Hyperthyroid heart disease in the elderly

Introduction to hyperthyroidism in the elderly Hyperthyroidism Heart disease (hyperthyroidism) is an endocrine of a series of symptoms and signs caused by thyroid disease excretion of excessive thyroid hormone on the direct or toxic effects of the heart, such as arrhythmia, heart enlargement, heart failure, angina pectoris, etc. Disordered heart disease. basic knowledge The proportion of illness: 0.0053% Susceptible people: the elderly Mode of infection: non-infectious Complications: angina pectoris heart failure arrhythmia myocardial infarction

The cause of hyperthyroidism in the elderly

Genetic factors (20%):

Genetic defects are the basis of the onset of GD and are based on:

1 The family aggregation of this disease is very obvious.

2 The co-observation rate of sequential twins in children is 30% to 60%, and astigmatism is 3% to 9%.

3 patients themselves or their families often have other autoimmune thyroid diseases, such as Hashimoto's thyroiditis, or other autoimmune diseases such as type I diabetes, myasthenia gravis, rheumatoid arthritis, systemic lupus erythematosus, Idiopathic thrombocytopenic purpura, pernicious anemia, and atrophic gastritis.

4HLA-B8, HLA-DR3, HLA-DR5, especially HLA-DQW2 and HLA-DR3-DQA1*0501-DQB*0201 are closely related to GD.

The frequency of 5 IgG heavy chain allotype determinant gene locus Gm in GD patients is significantly higher than that of normal people. However, the genetic pattern of this disease is still unclear, and the result of genetic factors may be inhibitory T cells (Ts). ) Functional defects.

Autoimmune (20%):

Immune abnormalities are the key to the pathogenesis of GD. It has been confirmed that there are abnormalities of humoral immunity and cellular immunity in GD patients. Among them, thyroid stimulating antibody (TSAb) is the main reason for the development of GD.

(1) humoral immune abnormalities: non-thyroid specific antibodies and thyroid specific antibodies can be detected in the blood of GD patients. The former includes antinuclear antibodies, anti-smooth muscle antibodies, anti-lymphocyte antibodies, anti-islet cell antibodies, anti-adrenal cell antibodies and Anti-gastric cell antibodies, etc. These non-specific antibodies are only a representation of GD and are not directly related to the onset of GD.

Thyroid-specific antibodies include thyroglobulin antibody (TGAb), thyroid peroxidase antibody (TPOAb), anti-thyroid hormone antibody, sodium/iodine transporter (NIS) antibody, TSH receptor antibody (TRAb), and thyroid stimulating immunoglobulin (TGI), etc., the latter two types of antibodies play an important role in the pathogenesis of GD.

Since Adoms and Purves discovered and named LD serum long-acting thyroid stimulants (LATs) in 1965, their functions, properties and relationship with GD have been studied in depth. It has been confirmed that LATs and their analogues belong to the same Abnormal immunoglobulins, mainly produced by lymphocytes in the thyroid gland, generally belong to IgG, collectively referred to as TRAb, which is divided into two types, stimulating and blocking. The former is called TSAb, and the latter is blocked by thyroid stimulation. TSBAb), TRAb can inhibit the binding of TSH to its receptor. The antibody detected based on this principle is called TSH-binding immunoglobulin (TBII). In fact, TBII includes two subtypes, one of which interacts with TSAb. Consistently, another has the activity of TSBAb. Both stimulatory and blocking antibodies can exist in GD patients. The growth and decline of activity is one of the reasons for the mutual transformation of hyperthyroidism and hypothyroidism. TGI has a higher examination in patients with GD. Outbreak rate, this antibody is closely related to the occurrence of goiter.

(2) Abnormal cellular immunity: autoantibodies in GD patients are associated with abnormal regulation of B lymphocytes. The study found that the number of activated T cells in the blood of GD patients, that is, the number of HLA-DR+ T cells increased, and its peripheral and/or thyroid gland The number of Ts cells decreased, the ratio of helper T cells (Th) to Ts increased, and the number and function of NK in the blood circulation or thyroid of the patients showed significant changes. In addition, -interferon and interleukin-6 (IL) were still present in GD patients. -6), abnormalities of various cytokines such as IL-8, IL-10, IL-13, IL-15 and IL-18, these factors are important for the occurrence and continuation of GD.

