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Cellular and humoral apoptosis markers in acute coronary syndrome combined with essential hypertension
Author(s) -
Л. В. Васина
Publication year - 2008
Publication title -
arterialʹnaâ gipertenziâ
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.126
H-Index - 5
eISSN - 2411-8524
pISSN - 1607-419X
DOI - 10.18705/1607-419x-2008-14-4-332-335
Subject(s) - annexin , apoptosis , unstable angina , peripheral blood mononuclear cell , medicine , myocardial infarction , acute coronary syndrome , pathogenesis , annexin a5 , immunology , cardiology , biology , flow cytometry , biochemistry , in vitro
The aim of this work was to examine the contents of annexin A5, sApo-1/Fas and sBcl-2 and the number of circulating mononuclear cells in apoptosis in order to clarify their role in the pathogenesis of acute coronary syndrome (ACS) combined with arterial hypertension (AH). We examined 83 patients with ACS (47 patients with unstable angina and 36 with myocardial infarction) and 14 healthy individuals. AH has been identified in 15 patients with unstable angina and in 17 with myocardial infarction. The number of viable mononuclear cells was significantly decreased and the number of mononuclear cells at the early stages of apoptosis (annexin A5-positive) was significantly increased as compared to control group in patients with the ACS, especially if combined with AH. At the same time there was a significant increase of sBcl-2 and sApo-1/Fas and annexin A5 in blood of the patients with myocardial infarction compared to patients with unstable angina, especially if combined with AH. The association between the level of sAro-1/Fas, annexin A5 and the number of circulating mononuclear cells at the early stages of apoptosis was shown in the study. Thus, in ACS, especially if combined with AH, enhanced cell apoptosis resulting from hemodynamic abnormal changes leads to activation of antiapoptotic mechanisms aimed at the decrease of the thrombophilia severity by reducing thrombogenic features of endotheliocytes subjected to apoptosis.

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