Keshan disease

Introduction to Keshan disease Keshandisease (Keshandisease) is an unidentified disease characterized by cardiomyopathy, also known as endemic cardiomyopathy. First discovered in Keshan County, Heilongjiang Province in 1935, it was named after Keshan disease. In the past, the mortality rate of this disease was high. After the founding of New China, the disease was actively prevented, and the incidence and mortality of the disease were greatly reduced. Some important advances have been made in prevention, treatment and etiology research. At present, the annual incidence rate has dropped below 0.07/100,000, and the incidence type has changed from emergency type to sub-acute type to potential type and slow type. Mainly. A large number of epidemiology, pathological anatomy, clinical prevention and laboratory research results show that the disease is an independent endocardial disease. basic knowledge The proportion of illness: 0.002% Susceptible people: no specific population Mode of infection: non-infectious Complications: arrhythmia hypokalemia cardiogenic shock congestive heart failure

Cause of Keshan disease

Causes of biogeochemistry (35%):

The study believes that the specific natural environment of the ward is related to the pathogenesis of Keshan disease. The chemical substances in the environment act on the human body through the soil-soil chain. Therefore, the research includes two aspects: one is the poisoning theory (including hydrazine, humic acid in water, nitrous acid). Salt, etc.), the second is the lack of or imbalance in the chemical substances (selenium, magnesium, molybdenum) in the diet. According to the investigation, the disease has obvious regional characteristics. The soil, water quality and food in the ward lack some trace elements such as human body needs. Selenium, molybdenum, magnesium, etc. or related nutrients, thereby interfering with myocardial metabolism, causing myocardial damage or rickets.

Biological cause (35%):

Some characteristics are consistent with the characteristics of biological factor infection. For example, many strains of virus can be isolated from the myocardial tissue of Keshan disease, including Coxsackie B virus. The results of serological research also indicate that about one third of the acute type and 67.9% are. The sub-acute Keshan disease patients with double serum Coxsackie B virus antibody was 4-fold increased with the isolated Coxsackie B virus inoculated low-selenium suckling mice caused by myocardial lesions, damage and lesion detection The rate is also significantly higher than the normal selenium group. In addition to the direct cytolytic effect of the virus, the virus can induce cytotoxic T cells, B cells, and T helper cells to proliferate, so the pathogenesis of Keshan disease is considered by biological etiology. Low selenium may be the basic factor, and some cases may occur when there is a Coxsackie B virus infection, and the resulting autoimmune reaction further aggravates myocardial damage.

Pathogenesis

Pathogenesis

(1) Causes of biogeochemistry: According to the theory, the cause of Keshan disease exists in the soil and water of the ward, and acts on the human body through the food chain. The amino acid, vitamins and trace elements are deficient or unbalanced, causing myocardial damage and causing disease.

1 Internal and external environment low selenium: low internal and external environment selenium is closely related to the occurrence of Keshan disease. A large number of studies have shown that Keshan disease occurs in the low selenium zone, and the selenium content in the diseased area is significantly lower than that in the non-disease area, hair and blood. Selenium content is significantly lower than that of non-disease residents, indicating that the selenium content in the environment outside the disease area is insufficient. More than 100,000 people in Heilongjiang, Shaanxi, Sichuan and other places have taken oral sodium selenite to prevent Keshan disease, and found that selenium supplementation is urgent. There is a significant effect on the onset of type and sub-acute Keshan disease. In addition, there are metabolic changes in the Keshan patient and the ward that are centered on low selenium, such as glutathione peroxidase in the tissues of patients and wards. The content of (GPX) was significantly lower than that of non-disease patients; plasma lipid peroxide (MDA), free fatty acid (FFA) and other components were significantly higher than non-disease areas; free radical content and hemoglobin oxidation rate in patients with red blood cells were significantly higher than non- Patients, ward children are also higher than non-disease children, but low selenium can not fully explain all the epidemiological characteristics of Keshan disease, such as not all low-selenium areas have Keshan disease; although the disease area is generally low selenium, but the incidence is only Occupy A small part of the disease; selenium levels in the ward do not change with the annual and seasonal occurrence of Keshan disease; there is no significant difference in selenium and selenium in the hair between the sick and non-disease children in the same ward, therefore, currently It is believed that selenium deficiency is a very important regional factor in the pathogenesis of Keshan disease, but it is not the only factor.