(3) Abnormal expression of HLA-DR antigen: thyroid cells of GD patients can express HLA-DR antigen abnormally. It has been thought that such thyroid cells can be used as antigen-presenting cells, present autoantigens to lymphocytes, and induce autoantibodies. In recent years, some people have questioned this. It is believed that the abnormal expression of HLA-DR antigen may be a secondary phenomenon, which has a protective effect on the body and can block the further development of GD.

(4) Abnormal adhesion molecules: the levels of soluble intercellular adhesion molecule (sICAM), vascular cell adhesion molecule (VCAM) and selectin in GD patients are increased, and thyroid cells can express ICAM, lymphocyte function. Antigen (LFA), etc. However, whether the abnormality of adhesion molecules is secondary to hyperthyroidism, or whether the pathogenic factors of GD need further study, 3. stress trauma, surgery, trauma and childbirth and other stress factors in the occurrence of GD It plays an important role in stress, causing a sharp rise in adrenal cortex hormones, further reducing Ts function, disorienting the Ts/Th ratio, leading to an increase in the body's immune response. In addition, the sympathetic nervous system is over-activated under stress, the latter directly or indirectly Causes abnormal synthesis and secretion of thyroid hormone.

Infection (20%):

Infection can lead to normal human cell destruction and antigen release, induce HLA-DR antigen expression and the production of various cytokines, and then promote GD. Some intestinal bacteria such as Yersinia and TSH receptors have a common antigenic determinant. When it is infected, an autoantibody similar to TRAb and/or an anti-TSH anti-idiotypic antibody can be produced, thereby causing the occurrence of GD.

Apoptosis (10%):

IgG in GD patients can regulate the expression of Fas protein in thyroid cells and its mediated apoptosis. Thyroid stimulating antibodies can participate in the development of GD goiter by inhibiting Fas-induced apoptosis, while blocking antibodies By inhibiting the action of TSH, increasing sensitivity to Fas-mediated apoptosis leads to destruction of thyroid in Hashimoto's thyroiditis (HT) or thyroid atrophy in patients with atrophic thyroiditis. On the other hand, soluble Fas in patients with GD and HT There is an abnormal serum concentration (sFas), which is a Fas that lacks a transmembrane region due to splicing abnormalities, which can block Fas-mediated apoptosis, sFas increase during GD hyperthyroidism, GD remission and HT thyroid function are normal. Time decreases, and remains normal during HT hypothyroidism and painless thyroid hyperthyroidism, and sFas values are associated with GD thyroid stimulatory antibody activity. This conclusion suggests an increase in Fas cleavage variant expression in GD patients. The reduction of normal Fas can promote the growth of thyroid gland by preventing thyroid cell apoptosis and increasing the production of thyroid stimulating antibodies by autoreactive B lymphocytes. , HT decrease in sFas means that normal Fas expression increased, thus leading to apoptosis by increasing thyroid damage.

Pathogenesis

1. The effect of thyroxine on the heart

There is thyroid catecholamine receptor on the inner side of myocardial cell membrane. Excessive thyroxine in hyperthyroidism can reduce the content of adenosine triphosphate (ATP) and creatine phosphate in the myocardium. According to the study, T4 has a direct positive inotropic effect. Adenylate cyclase activity is enhanced, and T4 works together to strengthen myocardial contractility, improve myocardial catecholamine action and sensitivity, and inhibit cardiac monoamine oxidase activity. Under excessive thyroxine, myocardial smooth muscle cell membrane slow sodium-calcium channel Activation, positive positive force effect and time change effect, the result of the above combined action can make tachycardia and increase cardiac output.

2. Changes in myocardial metabolism

It is known that thyroxine acts on the heart by changing the synthesis of proteins. When hyperthyroidism is excessive, thyroxine accelerates myocardial metabolism and oxygen consumption. The energy released in oxidation cannot be stored as high-energy phosphate bonds, but in the form of heat. This oxidative phosphorylation separation causes an increase in myocardial catabolism, anabolic inhibition, resulting in insufficient adenosine triphosphate and creatine content, reduced glycogen and protein synthesis, and more heat energy per myocardial excitation-contraction coupling reaction. Being released, the myocardial work is not efficient.

