Pathogenic connections of hypertension and chronic obstructive pulmonary disease (COPD) are poorly understood. According to several studies in patients with COPD, the cardiovascular causes of death are about 25%. The function of the right ventricle is the most important determinant of longevity in patients with pulmonary arterial hypertension. The most evidence-based inflammatory marker, which closely connected with exponential function of external respiration, is the C-reactive protein. Matrix metalloproteinases-9 plays an important role in cardiovascular diseases, providing stabilization of atherosclerotic plaque. The purpose of the study was to examine the parameters of right ventricular myocardium deformation and systemic inflammatory response indices under the influence of therapy. Materials and methods. 38 patients with COPD 2-3 stages in the acute phase against the background of hypertension, which were divided into two subgroups, were examined. The control subgroup included 19 patients taking standard therapy, the main group included 19 patients with a comorbid course of COPD 2-3 st. and GB 2 stage, to which standard therapy was prescribed rosuvastatin in a dose of 20 mg and amlodipine 5 mg. All patients underwent a general examination, collection of complaints and anamnesis, spirographic research to determine the parameters of the function of external respiration, echocardiographic study, determination of MMP-9 and hr-CRP, ET-1 levels in blood plasma. Results and discussion. Analysis of the obtained data showed that after 24 weeks of treatment with rosuvastatin and amlodipine, there was a significant decrease in Endothelin 1 (-64.69 [-74.06, -57.77] Δ% vs. -48.26 [-58.87, -20 48 ] Δ%), high-sensitivity C-reactive protein -70.00 [-80.00; -66.67] Δ% against -60.00 [-66.67; -42.86], matrix metalloproteinase -9 (-57.54 [-66.84, -49.07] Δ% vs. -47.84 [-62.13, -38.65] Δ%, respectively) when taking therapy compared to the group receiving the standard therapy regimen. Significant improvement in longitudinal deformation of the myocardium of the prostate in the main group by 6.54% in comparison with the control (-17.90 [-17.55, -18.30]% vs. -16.80 [-15.90, -17.80]%). Conclusions. Additional therapy with amlodipine and rosuvastatin in patients with GB in combination with COPD significantly improves the myocardium deforming functions of the prostate as compared to the subgroup of patients with GB and COPD on the background of standard therapy. A significant decrease in biochemical markers: Endothelin-1, a highly sensitive C-reactive protein, and matrix metalloproteinase-9 in a subgroup of patients with GB and COPD was additionally prescribed therapy with amlodipine and rosuvastatin.

Keywords: hypertension, chronic obstructive pulmonary disease, treatment, biomarkers

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