Thyrotoxic heart is a syndrome of damage to the cardiovascular system in patients with thyrotoxicosis. Pathology mainly occurs with Basal disease, less often its causes are thyroiditis, TSH-producing pituitary tumors, thyroid neoplasm. Symptoms of the disease include tachycardia and other cardiac arrhythmias, signs of heart failure. For diagnosis, ECG and EchoCG, hormonal profile examination, thyroid scintigraphy are prescribed. Treatment involves correction of euthyroidism, taking beta-blockers, antiarrhythmics and other pathogenetic therapy drugs.
The negative effect of an excess of thyroid hormones on the work of the heart was first established by the English physician K. Parry in 1785. In 1835, the Irish doctor Robert Graves and the German specialist Karl von Bazedov described tachycardia associated with an increase in the thyroid gland. Manifestations of thyrotoxic heart of varying degrees of intensity occur in all patients with toxic goiter, severe cardiovascular diseases are observed in 12-68% of patients. The risk of cardiovascular complications has a direct correlation with the experience of thyrotoxicosis.
Thyrotoxic heart most often develops with diffuse toxic goiter (DTG, Basedova disease). In rare cases, the disease occurs with other pathologies of the thyroid gland, accompanied by:
- Hyperthyroidism: Basedova disease. Pathology has an autoimmune nature, characterized by constant immune stimulation of thyroid cells. As a result, the amount of thyroid hormones in the blood increases, which cause damage to the myocardium.:
- Thyroiditis. When glandular tissue is inflamed against the background of viral subacute thyroiditis or Hashimoto’s autoimmune thyroiditis, part of the organ cells are destroyed. In this case, hyperthyroidism lasts for several weeks or months, so the heart lesions are functional.
- Tumors. The phenomena of thyrotoxicosis are observed against the background of TSH-secreting tumors of the pituitary gland, toxic thyroid adenoma. It is extremely rare for cardiac pathologies to occur in women with an ovarian stroma that produces thyroid hormones.
Independent risk factors include late diagnosis of endocrine pathologies, low adherence of patients to treatment, incorrect regimen of thyrostatics. Symptoms of cardiovascular disorders are possible in people who take synthetic thyroid hormones uncontrollably. The disease is more often observed in women with a tendency to autoimmune disorders, burdened with a family history.
With a thyrotoxic heart, myocardial dystrophy is observed, which develops under the influence of two main mechanisms. Firstly, with thyrotoxicosis, persistent hyperfunction of the heart muscle is noted against the background of activation of the sympathetic part of the autonomic nervous system. Secondly, thyroxine and triiodothyronine have a direct toxic effect on the myocardium.
Thyroid hormones affect the myocardium at the level of the nuclei, regulate the flow of ions through cell membranes, change the activity of mitochondria. The molecular mechanisms of toxic effects are realized through phospholipid-dependent protein kinases, the caldomodulin-Ca complex, and cMAF protein kinase. An increase in total vascular resistance in thyrotoxicosis increases the severity of the resulting disorders.
Pathomorphologically, mosaic disorders of the structure of cardiomyocytes, the presence of destroyed and intact mitochondria within a single cell are determined. Thyrotoxic effects cause the development of intracellular edema, an increase in the number of glycogen inclusions. With the long-term existence of the disease, irreversible foci of myocardiofibrosis occur.
According to WHO recommendations, cardiac dysfunction in thyrotoxicosis is defined as a subspecies of metabolic cardiomyopathy. In the absence of appropriate treatment for thyrotoxicosis, cardiac disorders are steadily progressive. In clinical cardiology , there are 3 stages of heart remodeling in patients with thyrotoxicosis:
- Hyperkinetic. It is observed at the first stage of thyrotoxic lesion, manifested by an increase in strength and heart rate. The hyperkinetic phase is characterized by an increase in the selection fraction up to 65% in the absence of organic changes in the myocardium.
- Normokinetic. At the second stage, there is a gradual increase in the mass of the myocardium of the left ventricle and the expansion of the cavities of the heart. Cardiac output and other functional parameters are within the normal range.
- Hypokinetic. At the third stage of thyrotoxic heart contractile function decreases sharply, chronic heart failure develops. Violations are accompanied by pronounced dilation of the left ventricle.
The most frequent manifestation of the disease is a feeling of palpitation, which is caused by constant sinus tachycardia. A person experiences a feeling of heaviness and dull pains in the heart area, severe weakness, fatigue when walking and habitual household activities. Shortness of breath often occurs, dizziness and pre-fainting states may occur.
