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Pol. Merkur. Lek (Pol. Med. J.), 2014, XXXVII/219: 170-174 Maximize

Pol. Merkur. Lek (Pol. Med. J.), 2014, XXXVII/219: 170-174

Title: Thyroid hormone and the cardiovascular system

Authors: Frączek M.M., Łącka K.

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SUMMARY IN POLISH & ENGLISH. FULL ARTICLE ONLY IN POLISH.

Thyroid hormone and the cardiovascular system


Frączek M.M.1, Łącka K.2

Medical University of Poznan, Poland: 1Medical Students’ Research Association, 2Department of Endocrinology, Metabolism and Internal Diseases

It is well established that thyroid hormones affect the cardiovascular system through genomic and nongenomic actions. TRα1 is the major thyroid hormone receptor in the heart. T3 suppresses increased mitotic activity of stimulated cardiomyocytes. Hyperthyroidism induces a hyperdynamic cardiovascular state, which is associated with enhanced left ventricular systolic and diastolic function and the chronotropic and inotropic properties of thyroid hormones. Hypothyroidism, however, is characterized by opposite changes. In addition, thyroid hormones decrease peripheral vascular resistance, influence the rennin-angiotensin system (RAS), and increase blood volume and erythropoetin secretion with subsequent increased preload and cardiac output. Thyroid hormones play an important role in cardiac electrophysiology and have both pro- and anti-arrhytmic potential. Thyroid hormone deficiency is associated with a less favorable lipid profile. Selective modulation of the TRβ1 receptor is considered as a potential therapeutic target to treat dyslipidemia without cardiac side effects. Thyroid hormones have a beneficial effect on limiting myocardial ischemic injury, preventing and reversing cardiac remodeling and improving cardiac hemodynamics in endstage heart failure. This is crucial because a low T3 syndrome accompanies both acute and chronic cardiac diseases.

Key words: thyroid hormones, cardiovascular system

Pol. Merk. Lek., 2014, XXXVII, 219, 170