMI was accompanied by elevation of IL-6.
Conclusions. Resistant AH was characterized by more expressed activation of low – grade inflammation, compared to controlled AH, which is associated with renin-angiotensin-aldosterone system activation and hypertensive injury of heart and kidneys.