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    Home > Active Ingredient News > Endocrine System > Refusal of mindset: Does hyperthyroidism necessarily lead to a fast heart rate?

    Refusal of mindset: Does hyperthyroidism necessarily lead to a fast heart rate?

    • Last Update: 2021-08-08
    • Source: Internet
    • Author: User
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    Recently, I have participated in the diagnosis and treatment of several patients with high or third degree atrioventricular block.
    Some patients have been diagnosed with diseases for several years.
    The normal heart rate is about 30-40 beats per minute, which is only about half of normal people.
    However, patients have long-term tolerance.
    No symptoms such as fainting or falling
    .

    In addition to the degenerative disease caused by age, are there other reasons for such patients? The author checked the literature and found some interesting cases, which I would like to share with readers
    .

    Author: Lin Gaofeng Department of Cardiovascular Medicine, Beijing Hospital.
    This article is published by Yimaitong authorized by the author, please do not reprint without authorization
    .

     Unusual case: A 41-year-old healthy man presented to the doctor with "sudden syncope".
    The patient denied that there were prodromal symptoms such as chest pain, dyspnea, or heart palpitations before the onset of syncope
    .

    However, before the onset of syncope, the patient had symptoms of fever and dry cough for several days without any obvious cause
    .

     The receiving doctor performed routine examinations for the patient, and the vital signs were stable, and the physical examination did not find obvious positive signs
    .

    The ECG examination results were unexpected.
    The results are shown in Figure 1: P wave and QRS wave are separated, sinus P wave frequency>100 beats/min, narrow QRS wave, ventricular rate is about 90-100 beats/min
    .

    Analysis of the electrocardiogram showed: sinus tachycardia, complete atrioventricular block, accelerated heart rhythm in the junction zone
    .

     Figure 1 The first electrocardiogram after the patient's visit.
    Other test reports were analyzed.
    No obvious abnormalities were found in routine blood and biochemical examinations, and electrolyte levels were within the normal range
    .

    Inflammation indicators are slightly elevated, C-reactive protein 48.
    9 mg/L, erythrocyte sedimentation rate 33 mm/h, which seems to be related to fever and dry cough symptoms in recent days
    .

    And the last revealed the cause of the patient’s abnormal thyroid function report: thyroid stimulating hormone (TSH <0.
    01 mIU/L), free tetraiodothyronine (FT4) 4 ng/dL (normal reference value 0.
    9–1.
    7 ng/dL)
    .

     In view of the obvious abnormality of the patient's electrocardiogram, in order to rule out the possibility of organic heart disease, the doctor perfected cardiac ultrasound (UCG) and magnetic resonance (MRI) examinations for the patient
    .

    The UCG results indicated that the patient's heart structure and function were normal (LVEF 59%), and the MRI results also ruled out the possibility of myocarditis and infiltrating cardiomyopathy
    .

    During hospitalization, the patient had repeated syncope episodes.
    Monitoring ECG showed that there was a long interval ranging from 10-13 seconds when syncope episodes occurred, and there was no junction zone or ventricular escape
    .

     Further examination results indicated that thyroid-stimulating hormone receptor antibody (TRAb) was also significantly increased, reaching 2.
    41 IU/L (normal reference value <1.
    75 IU/L), and the patient was eventually diagnosed with Graves disease
    .

    After the diagnosis, the patient began to receive methimazole drug treatment.
    At the same time, considering that the patient had repeated long intermittent and cardiogenic syncope episodes, the doctor implanted a temporary pacemaker for him
    .

    Analysis after implantation showed that the proportion of patients with ventricular pacing was not high, and most of the time was escape rhythm in the junction zone
    .

    Taking into account the recurrent episodes of syncope symptoms and long intervals, after communication, the patient finally received a permanent pacemaker implantation
    .

     After 5 months of treatment, the patient was followed up, and the thyroid function had returned to normal (see Figure 2)
    .