3. Hemodynamic changes

Excessive thyroid gland hyperthyroidism causes hypermetabolism, skin telangiectasia, increased vascular volume, and establishment of arteriovenous shunt in the microcirculation, increased blood flow to the heart, resulting in a significant increase in cardiac output, stroke volume of hyperthyroidism patients, The average systolic ejection rate, the wall shortening rate and the coronary blood flow rate were increased, while the contraction ejection interval and the pre-ejection period were shortened, the pulse pressure difference was widened, the systemic circulation resistance was decreased, the venous return flow was increased, and the pulmonary artery and Right ventricular pressure is significantly increased, myocardial oxygen consumption is increased, continuous overload can expand the heart, resulting in myocardial failure, due to the right ventricular myocardial reserve capacity, so hyperthyroidism first appeared right heart failure, and excessive thyroid hormone can make myocardium The Na/K-ATPase activity on the cell membrane is enhanced, and the Na efflux and K influx are promoted, which affects the electrophysiology of cardiomyocytes. In particular, the action potential duration of atrial myocytes is shortened, the electrical excitability is increased, and arrhythmia such as atrial fibrillation is easily caused. At the same time, hyperthyroidism is divided into myocardial metabolic oxidative phosphorylation, myocardial sensitivity to hypoxia is increased, easy to cause coronary artery spasm, and cause myocardial ischemia.

Elderly hyperthyroidism prevention

Primary prevention

Avoid the occurrence of hyperthyroidism by preventing various causes, including prevention of Hashimoto's thyroiditis, avoiding iodine deficiency and excessive iodine intake, preventing infection (infection of Yersinia enterica), avoiding mental stimulation and trauma, and passing Fishing, raising flowers, calligraphy, painting to cultivate the feelings, soothe the nerves, and actively participate in social activities, enrich the old age of life, maintain optimism, cheerful personality, avoid worrying about tension all over the world, overcome loneliness, pessimism, disgusting, narrow, violent Wait for bad personality and emotions to maintain a good and comfortable state of mind.

2. Secondary prevention

That is, early detection, diagnosis of sick elderly, regular (six months to 1 year) physical examination is very important, especially for high-risk elderly, thyroid function measurement, thyroid ultrasound should be used as a routine physical examination program, in order to early detection of early treatment.

3. Three levels of prevention

For the elderly with clear diagnosis, regular systemic treatment should be patiently explained, comforting the work, preventing the patient from fluctuating and external mental stimulation. During the onset, pay attention to rest, and should be bedridden in the early stage. The diet is light and nutritious. Easy to digest, it is advisable to add enough calories and nutrients, such as sugar, protein and vitamin B, to supplement the body's consumption.

Elderly hyperthyroid heart disease complications Complications angina pectoris heart failure arrhythmia myocardial infarction

Concurrent with angina, heart failure, arrhythmia, atrial fibrillation or myocardial infarction.

Elderly hyperthyroidism symptoms common symptoms goiter, weight loss, fatigue, abdominal pain, edema, depression, nausea, weakness, acute osteoporosis

The clinical manifestations of hyperthyroidism include: T3, T4 hypersecretion group, goiter and eye signs, but in the elderly, hyperthyroidism is more atypical, often with a special performance and easy to be misdiagnosed.

1. Typical clinical symptoms of senile hyperthyroidism

(1) High metabolic syndrome group: Due to excessive secretion of T3 and T4, the three major nutrients of sugar, fat and protein are hypermetabolized, oxidation is accelerated, heat production and heat dissipation are obviously increased, and patients often suffer from heat and sweat, and the skin is moist. The hand, the palm, the back, the chest, the armpit and other parts are obvious, and may be accompanied by low heat. At the same time, due to the high energy consumption, the protein catabolism accelerates to cause a negative nitrogen balance, resulting in excessive consumption of muscles and other tissues, and the patient often suffers from weight loss. Complained of fatigue, weight loss, about 80% of elderly patients with hyperthyroidism have weight loss, often the first symptom.

(2) Cardiovascular symptoms: Sinus tachycardia is a common manifestation of senile hyperthyroidism, usually 90-120 beats/min, and persists at night. Rest and general sedatives are difficult to relieve, which is one of the characteristics of this disease. However, the heart rate of about 40% of elderly patients with hyperthyroidism is <100 beats/min, which is due to the increase of diastolic depolarization rate and the shortening of the action potential interval in sinus node cells. The degree of tachycardia is usually proportional to the severity of the disease. The patient complained of palpitations, shortness of breath, chest tightness, and increased during activities.