2 Vitamin E (VE) deficiency: In recent years, it has been found that the content of alpha-tocopherol (-toco), which has the strongest antioxidant activity in VE components, is generally lower than that in non-disease areas, and it is also confirmed The total amount of -toco and VE in the plasma of the population (including patients with Keshan disease and healthy people) was significantly lower than that of non-disease healthy people. The total amount of -toco and VE in the erythrocyte membrane was also significantly lower than that of non-patients. Normal people in the ward, indicating that patients with Keshan disease are generally in a low VE state, the levels of polyunsaturated fatty acids (PUFAs) in the ward are generally higher than those in the non- ward, and the ratio of -toco (mg) to PUFAs (g) is generally low. In non-disease areas, PUFAs in living organisms depend on the protection of VE, suggesting that there may be a relative deficiency of -toco in the ward, which further reduces the body's antioxidant capacity.

3 Proteins and amino acids: The intake of animal and plant protein in the ward is significantly lower than that in the non-disease area; the content of essential amino acids in the ward is lower than that in the non- ward, and the sulfur-containing amino acids in the plasma of the ward (S-AA) As methionine deficiency, selenomethionine ingested from the diet instead of methionine is involved in protein synthesis, resulting in selenium not functioning properly. S-AA is also a precursor of glutathione, and its insufficient intake will lead to valleys. The synthesis of glutathione is not only a specific substrate for GPX reaction, but also a free radical scavenger. It can be seen that low selenium, insufficient S-AA intake and low VE can lead to antioxidant capacity of the body. decline.

4 Dietary high manganese: Previous studies have shown that in most low selenium areas, there are relatively high manganese phenomena in the internal and external environment. Experiments show that when the protein supply is insufficient, exogenous manganese can accumulate in the body, resulting in increased selenium excretion and decreased selenium content. It affects the antioxidant capacity of cells, especially red blood cells and myocardium, and the combination of selenium-depleted and manganese-rich, and affect each other, can further reduce the antioxidant capacity of the myocardium and aggravate myocardial damage.

5 Dietary low calcium: the residents in the ward have a single diet, and the calcium intake is not obvious. Animal experiments have found that low calcium can aggravate myocardial necrosis caused by low selenium. Therefore, dietary low calcium may also be important in the combined pathogenic factors of Keshan disease. Role, this can explain why Keshan disease occurs mostly in women of growth and children who have a large amount of calcium.

(2) Biological causes:

1 Enterovirus: A variety of viruses can be isolated from the blood of Keshan disease patients and the myocardium and other organs of the deceased, such as coxsackievirus A9, B1, B2, B3, B4, etc., Echovirus type 12 , adenovirus type 7, etc., serological investigation found that Keshan disease patients with intestinal virus neutralizing antibody positive rate is much higher than non-disease control group, only Coxsackie B virus neutralizing antibody positive rate as high as 68.6 %90%, and found that about 1/3 of the sub-acute type, the antibody titer of the acute patient increased by 4 times, the positive rate of Coxsackie virus IgM in the serum of the child was as high as 69.4%, indicating that most patients with Keshan disease have The newly occurring enterovirus infection, domestic in situ nucleic acid hybridization and nested polymerase chain reaction and other techniques, found that all types of Keshan disease myocardial specimens have intestinal virus RNA, the positive rate was 85.7% and 90% These findings suggest that attention should be paid to the role of enteroviruses, particularly Coxsackie B virus infection, in the pathogenesis of Keshan disease.

Foreign animal experiments have shown that in the absence of selenium and low VE, mice are more susceptible to Coxsackie virus, in the Coxsackie virus infection, low VE conditions of the myocardium, it can be seen that the disease changes severely; usually does not cause myocarditis benign The strain CVB3/0 also caused myocardial lesions in mice with low VE; at the same time, the virus isolated from the myocardium, when inoculated by cells to mice that had been supplemented with VE, also caused significant myocardial damage, indicating Benign CVB3/0 may have a phenotypic change under low VE conditions, and selenium deficiency has a similar situation. For example, the nucleotide sequence analysis of CVB3 and benign CVB3/0 isolated from the myocardium of selenium-deficient mice is found to have 6 (p. 234, 788, 2271, 2438, 3324, 7334) nucleotides undergo point mutations, and these mutations are consistent with the nucleotide sequence of the known myocarditis strain CVB3/20, CVB3/M1, Selenium protein such as GPX can be synthesized not only by higher biological cells but also by CVB3, while the partial amino acid sequence of GPX is homologous to CVB3, and the fusion protein can be formed with the capsid protein VP3. The above-mentioned selenium-deficient or selenoproteinase knock-out CVB3 /0 mutation site has It is located in this area, therefore, it was speculated that disease-causing mutant may also function with this GPX fusion protein inactivation.

