COMPLEMENT-MEDIATED AND CYTOKINE-DRIVEN INFLAMMATORY MECHANISMS IN SUBCLINICAL MYOCARDIAL INJURY IN PATIENTS WITH ARTERIAL HYPERTENSION
Keywords:
arterial hypertension, ischemic heart disease, subclinical myocardial injury, high-sensitivity troponin, immunoinflammation, cytokines, complementAbstract
The article presents the results of a study of pro-inflammatory and complement-dependent mechanisms in patients with arterial hypertension (AH) and in those with combined pathology of AH and ischemic heart disease (IHD). A total of 78 patients were examined and divided into two groups: patients with isolated AH (Group I) and patients with AH complicated by IHD (Group II). The control group consisted of conditionally healthy individuals. The study included the analysis of pro-inflammatory cytokines (IL-6), C-reactive protein (CRP), and complement component C3a depending on the degree of subclinical myocardial injury assessed by high-sensitivity cardiac troponin (hs-cTn). It was found that an increase in hs-cTn levels is accompanied by a stepwise activation of inflammatory processes: IL-6 increased up to 4.9-fold, CRP up to 6.5-fold, and C3a up to 36.7-fold (p<0.001), reflecting pronounced activation of innate immunity and complement-dependent mechanisms. The highest levels of IL-6 and CRP were observed in patients with manifest IHD, whereas the peak activity of C3a was detected at the stage of pronounced subclinical myocardial injury.
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