Opacity of cardiomyocytes

Introduction Cardiomyocyte bioelectricity: The transmembrane potential of cardiomyocytes is much more complex in terms of waveform and formation mechanism than skeletal muscle. Not only that, the transmembrane potential of the above different types of cardiomyocytes is not only different in amplitude and duration, but also has a certain difference in the waveform and the formed ion basis. The inconsistency of electrical activity of various types of cardiomyocytes is the cause of cardiac excitability and the special law of excitement showing throughout the heart. The basis of bioelectrical production of cardiomyocytes: The transmembrane potential of cardiomyocytes depends on the transmembrane electro-chemical gradient of ions and the selective permeation of ions by membranes.

Cause

Hyperthyroidism is one of the special clinical manifestations of hyperthyroidism, which can not only aggravate the original cardiovascular disease, but also cause arrhythmia alone, or even heart failure or sudden death.

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Electrocardiogram dynamic electrocardiogram (Holter monitoring) Doppler echocardiography

Hyperthyroidism is one of the special clinical manifestations of hyperthyroidism, which can not only aggravate the original cardiovascular disease, but also cause arrhythmia alone, or even heart failure or sudden death.

(1) Arrhythmia: Approximately 50-90% of patients with hyperthyroidism have arrhythmia, of which 85% to 100% of patients show tachycardia, and about 10% to 20% of patients show atrial fibrillation. Clinical electrocardiographic findings revealed arrhythmia, including sinus arrhythmia, atrial flutter, ventricular tachycardia, atrioventricular block, bundle branch block, and ST-segment depression and T-wave low-level or inversion.

(2) Heart failure: It is reported that 34.4% of elderly patients with hyperthyroidism have heart enlargement and heart failure. Echocardiography revealed that the cardiac output and cardiac index were higher than normal in patients with hyperthyroidism, and the left and right atrium and ventricles were both enlarged.

(3) ischemic heart disease: hyperthyroidism patients, especially elderly hyperthyroidism patients, prone to coronary artery insufficiency symptoms, clinical manifestations of angina or myocardial infarction, etc., most patients (67.2%) are often misdiagnosed as coronary heart disease. However, coronary angiography rarely shows arterial stenosis or sclerosis.

(4) mitral valve prolapse: It has been reported in the literature that 17 of the 40 patients with hyperthyroidism (43%) have mitral valve prolapse, which is significantly higher than the control group (18%).

Differential diagnosis

There is a thyroid hormone (T3) receptor in the nucleus of cardiomyocytes. T3 directly affects the mechanism of myocardial contraction and exerts a positive inotropic effect. T3 enters the cytoplasm and binds to specific receptors on the nuclear membrane, and stimulates myocardial contractile protein through intranuclear mechanism. Increased synthesis, thereby increasing myocardial contractility.

Another way T3 acts on the myocardium is to act on non-nuclear sites outside the nuclear receptor to rapidly increase myocardial contractility, the "extra-nuclear mechanism." Through these sites, T3 can increase the calcium ATPase activity on the sarcoplasmic reticulum, increase the intracellular calcium concentration and increase the myocardial contractility; up-regulate the sodium channel of the cell membrane, increase the sodium ion influx, cause the contractile force of cardiomyocytes to increase; activate mitochondria The medial aspect of adenine nucleotide transferase regulates the exchange of ADP and ATP in vitro and in vivo, promotes ATP production, and improves cell energy supply.

Thyroxine can increase the activity of the renin-angiotensin system (RAS) and increase the mRNA expression of both cardiac renin and angiotensin II (ANGII) through receptor-dependent and voltage-dependent calcium channels. Increases the intracellular calcium concentration in the cardiomyocytes, which adversely affects the cardiovascular system.

Serum cardiac troponin 1 (CTn1) and myoglobin (Mb) are serum markers that have been found to reflect myocardial damage in recent years and are ideal indicators for early diagnosis of myocardial injury and myocardial infarction. Experiments have shown that serum CTn1 and Mb in patients with hyperthyroidism are significantly higher than those in the normal group, which may be the effect of excessive thyroxine on myocardial metabolism.

Hyperthyroidism is one of the special clinical manifestations of hyperthyroidism, which can not only aggravate the original cardiovascular disease, but also cause arrhythmia alone, or even heart failure or sudden death.

(1) Arrhythmia: Approximately 50-90% of patients with hyperthyroidism have arrhythmia, of which 85% to 100% of patients show tachycardia, and about 10% to 20% of patients show atrial fibrillation. Clinical electrocardiographic findings revealed arrhythmia, including sinus arrhythmia, atrial flutter, ventricular tachycardia, atrioventricular block, bundle branch block, and ST-segment depression and T-wave low-level or inversion.

(2) Heart failure: It is reported that 34.4% of elderly patients with hyperthyroidism have heart enlargement and heart failure. Echocardiography revealed that the cardiac output and cardiac index were higher than normal in patients with hyperthyroidism, and the left and right atrium and ventricles were both enlarged.

(3) ischemic heart disease: hyperthyroidism patients, especially elderly hyperthyroidism patients, prone to coronary artery insufficiency symptoms, clinical manifestations of angina or myocardial infarction, etc., most patients (67.2%) are often misdiagnosed as coronary heart disease. However, coronary angiography rarely shows arterial stenosis or sclerosis. (4) mitral valve prolapse: It has been reported in the literature that 17 of the 40 patients with hyperthyroidism (43%) have mitral valve prolapse, which is significantly higher than the control group (18%).

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