2 Fusarium oxysporum: Some people extracted the beetle oxysporum from the ward, and speculated that the food contamination of Fusarium oxysporum was the cause of Keshan disease, but Fusarium oxysporum was found in both Keshan disease and non-disease areas. Distribution, and not the dominant bacteria; the difference between the different types of grain contamination is greater than the difference between the same type of food in the diseased and non-disease areas; the pollution distribution is not consistent with the regional distribution of Keshan disease; The toxicity of Fusarium was not related to the selenium status of the infected subjects. Selenium supplementation or supplementation of VE did not inhibit or reduce the toxicity of Fusarium oxysporum, which was inconsistent with the practice of selenium prevention of Keshan disease; Myocardial enzymology and pathological changes similar to Keshan disease have not been seen in myocardial damage. Therefore, the role of Fusarium oxysporum in the etiology of Keshan disease is still to be further explored.

In conclusion, it is currently believed that Keshan disease is an endemic cardiomyopathy caused by compound pathogenic factors. The basic cause is the combination of biogeochemical factors and dietary nutrition factors, resulting in low selenium and closely related VE (). - Tocopherol) Insufficient intake, low selenium, low VE generally affects people in the ward, usually only cause myocardial metabolic disorders or potential subclinical damage, to cause myocardial sharp necrosis and clinical morbidity, there must be some predisposing factors ( Conditional factors) Participation, these factors do not have obvious regional differences, but can play an important role in the clinical onset of Keshan disease, annual multiple, seasonal multiple, such as Coxsackie virus infection is an important condition factor.

2. A large number of autopsy confirmed that the pathological features of Keshan disease in Northeast China, North China, Northwest China and Southwest China were basically the same. Metabolic cardiomyopathy was mainly caused by mitochondrial damage of myocardial cells. Sexual expansion, the ventricle generally expands to the sides, severely spherical, ventricular wall often does not thicken, the cut surface sees the myocardial parenchyma intertwined degeneration, necrosis and fibrotic lesions, endocardial patchy thickening, 20% The patient has a wall thrombus and embolism of the lung, brain, kidney, spleen, mesentery and peripheral blood vessels. The heart valve and coronary artery are basically normal. Under light microscope, diffuse degeneration and focal necrosis of myocardial cells can be seen, with left ventricle and ventricular septum. More common, and the degree is heavier, while the right ventricle is lighter; the ventricle is heavier than the atrium; the inner chamber, the middle layer is heavier than the outer layer; the acute type of Keshan disease subendocardial myocardial necrosis can reach 95%, but the child's ventricle is outside The lesions of the layer are heavier than the endocardium. The myocardial lesions are closely related to the progressive branching of the coronary arteries. In children with subacute type, the myocardial cells are granular degeneration, and there may be vacuolar degeneration of varying sizes. Row Sterilization of myocardial necrosis due to neat degeneration, coagulopathy and lytic necrosis can be mixed in the same lesion, of which acute septic type is mainly coagulative necrosis, while subacute type is mainly composed of dissolved necrosis, often accompanied by Different degrees of secondary inflammatory reaction, lesions can invade the conduction system, and bilateral bundle branches, especially right bundle branch disease, change severely.

Electron microscopy mainly showed mitochondrial swelling, hyperplasia, mitochondrial mites destruction, myocardial cell outer membrane damage and capillary endothelial damage. Combined with histochemical analysis, it can be seen that this pathological change is related to myocardial cell oxidation and reductive metabolic system disorders. Disease is a primary metabolic cardiomyopathy (myocardial mitochondrial disease) characterized by myocardial cell mitochondrial damage. Endocardial myocardial biopsy is used to observe the myocardium of latent and slow Keshan disease. The membrane system of the cells has been significantly altered, endoplasmic reticulum, T-tube, disc expansion, mitochondrial hyperplasia, atypical, abnormal myofibrils and microscopic myolysis and interstitial fibrosis.