    The results of Holter and pacemaker programming show that the patient has basically returned to normal sinus rhythm, occasionally atrial pacing, and atrioventricular block has been corrected
    .

     Figure 2 The change curve of patient's thyroid function during treatment: A is FT4, B is TT3 Graves' disease (Graves' disease, GD), also known as toxic diffuse goiter, is one of the organ-specific autoimmune diseases and targets the thyroid An autoimmune disease caused by antibodies (TRAb) produced by the thyroid-stimulating hormone receptor (TSHR) on the follicular cell membrane
    .

    Since thyroid hormone can promote the body's metabolism, the major clinical manifestations of high metabolic-related symptoms, such as palpitations, tachycardia, insomnia, emotional irritability, anxiety, sweating, heat intolerance, eating and increased stool frequency, and weight loss
    .

     Table 1 Common symptoms, signs and occurrence probability of Graves’ disease Graves’ disease and the cardiovascular system As mentioned in the table above, Graves’ disease and other hyperthyroidism in the cardiovascular system are mainly manifested as palpitations and tachyarrhythmias (Tachycardia).
    Sinus tachycardia and atrial fibrillation are the most common
    .

    Among them, the relationship between hyperthyroidism and atrial fibrillation has been a hot research topic in recent years
    .

    Among the risk factors for atrial fibrillation summarized in the guidelines for the management of atrial fibrillation issued by the European Society of Cardiology (ESC) in 2016, symptomatic hyperthyroidism and subclinical hyperthyroidism are both related to the onset of atrial fibrillation (RR values ​​are respectively 1.
    42 and 1.
    31, see Table 2)
    .

    In addition to causing arrhythmias, thyroid hormones can increase cardiac output by enhancing myocardial contractility and reducing peripheral vascular resistance (see Figure 3)
    .

     Table 2 Hyperthyroidism is a common risk factor for atrial fibrillation Figure 3 The mechanism of action of thyroid hormones in the cardiovascular system The mechanism of atrioventricular block caused by hyperthyroidism is very rare, and only appears in individual case reports.
    The current mechanism It is not fully elucidated.
    Combined with relevant literature, its possible mechanism and precautions are as follows: ➤ The function of the atrioventricular node is regulated by autonomic nerves (including sympathetic nerves and parasympathetic nerves).
    Thyroid hormones can affect calcium ion flow (such as sarcoplasmic reticulum).
    And Ca2+-ATPase) participate in autonomic nerve regulation; ➤ Clinically, atrioventricular block caused by hyperthyroidism is often associated with some comorbidities, such as acute infection, coronary heart disease, electrolyte disorders (hypokalemia and hypocalcemia), Lyme Diseases, etc.
    ; ➤ Beta blockers are often used to control the ventricular rate of patients with hyperthyroidism.
    During the application, attention should be paid to monitoring the changes in the electrocardiogram, and to be alert to the risk of atrioventricular block caused by overdose
    .

     References: [1] El-Harasis MA, DeSimone CV, Stan MN, et al.
    Graves' disease-induced complete heart block and asystole.
    HeartRhythm Case Rep.
    2017; 4(3): 105-108.
    doi: 10.
    1016/ j.
    hrcr.
    2017.
    12.
    001.
    [2] Jin Shi.
    Graves Disease.
    Chinese Journal of Practical Rural Doctors.
    2018; 25(10): 12-13.
    [3] Burch HB, Cooper DS.
    Management of Graves Disease: A Review .
    JAMA.
    2015; 314(23): 2544-54.
    doi: 10.
    1001/jama.
    2015.
    16535.
    [4] Kirchhof P, Benussi S, Kotecha D, et al.
    2016 ESC Guidelines for the management of atrial fibrillation developed in collaboration with EACTS.
    Europace.
    2016; 18(11): 1609-1678.
    [5] Klein I, Ojamaa K.
    Thyroid hormone and the cardiovascular system.
    N Engl J Med.
    2001; 344(7): 501-9.
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