1 arrhythmia: premature beats are most common, atrial, ventricular, borderline can occur, especially in pre-atrial contractions, sometimes paroxysmal or persistent atrial fibrillation and atrial flutter, occasional room Ventricular conduction block, atrial fibrillation and conduction block are relatively common in elderly patients, with the increase in age, hyperthyroidism caused an increase in the incidence of atrial fibrillation, hyperthyroidism over 60 years old, the incidence of atrial fibrillation is 25%, some scholars suggest For the new generation of atrial fibrillation in the elderly should consider the possibility of eliminating hyperthyroidism, in addition, elderly hyperthyroidism combined with slow arrhythmia is also reported, including significant sinus tachycardia, sinus rest, sinus block and varying degrees of room Ventricular conduction block, very few occurrence of repeated syncope or threatened syncope, even if a cardiac pacemaker is implanted due to severe sinus node dysfunction or complete atrioventricular block, the cause of slow arrhythmia in patients with hyperthyroidism is unknown It may be caused by autoimmune inflammatory changes involving the conduction system. This type of slow arrhythmia can restore normal sinus node and atrioventricular conduction function after anti-thyroid drug treatment returns to normal. , Unexplained clinically sick sinus syndrome and atrioventricular block, should consider this rare cause of hyperthyroidism heart, in order to avoid improper placement of a permanent artificial heart pacemaker.

2 heart enlargement and heart failure: early morphological changes of the hyperthyroidism are prominent in the pulmonary artery segment, the left edge of the heart is straightened, the left heart is enlarged in the heart, or the right ventricular hypertrophy and whole heart hypertrophy can be called hyperthyroidism. Cardiomyopathy, elderly patients with hyperthyroidism, if the disease is long, the disease is not well controlled, the heart of the hyperthyroidism is easy to develop into heart failure, the incidence of congestive heart failure in elderly patients with hyperthyroidism is 10% to 25%, with atrial fibrillation Compared with sinus rhythm, the incidence of heart failure is 4 times higher, but in hyperthyroidism, due to pulmonary artery pressure and right intraventricular pressure is significantly increased, it is prone to right heart failure, simple left heart failure, pulmonary edema is rare.

3 ischemic heart disease: the incidence of coronary artery insufficiency in patients with hyperthyroidism is about 10% to 20%, manifested as angina pectoris and myocardial infarction, which is mostly combined with angina pectoris, with myocardial infarction rare, hyperthyroid ischemic heart disease, Coronary angiography is normal and can be completely restored with the healing of hyperthyroidism.

4 Possible mechanisms of hyperthyroidism include: A. tachycardia, increased myocardial oxygen consumption, cardiac hypertrophy, imbalance of myocardial blood supply and demand, B. tachycardia, diastolic phase shortening, diastolic blood pressure, resulting in insufficient coronary blood supply, C. Cardiac autonomic nervous system dysfunction, parasympathetic nerves inhibit myocardial inhibition, coronary artery spasm and excessive accumulation of lactic acid, D. microvascular embolism, microcirculatory disorders.

(3) In addition to cardiac symptoms, hyperthyroidism can be accompanied by atypical symptoms such as digestive system, blood system and mental nervous system.

1 digestive system: appetite hyperthyroidism, but significant weight loss is one of the characteristics of hyperthyroidism, but elderly patients, less than a quarter of appetite hyperthyroidism, the opposite 1/3 to 1/2 of patients anorexia, accompanied by other gastrointestinal symptoms For example, abdominal pain, nausea and intractable vomiting, the elderly can also have constipation.

2 symptoms of the nervous system: T3, T4 on the nervous system often makes the patient nervous, prone to excitement, irritability, etc., but only 25% of the elderly have the above symptoms, on the contrary, the elderly of hyperthyroidism are dumb, lethargic, Depression and apathy, and appear aging, and even cachexia, this condition is often referred to as "apathetic hyperthyroidism."

3 blood system: most patients with hyperthyroidism have red blood cell count size, normal morphology, normal hemoglobin concentration, and neutrophils often decrease, sometimes less than 3.0 × 109 / L, but the absolute value of lymphocytes, percentage and mononuclear cells increase; The lifespan of platelets is shortened, and the skin is prone to purpura.

4 Musculoskeletal system: The clinical manifestations are acute and chronic myopathy. The patient complains of weakness and weakness, and the action, especially the landing, the standing up, the continuous combing and the overhead, and the elderly are also occasionally recurrent. At the same time, due to systemic hypermetabolism, the protein matrix in the bone is insufficient, leading to osteoporosis, especially for older women who have been menopausal, osteoporosis can be more obvious, increasing the risk of fracture, a small number of patients can develop pathology Sexual fractures, especially vertebral compression fractures and femoral neck fractures.