Using molecular biology techniques, apoptotic cardiomyocytes are distributed around or scattered in the myocardial lesions, suggesting that cardiomyocyte apoptosis is also involved in the occurrence and development of myocardial damage.

In addition to the myocardium, other organs such as skeletal muscle, lung, pancreas, and thyroid are mostly congestive changes.

Keshan disease prevention

(1) Comprehensive preventive measures Pay attention to environmental sanitation and personal hygiene, protect water sources, improve water quality, improve nutritional conditions, and prevent partial eclipse. Especially for pregnant women, mothers and children, it is necessary to strengthen the supplement of protein, various vitamins and essential trace elements. Including magnesium, iodine, etc., and prevention of Kashin-Beck disease, endemic thyroid disease.

(2) Popularized areas to promote preventive medication using sodium selenate as a preventive medication, after years of promotion, it can be proved that the incidence can be significantly reduced, usually once every 10 days, 1 to 5 years old 1mg, 6 to 10 years old 2mg, 11 ~15 years old 3mg, 16 years old and above 4mg, non-incidence season can be stopped for three months, getting rid of poverty and getting rich, improving the living standards of people in the ward, is also an important preventive measure.

Researchers have learned that the composition of food is different, and the prevalence rate is significantly different. The diet of Keshan disease patients is low in beans, vegetables, animal foods, oils, etc. Vitamin A, vitamin B12 and selenium are especially low. The content of calcium in food is also obviously insufficient. The observation results show that the improvement of diet has obvious preventive effect. It is proposed to change or improve the dietary composition of residents in the ward, reasonably arrange food supply, and rationalize the nutrition of residents, which will control the occurrence of Keshan disease.

(3) Pay attention to rest and strengthen management According to the patient's heart function state, limit or avoid physical and mental activities, promote life rules, work and rest, rest can reduce the burden on the heart, promote the recovery of damaged myocardium, avoid upper respiratory tract infection and mental stimulation. Patients with unstable conditions should be followed up for observation.

In addition, it is recommended to use selenium-containing salt in popular areas, seed-soaked seeds in rural areas, and selenium-containing fertilizers in plant roots to increase selenium content in crops.

Epidemiology

(1) In popular areas, this disease has occurred in foreign countries. North Korea and Japan have also reported that China mainly occurs in a transitional zone from northeast to southwest, namely Heilongjiang, Jilin, Liaoning, Inner Mongolia, Hebei, Henan, Shandong, Shanxi, and Shaanxi. In Gansu, Ningxia, Sichuan, Yunnan, Tibet and other provinces and autonomous regions, the ward is mainly in the deserted hills, the plateaus and the grasslands in the rural areas, and the urban areas are less likely to occur.

(2) In the onset season, the disease has obvious multiple and multiple seasons. In the northeast region, the incidence of acute patients is mostly in the cold winter, while in the southwest region, the hot summer is the best season.

(3) Population distribution The disease mainly occurs in rural young and middle-aged women and children. In the northeast and northwest regions, there are significantly more young and middle-aged women than men. In Sichuan and Yunnan, children aged 2-6 years are more common, and there is also a family. The number of people has been ill, according to the survey of epidemic areas, the number of agricultural population is high, while the urban population is rarely ill.

Keshan disease complications Complications arrhythmia hypokalemia cardiogenic shock congestive heart failure

The diseases that are easily complicated by the disease are as follows:

I. Arrhythmia

(1). Acute cardiac insufficiency with cardiogenic shock and ventricular ectopic rhythm (premature beat, tachycardia, fibrillation) or I, II, III degree atrioventricular block, more than large dose of VC intravenous injection After expansion or sub-hibernation therapy, it disappears within a few hours with the relief of shock, and antiarrhythmic drugs are generally used.

(2). Chronic cardiac insufficiency complicated by ventricular arrhythmia, more than the effective dose of cardiotonic agent, and ventricular arrhythmia or reduced or disappeared when cardiac dysfunction is improved.

(3). After acute or chronic cardiac insufficiency is invalid after the above treatment and observation, antiarrhythmic drugs may be added, but attention should be paid to the negative muscular effect of the latter, arrhythmogenic effect and its cardiotonic agent, diuretic Interacting, so as not to inhibit the myocardium, increase cardiac dysfunction or lead to digitalis poisoning, and even cause cardiac arrest.

