Correction of systemic inflammation and endothelial dysfunction in patients with chronic obstructive pulmonary disease in combination with arterial hypertension under the influence of the therapy

One of the main pathogenetic mechanisms combining chronic obstructive pulmonary disease (COPD) and arterial hypertension (AH) is a persistence systemic inflammation leading to the formation of endothelial dysfunction (ED), which serves as an independent predictor of the adverse prognosis of most cardiovascular diseases (CVD), while the treatment of patients with COPD in combination with AH requires the inclusion of drugs that have a beneficial effect on these pathological conditions. Prolonged-release indapamide has a number of pleiotropic effects, but most studies to study its effect on the state of endothelium and the intensity of systemic inflammation were conducted in patients with AH without associated bronchial obstructive diseases. The works carried out in conditions of comorbidity with COPD and according to the data of which the influence of diuretic drugs on the markers of systemic inflammation and ET in patients would be evaluated, were not found out, in this connection the present research was initiated and carried out.

The aim of the study was to evaluate the dynamics of markers of systemic inflammation and ET in the inclusion of diuretics in the complex therapy of patients with COPD in combination with BA.

Materials. Patients (n = 65: 50 men and 15 women) with stage I – IV COPD suffering from arterial hypertension (AH) I – III with initially elevated levels of systemic inflammation markers and ET, in whom the antihypertensive therapy performed was not effective enough, were included in the study.

Results. The results of the research on estimation of dynamics of markers of system inflammation – highly sensitive C-reactive protein (hsСRP), an intercellular adhesion molecule of type 1 (sICAM-1) and ET – endothelin-1, sP-selectin at the inclusion of diuretics in the therapy of patients with COPD with AH are presented. When analyzing the dynamics of the studied markers, a decrease in their level was noted, but statistically significant changes were obtained only in patients against the background of prolonged-release indapamide treatment. Additional pleiotropic effects of indapamide, consisting in reduction of activity of markers of systemic inflammation and ET, are also shown. Its high efficiency in achieving and maintaining the target AH levels compared to hydrochlorothiazide has been demonstrated.

Conclusion. The expediency of the inclusion of prolonged-release indapamide in the complex therapy of patients with COPD in combination with AH on the first line of antihypertensive therapy has been demonstrated due to its additional pleiotropic properties, which consist in the influence on the general pathogenetic links of the formation and progression of AH in COPD and its high antihypertensive efficiency in comparison with hydrochlorothiazide.

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