OVERVIEW
Hypothyroidism is a clinical syndrome caused by insufficient secretion of thyroid hormones and low body metabolism. Hypothyroidism can develop in fetuses, neonates (cretinism), children, adolescents (juvenile-type hypothyroidism) and adults (adult-type hypothyroidism). Clinical manifestations vary greatly depending on the age of onset of the disease, but all of them may involve the cardiovascular system to varying degrees, causing hypothyroidism heart disease.
Causes
1. Primary hypothyroidism
Hypothyroidism is caused by the pathology of the thyroid gland itself.
2. Secondary hypothyroidism
It includes hypothyroidism caused by insufficient secretion of thyroid stimulating hormone (TSH) due to pituitary lesions and hypothyroidism caused by decreased secretion of thyrotropin-releasing hormone (TRH) in the hypothalamus, resulting in decreased production of TSH by the pituitary gland.
3. Peripheral hypothyroidism (thyroid hormone resistance syndrome)
Hypothyroidism is caused by the lack of response of peripheral tissues to thyroid hormones.
Symptoms
1. Adult-onset hypothyroidism
Mostly seen in middle-aged women, the ratio of male to female is 1:5, with insidious onset and slow progression. Typical symptoms are as follows:
(1) General manifestations: fear of cold, dry skin with little sweat, thick, yellowish and cold, sparse and dry hair, brittle and cracked nails, fatigue, drowsiness, poor memory, mental retardation, slow reaction, mild anemia and weight gain.
(2) Special Facial Features Pale and waxy face, puffy face, dull gaze, loose and swollen eyelids, apathetic expression, few words, hoarseness when speaking, slurred speech.
(3) Cardiovascular system Slow heart rate, weak heart sounds, generalized enlargement of the heart, often accompanied by pericardial effusion, called hypothyroid cardiomyopathy. Patients may have obvious lipid metabolism disorders, showing hypercholesterolemia, hypertriglyceridemia and hypertriglyceridemia, often accompanied by atherosclerosis, and the incidence of coronary heart disease is higher than that of the general population. However, due to the low metabolic rate of the peripheral tissues, the cardiac blood volume is reduced, and the myocardial oxygen consumption is reduced, so angina pectoris and cardiac failure seldom occur. Sometimes the blood pressure is high, but it is mostly seen in diastolic blood pressure.
(4) Digestive system Patients have loss of appetite, constipation, abdominal distension, and even paralytic intestinal obstruction. About half of the patients have complete gastric acid deficiency.
(5) Muscle and joint system Muscle contraction and relaxation are slow and delayed, and muscle pain and stiffness are often felt. Bone metabolism is slow, and bone formation and resorption are reduced. Joints are painful, inactive, and have a feeling of ankylosis, which is aggravated by cold, as in chronic arthritis. Occasionally, joint effusion is seen.
(6) Endocrine system Impotence in men, excessive menstruation in women, and amenorrhea in patients with prolonged illness. The function of tight adenocortex is low, and blood and urine cortisol are lowered. Primary hypothyroidism can sometimes be accompanied by autoimmune hypoadrenocorticism and/or type 1 diabetes mellitus, known as Schmidt’s syndrome.
2. Cretinism
Hypothyroidism in newborns in iodine-deficient areas is called cretinism, in which the child is demented, has poor appetite, difficulty in feeding, has no sucking power, is quiet, cries less, is lethargic, has fewer spontaneous movements, has flaccid muscles, is pale, has dry skin, is cold, is coarse and thick, has a hoarse voice, has dry and constipated stools, and has weak tendon reflexes.
3. Juvenile hypothyroidism
In older children, the symptoms are like those of adult-type hypothyroidism, and growth and development are affected, with delayed bone age, delayed pubertal development, and poor intellectual and academic performance.
Regardless of the type of hypothyroidism, when the symptoms are severe and not reasonably treated, under certain circumstances, such as infection, cold, surgery, anesthesia or the use of sedatives can be induced coma, resulting in mucous edema coma (or hypothyroidism crisis). The patient first has drowsiness, body temperature does not rise, even below 35ºC, blood pressure drops, respiration is shallow and slow, heartbeat is weak and slow, muscle flaccidity, tendon reflexes disappear, and may be accompanied by shock, cardiac and renal failure, which may be life-threatening.
Examination
Decrease in serum T3 and T4 and increase in TSH are due to the pathology of the thyroid gland itself. If TSH is decreased or normal, further use of thyrotropin-releasing hormone excitation test. If TSH is elevated, it is hypothalamic hypothyroidism; if TSH is unresponsive, it is pituitary hypothyroidism. Cardiac function tests show prolonged arm-to-lung and arm-to-lingual circulation times, prolonged pre-ejection period (PEP), and increased pre-ejection to left ventricular ejection time ratio (PEP/LVET).
1. Electrocardiogram (ECG)
Electrocardiogram (ECG) shows slow heart rate, low voltage of QRS wave group, low or inverted T wave, decreased amplitude of P wave, occasionally prolonged P-R interval and QRS interval, ischemic changes of ST segment can also be caused by coronary atherosclerosis complicated by this disease.
2. Chest X-ray
Plain film shows generalized enlargement of the heart shadow, and the heart beats are sluggish and small in amplitude under fluoroscopy.
3. Echocardiography
In addition to the detection of pericardial effusion, there are signs of myocardial hypertrophy (caused by myocardial pseudohypertrophy), and some cases even show asymmetric septal hypertrophy and are misdiagnosed as primary hypertrophic cardiomyopathy.
Diagnosis
For the diagnosis of hypothyroidism cardiomyopathy, in addition to the evidence of hypothyroidism, the following conditions are needed:
1. Clear signs of cardiac disease, such as slow heart rate or diminished heart sounds.
2. Enlargement of the heart on imaging.
3. An abnormal electrocardiogram.
4. Other causes of heart disease are excluded.
5. The above changes improve with thyroid hormone therapy. If there is no clinical cause for the enlarged heart or pericardial effusion with slow heart rate, especially in female patients, the possibility of hypothyroid cardiomyopathy should be considered.
Treatment
Patients with hypothyroidism require thyroid hormone replacement therapy, which is often lifelong. Thyroid preparations include levothyroxine sodium (L-T4), triiodothyronine (L-T3), and thyroid tablets, in addition to Euthroid (containing T40.06mg and T315μg per tablet) and Thyrolar (containing T40.05mg and T312.5μg per tablet). The commonly used domestic preparation is Thyrolar tablets. Due to the direct stimulation of the heart by T3 and the fact that T4 can be converted to T3 more peripherally for its own needs, there are no more T3 preparations on the market.
In addition to thyroid preparation replacement therapy, patients with anemia should be supplemented with iron, vitamin B12, and folic acid according to the type of anemia. Those with gastric acid deficiency should be supplemented with dilute hydrochloric acid.
Prognosis
Most patients with hypothyroidism experience significant improvement in clinical symptoms with effective treatment. Cardiac lesions can be expected to normalize in a short period of time. Without timely treatment, the lesions worsen year by year, and some of them even complicate hypothyroidism coma, which is life-threatening.