(4). Permanent complete atrioventricular block with ineffective drug therapy, artificial cardiac pacemaker can be placed; for patients with persistent ventricular tachycardia or ventricular fibrillation, electrical cardioversion is feasible.

2. Thrombosis, embolization according to thrombosis, embolization treatment routine treatment.

III. Infection with pulmonary infection can often induce or aggravate cardiac dysfunction. The corresponding antibiotic treatment or prevention should be used. Intestinal ascariasis in children should be treated with mites after heart failure control.

Water, electrolyte disorder

(1) Diuretics should be applied intermittently to avoid water, electrolyte imbalance and acid-base balance imbalance.

(2). For patients who use diuretics for a longer period of time, it is not appropriate to strictly limit the intake of sodium salt.

(3). When conditions permit, blood volume, serum sodium, potassium, chlorine, calcium, magnesium and other plasma changes should be monitored, water should be adjusted in time, salt metabolism disorders, pay attention to correct acid-base imbalance.

(4). In order to prevent hypokalemia, the potassium-diuretic diuretic can be alternately or combined with the potassium-sparing diuretic, and the supplement of magnesium salt should be emphasized.

5. Cardiogenic shock accounts for about 75% of acute severe Keshan disease. Patients often suffer from nausea, severe vomiting, dizziness, chest tightness, palpitations and dyspnea. The severe cases die within a few hours. If the patient can get timely Rescue, 90% of patients can recover within 24 to 36 hours.

Sixth, congestive heart failure due to diffuse severe degeneration of the myocardium, necrosis and scar formation, so Keshan disease patients may have varying degrees of congestive heart failure.

Common symptoms of Keshan disease, nausea, dark, dizziness, difficulty breathing, loss of appetite, dizziness, chest tightness, abdominal pain, asthma, ascites

According to the state of cardiac function, Keshan disease is clinically divided into acute type, sub-acute type, slow type and latent type. The first three are cardiac decompensation type, the latter is compensatory type, and the acute type is acute heart. Insufficient function, often combined with cardiogenic shock and severe arrhythmia, subacute type mainly occurs in children, mainly with systemic edema and congestive heart failure, slow type mainly manifests as chronic congestive heart failure, can occur gradually, or Acute or sub-acute transition, the potential heart function is good, there are no symptoms, and occasional arrhythmia and ECG changes.

1. Acute type is more common in winter, rapid onset, rapid change, often in the cold, overwork, cold, mental stimulation, overeating or women's childbirth and other causes of increased cardiac load, the most common manifestation is Cardiogenic shock, accounting for about 75% of acute severe Keshan disease, patients often with nausea, severe vomiting, dizziness as the main symptoms, but also often with dizziness, upper abdominal discomfort, chest tightness, palpitations, dyspnea, Severe cases can die within a few hours, physical examination 67% ~ 82% of patients have heart enlargement, may have galloping, lung voice, liver, edema and shock and other clinical manifestations, this type often combined with severe arrhythmia, performance For multi-source and multiple ventricular premature contractions, ventricular tachycardia and various degrees of atrioventricular block, 20% can appear A-S syndrome, a few (<5%) can be manifested as pulmonary congestion Acute left heart failure or pulmonary edema, cardiogenic shock, arrhythmia and pulmonary edema often exist together. If the symptoms of liver and edema in acute patients do not disappear for more than 3 months, the prompt changes from urgent to slow. type.

2. Sub-acute type occurs in post-weaning and pre-school children (2 to 5 years old), frequent in summer and autumn, slow onset, often with systemic edema, apathetic, loss of appetite, dark complexion as the main symptom, often in the presence of symptoms Chronic cardiac insufficiency occurred about 1 week later, a small number of cases may occur with cardiogenic shock, physical examination showed facial and systemic edema, heart enlargement, heart rate increased, often galloping and congestive liver, if the disease 3 months after the onset of illness If it still fails to ease, it will turn into a slow type.

3. Slow onset is slow, can gradually develop from the asymptomatic stage, can also be caused by other types of transition, mainly for the clinical manifestations of chronic congestive heart failure, may have heart palpitations, difficulty breathing, edema, liver congestion, heart expansion, The first heart sound is weakened, galloping and various arrhythmia, especially ventricular premature contraction and atrial fibrillation. There may be relative murmur of tricuspid and tricuspid regurgitation, and pleural effusion may also occur. Ascites and pericardial effusion and corresponding symptoms and signs, complications of chronic cardiac insufficiency, such as pulmonary infarction, may also occur. In addition, embolism of the brain, kidney, spleen, mesentery, etc. may occur due to thrombus detachment of the heart. .

