Clinical Physiology of Circulation

Chief Editor

Leo A. Bockeria, MD, PhD, DSc, Professor, Academician of Russian Academy of Sciences, President of Bakoulev National Medical Research Center for Cardiovascular Surgery


Endothelial dysfunction in the pathogenesis of disorders of cerebral circulation in atrial fibrillation

Authors: L.A. Bockeria, V.Yu. Taskina

Company:
A.N. Bakoulev Scientific Center for Cardiovascular Surgery of Russian Academy of Medical Sciences, Rublevskoe shosse, 135, Moscow, 121552, Russian Federation

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Link: Clinical Physiology of Blood Circulaiton. 2013; (): -

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Abstract

Atrial fibrillation is traditionally considered as a significant factor of cerebral blood flow dysfunction.
Cerebrovascular complications at atrial fibrillation are generally associated with cardiogenic
thrombembolia. Abnormalities of microcirculation and endothelial dysfunction at the level of final link
of the vascular tree, accompanying the atrial fibrillation, may further increase the risk of local clotting
in cerebral miscrovessels with the progression of clinical findings of ischaemic stroke.

Endothelium dysfunction, caused by these or those factors, is detected at various diseases and
states and always worsens the course of the primary disease, promoting its complications. Slow
blood flow, which furthers increase of blood viscosity and increase of shear stress appear to be the
reason of the progressing endothelial dysfunction in the final link of the vascular tree in addition to
atrial fibrillation. Continuous impact of such factor may lead to overstress and further decompensation
of compensatory mechanisms, related to products and effects of NO. Increase of protrombothic
state will be the result of such abnormality, which in addition to the cerebral blood flow, shall mean
increase of the risk of local clotting with the progression of clinical findings of ischaemic stroke. Nonregular
and impact with different amplitudes concerning its strength on endothelial cells of the pulse
wave may make an additional contribution into progression of endothelial dysfunction in the final link
of the vascular tree at atrial fibrillation

Despite the theoretical grounds of existence of endothelial dysfunction at the level of tissual miscrovessels
at atrial fibrillation, such an assumption shall be confirmed in practice. It is explained by
the fact that the investigations concerning this subject, conducted before, were not correct from the
point of view of the selected cohort of subject matter patients, many of which had coexisting diseases
that could easily damage endothelial function, notwithstanding the presence or absence of
atrial fibrillation itself. Apart from this, diagnostic potential of the methods of confirmation of
endothelial dysfunction in a miscrocirculatory course at atrial fibrillation, applied in the past year, was
obviously not sufficient.

The current situation with clarification of significance of endothelial dysfunction in the mechanisms
of cerebrovascular complications at atrial fibrillation necessitates continuation of appropriate
research. One should note, that such investigations, first of all, should include patients with exceptional
essential atrial fibrillation, and, secondly, shall be supported by the methods, providing the
most objective characteristics of endothelial state right at the level of tissual microvessels. The information
received in such a way, may become a basis for inclusion of cytoprotectants, applied for correction
of endothelial dysfunction into comprehensive treatment of patients with atrial fibrillation.

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