5 Goiter: Goiter is one of the main clinical manifestations of hyperthyroidism, but many elderly patients often have no obvious goiter.

Most of the elderly patients with hyperthyroidism have the above typical and atypical symptoms, and asymptomatic are rare. There is no report yet.

2. Signs of elderly hyperthyroidism

(1) Typical signs: the impulse in the anterior region is enhanced, the first heart is loud, the second sound of the pulmonary artery is hyperthyroidism, the third heart sound appears, and the audible period is clicked. The heart sound of the atrial fibrillation is different, and the rhythm is absolutely Incomplete, the pulse rate is not less than the heart rate, and the heart is enlarged.

(2) atypical signs: premature beats, tachycardia.

First of all, in order to meet the diagnosis of hyperthyroidism, in addition to clinical symptoms and signs, laboratory tests are very important, especially in atypical elderly patients with hyperthyroidism, except for T4, free T4, T3 and free T3, TSH levels are low or even undetectable. It is an important indicator for the diagnosis of hyperthyroidism.

Elderly hyperthyroidism examination

Blood routine

The total number of white blood cells decreased, the absolute value and percentage of lymphocytes increased, and red blood cells and hemoglobin were mostly normal.

2. Blood sugar

Fasting blood glucose is normal, and blood glucose peaks increase after meal or oral glucose tolerance test, even diabetes-like type, plasma insulin is also increased, but there is no obvious delay in insulin secretion and thyroid gland not only increases the utilization of glucose in surrounding tissues, but also promotes sugar. The original decomposition is related to the acceleration of intestinal glucose absorption.

3. Blood lipids

At the time of hyperthyroidism, the synthesis and decomposition of cholesterol and triacylglycerol are enhanced, and the decomposition is more than synthesis, so cholesterol is often low, and triacylglycerol can be slightly lower.

4. Basal metabolic rate determination

The basal metabolic rate refers to the amount of heat generated per square meter of body surface area per hour after the human body is fasted for 14 to 16 hours, and the absolute value of the ambient temperature is 16 to 20 ° C. The normal value is -10% to +15. %, 95% of patients with hyperthyroidism are higher than normal, the degree of increase is consistent with the severity of the disease, clinically +15% ~ +30% is light, +30% ~ +60% is medium, > +60% is heavy, but measured Other influencing factors such as fever, cardiopulmonary dysfunction, malignant tumor and anemia should be excluded. The following formulas are commonly used in clinical practice: the method is fasted for 12 hours, and the pulse rate and blood pressure are measured in the morning after 8 hours of sleep, and then calculated by the formula:

Basal metabolic rate (%) = (pulse rate + pulse pressure difference) - 111

Basal metabolic rate (%) = 0.75 × [pulse rate + (0.74 × pulse pressure difference)] - 72

5. Determination of thyroid function

(1) TT4 (serum total thyroxine) is not affected by iodine in food and drugs, but is affected by TBG (serum thyroxine binding protein), which increases or decreases with increasing or decreasing TBG, while TBG is affected by Estrogen, pregnancy, viral hepatitis and other factors are increased, and are affected by androgen, severe liver disease, and hypoproteinemia. TT4 is reduced in many acute and chronic diseases due to the conversion of T4 to T3 in peripheral tissues. High TT4emia is formed, but at this time the thyroid function is normal, such as systemic infectious diseases, myocardial infarction, liver and kidney dysfunction and malignant tumors, so the increase of TT4 can not be used as a positive diagnosis of hyperthyroidism.

(2) TT4 (serum total triiodothyronine) was measured by radioimmunoassay (RIA) and was also affected by TBG. The normal value was 100-150 g/dl. In the early stage of hyperthyroidism, T3 increased earlier and faster. T4 is more sensitive and is meaningful for the diagnosis of T3 hyperthyroidism. In elderly people with normal thyroid function, the T3 value is generally normal or decreased, so the increase in T3 is likely to be hyperthyroidism.