In the course of chronic Keshan disease, if acute symptoms and signs of cardiogenic shock occur, it is called a slow type of acute attack.

4. The latent type is often asymptomatic, the cardiac function is well compensated, but there may be a slight increase in the heart. The ECG may have ventricular premature contraction or complete right bundle branch block or ST-T change. It is a latent type, called the potential type of stability, and has a good prognosis; it can also be derived from other types, which is called the latent potential type, and the prognosis is worse than the stability potential type.

Keshan disease check

(1) Blood tests for acute and sub-acute patients, the total number of white blood cells and neutrophils can be increased, erythrocyte sedimentation rate can be increased, serum aspartate aminotransferase (SGOT), creatine phosphokinase (CPK) and its isoenzymes in acute and severe cases The activity of lactate dehydrogenase (LDH) and its isoenzymes may increase to varying degrees, mostly rising several hours after onset, reaching a peak in 1 to 3 days, gradually returning to normal after 1 to 2 weeks, and resistance in recent years. The preparation of human cardiac myosin heavy chain monoclonal antibody is successful, which also helps the diagnosis of early myocardial necrosis, slow and latent visible albumin dynacle, globulin increased, serum protein electrophoresis a1 and a2 globulin increased, part Intestinal viral IgM was significantly elevated in patients' serum, and enterovirus RNA in blood and myocardial samples was positive.

(B) ECG examination This disease can have a variety of ECG changes, and often a variety of changes exist at the same time, with cardiac hypertrophy, myocardial damage and arrhythmia are the most common.

1. Heart damage can be seen in the ST segment rising or depression, which is related to epicardial or subendocardial myocardial damage, more common in acute type, a small number of QS can be seen in the limb joint or pre-cardiac lead-like myocardial infarction Wave or Qr wave, which is caused by myocardial necrosis or myocardial fibrosis. In addition, T wave is low level, biphasic or inverted, QT interval is prolonged, and low voltage is also common.

2. Arrhythmia is divided into ectopic heart rhythm, conduction block, ectopic heart rhythm with ventricular premature contraction most common, often multiple sources, frequent, followed by paroxysmal tachycardia and atrial fibrillation, the latter more common in In patients over 40 years of age or children with enlarged heart, conduction block is most common with complete right bundle branch block, which accounts for about 50% of adult abnormal ECG, and is often the only type of potential ECG change; followed by room Ventricular block.

(3) X-ray examination X-ray examination in rural areas is an effective means to find Keshan disease. It can be seen that the heart is enlarged, the myogenic expansion is performed, the pulsation is weakened, and the slow and sub-acute type is most obvious, mostly universal. Moderately above expansion can be generally increased in spherical shape, often accompanied by pulmonary congestion, urgency is generally mild to moderately enlarged, and a few hearts do not expand, the enlarged heart moves down the transverse direction, the heart is triangular and weak, pulsating Attenuation or disappearance, called myogenic expansion; while children's heart often expands in a spherical shape, pulmonary vascular venous congestion or mixed hyperemia, early pulmonary angiography increased, widened, acute lungs still visible Pulmonary vein hypertension, such as the blurring of the blood vessels, the enlargement of the hilar and the cloud-like shadow of the lungs, sometimes shows the manifestations of pulmonary embolism.

(4) Echocardiographic examination Echocardiographic changes in this disease are very similar to dilated cardiomyopathy, often manifested as dilated cardiomyopathy-like changes, slow and sub-acute type left atrium, left ventricle, right ventricular cavity are more common Sexual enlargement, widening left and right ventricular outflow tract, thin ventricular wall, weakened ventricular diffuse activity, and segmental dyskinesia, left ventricular ejection fraction decreased, sometimes with wall thrombus, acute left ventricular enlargement See, Doppler echocardiography can be found in 49.2% of patients with mitral regurgitation, tricuspid regurgitation is also common, valve failure after heart failure cure can be alleviated or even disappeared.

(V) Systolic time interval regulation This test shows that the ratio of PEP/LVET (the ratio of pre-spray time to left ventricular ejection time) is higher than normal (normal value 0.345 ± 0.036), reflecting the weakened myocardial contractility of the disease.

