Abstract
Introduction: The study of indicators of innate immunity in patients with arterial hypertension in clinical trials makes it necessary to correct them in order to reduce vascular inflammation in arterial hypertension to prevent damage to target organs and development of cardiovascular complications. The aim of the study was to assess the effectiveness of antihypertensive therapy to correct indicators of innate immunity in patients with essential arterial hypertension.
 Materials and methods: Patients with essential arterial hypertension (EAH) (II stage, 3rd degree) were divided into 3 groups: the 1st group included the patients with hypertrophy of the left ventricular myocardium; the 2nd group included the patients with atherosclerotic vascular lesions; the 3rd group included the patients with chronic kidney disease. As an initial antihypertensive pharmacotherapy, all the patients with essential arterial hypertension were prescribed perindopril (5–10 mg/day) and amlodipine (5–10 mg/day).
 Results and discussion: Changes in innate immunity indices in patients with essential arterial hypertension (II stage, 3rd degree) are differentiated depending on the affected target organ. The antihypertensive pharmacotherapy with perindopril and amlodipine in patients with essential arterial hypertension has various corrective effects on impaired innate immunity, depending on the nature of target organ damage. Regardless of target organ damage, ноу antihypertensive therapy with perindopril and amlodipine does not affect the reduced functional and increased metabolic activities of peripheral blood neutrophils.
 Conclusion: The results obtained dictate the need for further clinical studies of other classes of antihypertensive drugs and their combinations in the correction of innate immunity indices in order to effectively prevent the progression of target organ damage.
 Graphical abstract:
Highlights
The study of indicators of innate immunity in patients with arterial hypertension in clinical trials makes it necessary to correct them in order to reduce vascular inflammation in arterial hypertension to prevent damage to target organs and development of cardiovascular complications
N/% Age, M ± m Anamnesis, M ± m SBP, M ± m DBP, M ± m Heart rate, M ± m Smoking, n/% Dyslipidemia (Total cholesterol over 4.9 mmol/L and/or cholesterol low density lipoprotein over 3.0 mmol/L), n/% Glucose concentration 5.6–6.9 mmol/L, n/% Impaired glucose tolerance, n/% Body mass index ≥ 30 kg/m2, n/% Waist circumference: ≥ 102 cm for men; ≥ 88 cm for women, n/% Family history of cardiovascular disease, n/% LVHM according to electrocardiography, n/% LVHM according to echocardiography, n/% Thickening of the wall of the carotid arteries, n/% Pulse wave speed > 10 m/s, n/% Ankle-brachial systolic pressure index < 0.9, n/% Chronic kidney disease, n/%
Clinical trials have identified chronic inflammatory diseases as a risk for cardiovascular diseases, and recent studies have identified the contribution of various inflammatory cells to vascular oxidative stress and inflammation
Summary
The study of indicators of innate immunity in patients with arterial hypertension in clinical trials makes it necessary to correct them in order to reduce vascular inflammation in arterial hypertension to prevent damage to target organs and development of cardiovascular complications. In experimental studies in mice, IL-6 suppression neutralized an increase in blood pressure in response to angiotensin II infusion and decreased the progression of chronic kidney disease, as measured by albuminuria (Lee et al 2006). This nephroprotection was associated with a decrease in the number of monocytes infiltrating the kidney and a decrease in the number of renal macrophages (Hashmat et al 2016). This indicates that intervention at the IL-6 application points can be an effective way to suppress target organ damage in hypertension by blocking the activation of myelomonocytic cells
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