(3) FT4 (serum free T4) and FT3 (serum free T3): most of the thyroxine in the blood is in a non-free state combined with TBG-based serum protein, while free thyroxine content is rare, FT4 only accounts for The total T4 is 0.03%, FT4 is only 0.3% of the total T3. The determination of free thyroxine is not affected by TBG, which directly reflects the thyroid function status. Its sensitivity and specificity are significantly higher than total T3 (TT3) and total T4. (TT4) is the most sensitive and most valuable indicator reflecting thyroid function status. Adult normal value, RIA (radioimmunoassay) FT4 9-25pmol/L, FT3 3-9pmol/L, hyperthyroidism patients significantly increased, diagnostic coincidence rate Above TT3 and TT4, the coincidence rate for the diagnosis of hyperthyroidism is as high as 100%.

(4) TSH (thyrotropin) measurement: When thyroid function changes, TSH fluctuation is more rapid and significant than T3, T4, so TSH in blood is a sensitive indicator reflecting hypothalamic-pituitary-thyroid axis function, hyperthyroidism, feedback Inhibition of TSH release, determination of normal TSH by IRMA (immunoradiography) is 0.4-3.0 mU/L or 0.6-4.0 mU/L. Recently, TSH was found by monoclonal antibody immunoradiometric assay (TSH-IMA), hyperthyroidism, and even In subclinical hyperthyroidism, TSH is reduced and is the most sensitive indicator for the diagnosis of hyperthyroidism. However, it must be pointed out that regardless of the sensitivity of the TSH measurement, clinical and other thyroid function tests must be combined to make a correct diagnosis, prognosis and treatment decision. The increase in TSH generally excludes the diagnosis of hyperthyroidism.

6.TRH (thyroid stimulating hormone releasing hormone) excitatory test

When hyperthyroidism, blood T3, T4 increased, inhibition of pituitary TSH cells, so TSH is not excited by TRH, such as intravenous injection of TRH 400g after TSH increased response, can rule out the disease, such as TSH does not increase the support for the diagnosis of hyperthyroidism, Also seen in subclinical hyperthyroidism, normal thyroid function, and pituitary disease with insufficient secretion of TSH, TSH insensitivity syndrome, TSH tumor, etc., so it is necessary to pay attention to the diagnosis. This test measures TSH in vitro without introducing nuclides. In vivo, the side effects are small, and it is safer for elderly patients with coronary heart disease or hyperthyroidism. It basically replaces the T3 inhibition test. In recent years, with the promotion of TSAB, UTSH and other detection methods, the TRH stimulation test has also been replaced.

7. Thyroid nucleus imaging

Including 131I measurement and thyroid scan of thyroid gland, if you want to understand thyroid function, radionuclide is generally not recommended for in vivo examination, but other in vitro tests should be performed first. The coincidence rate of thyroid gland 131I rate diagnosis of hyperthyroidism is 90%, iodine deficiency thyroid gland The swelling can also be elevated, but generally there is no peak advancement. If necessary, it can be identified by T3 inhibition test. This method can not reflect the severity of the disease and the changes in the condition of the treatment, but can be used to identify hyperthyroidism of different causes, but this law is subject to The effects of various foods and iodine-containing drugs are also affected by many diseases. Therefore, the use of thyroid 131I rate to diagnose hyperthyroidism is now rarely used. If you need morphological information in addition to understanding the function of the thyroid, you must have a thyroid scan. Commonly used nuclides are 131I, 125I, 123I and 99Tc, of which 99Tc has low radiation, is not organicized by thyroid, and can be scanned for 30 minutes after intravenous injection. It is not affected by antithyroid drugs, and can also understand the blood supply of thyroid. , has certain advantages.

8. Imaging examination

Ultrasound, CT, MRI, etc. help to understand the size of the thyroid gland. The space is cystic or solid. It is sensitive to small nodules that are difficult to detect in clinical practice. In addition, color Doppler ultrasound can still measure the thyroid gland. Blood flow.

Diagnosis and diagnosis of hyperthyroidism in the elderly

diagnosis

On the basis of hyperthyroidism, the following 1 or more cardiac abnormalities occur, and other causes are excluded. After the hyperthyroidism is controlled, the following abnormalities of the heart can be diagnosed as hyperthyroidism.

1. Obvious arrhythmia (paroxysmal or persistent atrial fibrillation, frequent atrial premature contraction or bundle branch block).

2. The heart is enlarged (one or both sides).

3. Angina or acute myocardial infarction occurs after suffering from hyperthyroidism.

Differential diagnosis

Clinical needs are differentiated from digestive tract tumors, coronary heart disease, rheumatic heart disease, neurosis, and diabetes.

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