(6) Endocardial Myocardial Biopsy This is a biopsy method combined with cardiac catheterization. The endocardial myocardium obtained by pathological biopsy is helpful for the diagnosis of this disease.

Diagnosis and differential diagnosis of Keshan disease

diagnosis

According to the epidemiological characteristics of Keshan disease: that is, the epidemic area, the epidemic season, the incidence of the population, combined with clinical emergency, chronic heart failure, heart enlargement, arrhythmia and other diagnoses are not difficult. In the northeast, there are Kashin-Beck disease and place in the northwest. In areas where sexual goiter is present, such as patients with similar manifestations of dilated cardiomyopathy, it should be considered that the heart condition may be slow Keshan disease.

Broadly speaking, Keshan disease is a kind of primary cardiomyopathy. Its clinical manifestations, electrocardiogram, X-ray, echocardiography and other manifestations are similar to dilated cardiomyopathy, but Keshan disease has significant local epidemic characteristics. The following points can be used for identification: 1 age: Keshan disease is more common in women and children of childbearing age, while more than 70% of domestic statistics of dilated cardiomyopathy are seen after 30 years old; 2 gender: Keshan disease is more common in women, and expansion type More common in men with cardiomyopathy; 3 grams of mountain disease mainly occurs in the self-produced agricultural population, non-agricultural population rarely occurs, dilated cardiomyopathy does not have this feature; 4 course: slow type Keshan disease seems to be more dilated Cardiomyopathy is long. In addition, oral selenite can be reduced to the population of the endemic population for many years, which can reduce the incidence of selenium, which indicates that selenium can prevent the disease. Finally, endomyocardial biopsy also helps to distinguish the two. .

Diagnostic criteria (revised in 1995) have the characteristics of Keshan disease, and can have any one or one of the following manifestations and can exclude other diseases:

(1) The heart expands.

(2) Acute or chronic cardiac insufficiency.

(3) arrhythmia: multiple ventricular premature contractions (more than 6 times per minute, increased after exercise); atrial fibrillation; paroxysmal ventricular or supraventricular tachycardia.

(4) Running horses.

(5) Embolization of the brain or other parts.

(6) ECG changes: atrioventricular block; bundle branch block (except for incomplete right bundle branch block); ST-T changes; QT interval is significantly prolonged; multiple or multi-source ventricular pre-term Contraction; paroxysmal ventricular or supraventricular tachycardia; atrial fibrillation or atrial flutter; P wave abnormalities (left or right atrial enlargement or bilateral atrial load increase).

(7) The heart is enlarged by X-ray.

(8) Echocardiography: left atrium, left ventricular internal diameter expansion; ejection fraction (EF%) often falls below 40%; may have segmental wall motion disorder; apical valve blood flow spectrum A peak is greater than E peak .

(9) Changes in the electrocardiogram: pre-ejection period (PEP)/left ventricular ejection period (LVET) 0.40; A wave rate (A/E-0) 15%.

(10) Laboratory examination: AST, ALT increased, AST/ALT>1; LDH and its isoenzyme LDH1 increased.

LDH1>LDH2; CK and its isoenzyme CK2 increased.

2. Clinical classification criteria are divided into the following 4 types according to the pathogenesis and cardiac function:

(1) urgency: acute onset of acute myocardial ischemia, necrosis or acute cardiac decompensation and any of the following manifestations are severe acute Keshan disease: 1 cardiogenic shock; 2 severe arrhythmia Cardio-cerebral syndrome; 3 acute pulmonary edema or acute left heart failure.

(2) slow type: the heart is mostly moderate to severely enlarged, showing chronic congestive heart failure,

1 natural slow type: is a group of patients with no acute, acute, slow and latent medical history, slow from mild onset of symptoms, the most common form of this type in recent years;

2 slow type acute attack: slow type in the ward and in the multiple seasons, there are acute manifestations;

3 slow classification: according to the classification of cardiac function, divided into chronic grade II, grade III, grade IV.

(3) Sub-quick type:

1 exact sub-acute type: occurred after weaning, Keshan disease of preschool children, the incidence is slower, more than 1 week after the symptoms appear congestive heart failure, or cardiogenic shock (a few), congestive heart failure Its main performance, may have facial edema, liver and gallop, etc.

