Cell and Organ Transplantology. 2023; 11(2):88-95.
DOI: 10.22494/cot.v11i2.154

The improvement of endothelial function by inhibition of platelet activity using acetylsalicylic acid in patients with arterial hypertension

Talaieva T., Mishchenko L., Tretyak I., Matova O., Vasilinchuk N., Vavilova L

• M. D. Strazhesko National Scientific Center of Cardiology, Clinical and Regenerative Medicine, National Academy of Medical Sciences of Ukraine, Kyiv, Ukraine

Abstract

In accordance with modern ideas about the pathogenesis of thrombotic complications of cardiovascular diseases (myocardial infarction, stroke), it should be noted that platelets and platelet humoral factors play a key role in the development of thrombosis. Activated platelets are able to activate both endotheliocytes and pro-inflammatory cells – monocytes/macrophages, which take a direct part in the formation and progression of atherosclerotic plaque.
The purpose of the study is to determine the possibility of improving the function of the endothelium by suppressing the activity of platelets using acetylsalicylic acid (ASA) in patients with arterial hypertension and atherosclerotic cardiovascular diseases.
Methods. 41 patients with arterial hypertension and atherosclerotic cardiovascular diseases were included in the study. All patients were divided into two groups: group 1 included 20 patients who were taking ASA before the start of the study; group 2 consisted of 21 patients who did not receive ASA before participating in the study. During the study, patients of both groups received ASA (75 mg once a day) for 6 months as part of basic therapy (antihypertensives, statins). In all patients, before the start of the study and at the final stage, the activity of platelets was determined by the expression of glycoproteins GPIIb (CD41), GPIIIa (CD61) and P-selectin, as well as the content in the blood of endothelial progenitor cells (CD45^–CD31⁺CD133⁺) and desquamated endothelial cells (CD45^–CD31⁺CD133^–) by flow cytometry. The content of C-reactive protein, cytokines TNF-α and IL-10 and asymmetric dimethylarginine (ADMA) in the blood was determined by ELISA. All patients underwent a test with flow-dependent vasodilation of the brachial artery.
Results. In patients who did not receive ASA before the start of the study, the activity of platelets in the peripheral blood was higher, signs of more pronounced endothelial dysfunction than in patients who received ASA were noted. After 6 months of taking ASA on the background of standard antihypertensive therapy, the level of activation of platelets decreased in patients of both groups. In the patients of group 1, the expression of CD41 decreased by 31.8 % (p < 0.01), CD61 – by 15.2 % (p < 0.01). In group 2, the suppression of platelet activity was even more pronounced: the level of CD41 decreased by 55.2 % (p < 0.001), CD61 – by 27.5 % (p < 0.05). In patients of group 1, the percentage of P-selectin-expressing platelets decreased by 78.1 % (p < 0.01); in group 2, the number of such platelets also decreased significantly – by 42.5 % (р < 0.05). The number of endothelial progenitors in the blood increased significantly in both groups: 3 times in patients of group 1 (p < 0.001); 2.3 times – in patients of group 2 (p < 0.001). In patients of both groups, a significant (2-fold) increase in the endothelium-dependent vasodilatation index was observed (p < 0.01). At the end of the study, a decrease in the blood level of CRP by 12.2 % and 18.8 %, pro-inflammatory cytokine TNF-α by 50.0 % and 57.0 %, respectively, was found in patients of groups 1 and 2 (p < 0.001).
Conclusion. The suppression of platelet activity in response to acetylsalicylic acid in patients with arterial hypertension and atherosclerotic cardiovascular diseases was accompanied by alterations in the intensity of systemic inflammation and the restoration of endothelial functions.

Key words: platelets; endothelial progenitor cells; endothelial dysfunction; arterial hypertension; acetylsalicylic acid

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