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Endothelial function in thyrotoxicosis and its relationship with cardiovascular remodeling

https://doi.org/10.18705/1607-419X-2011--2-

Abstract

The data on the endothelial function in thyrotoxicosis is insufficient. There are many case reports of trombosis in patients with high level of von Willebrand factor (VWF). Present study addresses the influence of thyrotoxicosis on the VWF level, endothelium-dependent vasodilatation and remodeling of the heart and vessels. 143 normotensive patients with thyrotoxicosis without known cardiovascular diseases were included. Mean level of thyroid hormones had been increased before the therapy and it decreased till the normal values after 3 weeks and was stable one year after the treatment. Our results demonstrated, that increase of VWF is associated with thyrotoxicosis, and normalization of thyroid hormones is associated with the decrease of VWF level. The endothelial dysfunction developed at thyrotoxicosis is related to the level of thyroid hormones and thyrotrophic hormone receptor remodeling of the heart and vessels, and, particularly, to the development of pulmonary hypertension.

About the Authors

A. Yu. Babenko
Almazov Federal Heart, Blood and Endocrinology Centre, St Petersburg
Russian Federation


E. N. Grineva
Almazov Federal Heart, Blood and Endocrinology Centre, St Petersburg
Russian Federation


M. I. Kadinskaya
Pavlov St Petersburg State Medical University, St Petersburg
Russian Federation


A. V. Lisker
Pavlov St Petersburg State Medical University, St Petersburg
Russian Federation


E. V. Shlyakhto
Almazov Federal Heart, Blood and Endocrinology Centre, St Petersburg; Pavlov St Petersburg State Medical University, St Petersburg
Russian Federation


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Review

For citations:


Babenko A.Yu., Grineva E.N., Kadinskaya M.I., Lisker A.V., Shlyakhto E.V. Endothelial function in thyrotoxicosis and its relationship with cardiovascular remodeling. "Arterial’naya Gipertenziya" ("Arterial Hypertension"). 2011;17(2):115-122. (In Russ.) https://doi.org/10.18705/1607-419X-2011--2-

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ISSN 1607-419X (Print)
ISSN 2411-8524 (Online)