2 suspected sub-acute type: if there is mental wilting, loss of appetite, cough, asthma, abdominal pain, vomiting, eyelid or lower extremity edema, and blood pressure lower pulse pressure difference, heart rhythm significantly increased, all heart sounds or first heart sounds weakened, etc. According to the suspected sub-acute type and timely treatment, once the heart failure manifests, the diagnosis can be confirmed.

3 sub-acute type turned into slow type: the sub-acute type Keshan disease did not heal after 3 months from the date of onset, which was renamed as "turning slow type".

(4) Potential type: cardiac function grade I (normal), cardiac function is in the compensation period, the heart can be normal or slightly enlarged, and the electrocardiogram is mostly ventricular premature contraction or complete right bundle branch block or ST- T changes.

The disease mainly manifests as acute and chronic cardiac insufficiency, heart enlargement, arrhythmia and embolism of organs such as brain, lung and kidney. It is mainly clinically to identify which type of Keshan, according to the national keshan in 1982 The disease prevention and treatment experience exchange meeting is divided into the following.

(1) Acute healthy people can have sudden onset, and can also be acutely attacked on the basis of potential or slow type. In the north, acute type occurs mostly in winter, often due to cold, overwork, infection, binge drinking, binge eating or childbirth. Such as the onset of the disease, the onset of acute, severe cases can be manifested as cardiogenic shock, acute pulmonary edema and severe arrhythmia, initial feeling dizziness, heart discomfort, repeated nausea and vomiting, spit yellow water, and then restless, severe Can die in a few hours or days, physical examination sees patients pale, limbs cold, weak pulse, body temperature does not rise, blood pressure lowers, shallow breathing, heart is generally mild, heart sounds weak, especially the first heart sound weakened Very, there may be diastolic galloping and mild systolic hairy murmurs, arrhythmia often seen, mainly ventricular premature beats, paroxysmal tachycardia and atrioventricular block, acute heart failure when the lungs appear rales In addition, hepatomegaly and lower extremity edema are also common.

(2) The subacute type is not as fast as the emergency type. Most of the patients are young children, accounting for 85% of 2 to 5 years old. In spring and summer, the incidence is mostly, and there may be cardiogenic shock or congestive heart failure. For the spirit of wilting, cough, shortness of breath, loss of appetite, gray complexion and body edema, but also heart enlargement, galloping and hepatomegaly, embolism in the brain, lungs, kidneys, etc. is not uncommon.

(3) The slow onset is slow, and the disease is unknowingly affected. It can also be caused by acute, subacute or latent type. The clinical manifestations are mainly chronic congestive heart failure. The main complaint is heart palpitations, shortness of breath, and fatigue. Aggravation, and may have less urine, edema and ascites, physical examination showed that the heart is significantly enlarged to both sides, low heart sounds, audible and mild to moderate systolic murmurs and diastolic galloping, late signs of right heart failure such as neck Intravenous excretion, hepatomegaly and lower extremity edema, severe cases may have chest, ascites, cardiogenic cirrhosis and other manifestations, arrhythmia often seen such as ventricular premature beats, tachycardia, conduction block, atrial fibrillation.

(4) The potential type can occur in healthy people, but also in other stages of improvement. The former is often asymptomatic and can work or work as usual. It is found in the census. This is a stable potential type, which is transformed by other types. The person may have symptoms such as palpitations, shortness of breath, dizziness, fatigue, electrocardiogram, ST-T changes, QT interval prolongation and premature beats. Although the potential heart is damaged, the heart function is well compensated and the heart does not increase. Or slightly increase.

Differential diagnosis

1. Acute type should be differentiated from acute myocarditis, acute myocardial infarction, acute gastritis, and biliary ascariasis.

2. Slow type needs to be differentiated from dilated cardiomyopathy, perinatal cardiomyopathy, coronary heart disease, chronic pericarditis, rheumatic valvular heart disease, especially with dilated cardiomyopathy. Some scholars believe that the two Identification of the disease should be linked to clinical and epidemiological, pathological data and life changes, for comprehensive analysis, the main identification points such as.

3. Subacute type needs acute, chronic glomerulonephritis or nephropathy, bronchial pneumonia (combined heart failure), endocardial fibroelastosis, pericarditis.

4. Potential type needs to be differentiated from focal myocarditis, non-obstructive hypertrophic cardiomyopathy, and cardiac neurosis.

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