With the progression of thyrotoxic heart syndrome, severe pain occurs in the left half of the chest, swelling of the lower extremities appears, there are attacks of suffocation and coughing. Some patients experience distension and enlargement of the abdomen, pain and heaviness in the right hypochondrium. The cervical and peripheral veins swell and contour well through the skin.
Cardiac symptoms are accompanied by typical manifestations of thyrotoxicosis. Patients become irritable, emotionally unstable, and have difficulty falling asleep. Digestive disorders are represented by frequent diarrhea and decreased appetite. There may be a fine-grained tremor of the extremities, muscle weakness, motor activity disorders.
High resting heart rate, which is observed in all patients with a thyrotoxic heart, is a predictor of the risk of fatal conditions. With constant tachycardia, the probability of acute transient ischemic attacks, strokes, and lethal ventricular fibrillation increases by 3 times. In patients with concomitant hypertension and coronary heart disease, there is a worsening of the course of diseases, a decrease in pharmacological control.
A serious complication of the disease is atrial fibrillation, which develops in 28% of patients. Up to 68% of patients with a long history of thyrotoxic heart experience manifestations of heart failure (HF). At first, the right ventricular type of heart failure develops, since the right parts of the heart deplete their functional reserve faster. In the absence of medical correction, a total form of heart failure is formed.
During a physical examination of the patient by a cardiologist, an increase in heart tones, systolic noises, and the emphasis of the second tone on the pulmonary artery are determined. Percussion reveals the expansion of the boundaries of the heart. To determine the nature and severity of organ-functional disorders, a comprehensive examination program is used, which includes the following methods:
- ECG. According to the results of electrocardiography, sinus tachycardia, an increase in the amplitude of the teeth is determined at the initial stage of the disease. At later stages, atrioventricular or intraventricular blockages occur, prolongation of the QT interval, inversion of the T wave, which reflects the process of myocardial remodeling.
- EchoCG. Ultrasound examination of the heart reveals a consistent increase and decrease in the fraction of blood ejection, dynamic observation reveals a gradual expansion of the ventricular cavities. When performing EchoCG at the hypokinetic stage, signs of myodystrophic cardiosclerosis are determined.
- Scintigraphy. A radioisotope scan of the gland is prescribed to determine its functional activity. According to the distribution of radioactive isotopes, it is possible to identify diffuse changes or focal hormonally active formations.
- Analysis of myocardial markers. To exclude acute myocardial damage, a troponin test is performed, the content of creatine phosphokinase and lactate dehydrogenase is determined. It is advisable to perform an analysis of acute-phase blood parameters.
- Hormonal studies. To confirm the thyrotoxic nature of cardiac pathology, tests are prescribed for hormones T3, T4 (their number is increased) and pituitary TSH, the level of which is more often reduced.
Signs of a thyrotoxic heart must be distinguished from toxic-allergic myocarditis, rheumatic valvular defects, and other variants of metabolic cardiomyopathies. Differential diagnosis is carried out with independent forms of arterial hypertension, coronary heart disease, tuberculosis intoxication.
Drug therapy is aimed at achieving the euthyroid state and the maximum possible relief of cardiac symptoms. The main group of drugs used are antithyroid (thyrostatics), which block the synthesis of thyroid hormones. As the levels of T3 and T4 decrease, their negative effects on the myocardium decrease. Complex treatment includes the following groups of medications:
- Beta-blockers. Most patients are prescribed non-selective blockers that contribute to the elimination of tachycardia and other types of arrhythmias. With subclinical thyrotoxicosis, it makes sense to prescribe selective beta-blockers that have a long half-life.
- Antiarrhythmic drugs. Repolarization inhibitors, which have a weak inotropic property, have the greatest activity in thyrotoxic cardiomyopathy. To enhance the effect, therapy is supplemented with cardiometabolic drugs, vitamin and mineral complexes.
- Diuretics. Diuretics are added to the treatment regimen of an advanced form of thyrotoxic heart, which is accompanied by heart failure. Cardiac glycosides in strictly controlled doses can also be used to support the work of the organ.
- Anticoagulants. Against the background of arrhythmias, there is an increased risk of thrombosis, which requires preventive administration of antiplatelet agents and anticoagulants. Since the plasma clearance of coagulation factors associated with vitamin K increases with DTG, the doses of drugs should be less than standard.
Prognosis and prevention
The outcome of the disease directly depends on the success of the treatment of the cause of thyrotoxicosis, patient compliance, timely diagnosis of cardiac pathology. When persistent euthyroidism is achieved, it is possible to eliminate arrhythmia and reduce the risk of cardiovascular crises. With the development of total heart failure, the prognosis is unfavorable. Prevention consists in the prevention, early diagnosis and comprehensive treatment of thyroid pathologies.