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№4' 2019


International Medical Journal, Vol. 25., Iss. 4, 2019, P. 67−71.



Irina Anatolevna Hryhorova, Aleksandr Rostislavovich Yeskyn, Vladimir Anatolevich Vodopianov

Kharkiv National Medical University
City Out−Patient Clinic N3, Mariupil, Ukraine

To establish criteria for the severity of pathogenetic disorders in the most common forms of transient ischemic attacks, i.e. cardioembolic and atherothrombotic, a differentiated approach to the treatment and primary prevention of vascular disorders of the cerebral ischemia and dysfunction of ischemia was substantiated. To objectify endothelial dysfunction, endothelin−1 was studied with its principal antagonist − a sodium oxide vasodilator and the major pro−inflammatory cytokine TNF−α. The blood was collected from the patients 12 hours after the first neurological symptoms appeared, the purpose of which was to determine the peak values of the disturbance of biochemical parameters. The data obtained indicate that with a transient ischemic cardioembolic attack, a milder clinical manifestations is caused by less pronounced pathogenetic changes in endothelial dysfunction. At the same time, in atherothrombotic form, the neurological symptoms grow more slowly and have a more pronounced character, which is also confirmed by the study of endothelial dysfunction. Thus, the study of endothelial dysfunction severity in patients with transient ischemic attacks can justify a differentiated pathogenetic approach to treatment and improve the prevention of vascular disorders. Primary prevention in a transient ischemic attack should be directed to causes that are extravasal in nature, and at atherothrombotic treatment to atherosclerosis, mainly reduction of atherosclerotic plaques. Despite quite similar correlation of major vasoconstrictor and vasodilator disorders, a mild and moderate clinical severity due to various occlusion factors is observed. To further determine the occlusion mechanisms, it is necessary to study rheological, coagulation and dynamic parameters of patients' blood.

Key words: cardioembolic transient ischemic attack, atherothrombotic transient ischemic attack, endothelial dysfunction, endothelin−1.


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