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Коморбідний ендокринологічний пацієнт

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Международный эндокринологический журнал 3 (59) 2014

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Role of thyroid hormones in development of atrial fibrillation in patients with thyroid pathology

Авторы: Rebrov B.A., Sorokina E.E. - DZ "Lugansk State Medical University", Department of Internal Medicine , Faculty of Postgraduate Education.

Рубрики: Эндокринология

Разделы: Справочник специалиста

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The thyroid gland is one of the most important organs of internal secretion. Thyroid hormones have an effect on almost all types of metabolism, organs and systems of the body, especially on the cardiovascular system.This contributes to the development of various diseases, particularly cardiac arrhythmias. The transition process of the thyroid hormones in the active form occurs with the participation of metallo-enzymes - selenium-dependent monodeiodinase. In micronutrient selenium deficiency develops thyroid failure, despite normal levels of T4 in the blood plasma, it is so-called subclinical thyroid dysfunction.

The persons suffering from diseases of the thyroid gland (TG) by the recommendations of the European Society of Cardiology (ESC, 2010, 2012) were isolated in a separate category, which underlines the importance of the problem. AF in these patients is recorded in the 9–23 %.

Typically, patients with thyroid diseases are divided into groups depending on changes in its functions to persons with hyperthyroidism, euthyroid and with hypothyroidism.

Hyperthyroidism is correlated with a higher risk of AF, because of different portions of the myocardium functional heterogeneity, which arises in hyperthyroidism.Any additional increasing this heterogeneity effect can lead to complete activity discoordination in the different heart muscle portions, that causes to the development of AF. Direct and exchange-mediated effect of thyroid hormones on the myocardium causes a positive inotropic, chronotropic, dromotropic and bathmotropic effect that leads to more strong heart muscle contraction and more frequent heart rate (HR), improvement of conduction of excitation along the myocardium and increase of the heart muscle excitability, as well as reduce systemic peripheral resistance.

The choice of treatment for each patientis individual, and determined on the basis of indications and contraindications:

1. Thyreostatics: tiamazol (praescribed 20–50 mg for not more than 3–6 weeks); reduce the dose gradually during 3–4 weeks tillthe maintenance dose (5–10 mg/d). To prevent the recurrence of the disease the given dose is recommended to take for about 1–1.5 yrs.

2. Combination therapy is used in patients with high risk of recurrence of hyperthyroidism and includes tiamazol 5-15 mg/d, and levothyroxine 50 mg/d.

3. Indications for use of lithium carbonate (900–1800 mg/d): mild form of hyperthyroidism or preoperative intolerant thyreostatics.

4. Application of beta-blockers used as symptomatic therapy (propranolol - 40–120 mg. or metoprolol – 100–150 mg).

However, according to ESC (2012), despite the importance of the problem of hyperthyroidism leads to an increased risk of cardiovascular death in patients with atrial fibrillation. To increase the risk of cardiovascular death in patients with AF is hypothyroidism.

In international studies found that when hypothyroidism effects on the heart is not so much due to a general effect on metabolism, as in hyperthyroidism, but rather because of the synchronous operation of the conduction system of the heart and thyroid.

It is now established that K+ channels (KCNQ1, KCNE2) exist not only in the heart, but also in thyrocytes and simultaneously regulate not only processes repolarization, but also biosynthesis of thyroid hormones. Mutations of respective genes (congenital hypothyroid condition) or under their functioning due to acquired hypothyroidism leads to a shortening of the atrial refractory period and predisposes to the appearance of AF to increased electrical activity ventricular arrhythmias and often to lethal ventricular fibrillation.

Treatment of hypothyroidism in AF based on substitution therapy with levothyroxine. In old age, with CHD and arrhythmia history starting dose is 25 mcg/d. Increase the dose every 4–6 weeks at 25–50 mcg, carefully controlled ECG and TSH, T4. The second part of the treatment is metabolic therapy.

Thus, the action of thyroid hormones on the cardiovascular system is diverse, but the mechanisms of disorders of impulse conduction, as in hyper- and hypothyroidism insufficiently studied. AF in combination with impaired thyroid function is a serious problem in modern medicine.



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