Cellular and humoral apoptosis markers in acute coronary syndrome combined with essential hypertension
https://doi.org/10.18705/1607-419X-2008-14-4-332-335
Abstract
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.
About the Author
L. V. Vasina
St Petersburg Pavlov State Medical University, Hospital №122 named after L.G. Sokolov, St Petersburg
Russian Federation
Russian Federation
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Review
For citations:
Vasina L.V. Cellular and humoral apoptosis markers in acute coronary syndrome combined with essential hypertension. "Arterial’naya Gipertenziya" ("Arterial Hypertension"). 2008;14(4):332-335. (In Russ.) https://doi.org/10.18705/1607-419X-2008-14-4-332-335
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