Overview: Keshan disease (Keshan disease) is a reason not clear to cardiomyopathy-based disease, also known as endemic cardiomyopathy. 1935 First found in Keshan County, heilongjiang Province, it is named in Keshan disease. Higher mortality of the disease in the past, the new China was founded to prevent and treat this disease, so that morbidity and mortality of this disease has been a significant decline. In the prevention, treatment and cause of the disease has also made some important progress. The current annual incidence has dropped to 0.07/10 million or less, the incidence of type from the acute type, subacute type is more to the potential-and slow-type-based. A large number of epidemiological, pathological anatomy, clinical control and laboratory results indicate that the disease is an independent endemic cardiomyopathy.[Cause]
Keshan disease is caused by what the?
cause of Keshan disease is not yet clear that the theory of the cause of up to 10 species, according to a large number of field investigations and laboratory analysis, the majority of theories have been eliminated, the current cause of Keshan disease research focuses on biogeochemical and biological causes of two major causes.
1. biogeochemical causes of that ward specific natural environment, and Keshan disease related to chemical substances through the soil and water environment - the food chain in the human body, so the research includes two aspects: one is the poisoning theory (including barium, humic acid, nitrite, etc.), two chemical substances to the diet (selenium, magnesium, molybdenum) the lack or imbalance theory. according to the survey of the disease have significant regional, ward of the soil, water and food in the lack of certain trace elements such as the human body needs selenium, molybdenum, magnesium, etc., or the nutrients, thereby interfering with myocardial metabolism, or injury caused by myocardial and morbidity. Institute of Keshan disease control group of non-ward ward and determination of selenium in internal and external environment, water and food found in the ward of selenium were significantly lower blood selenium ward populations and hair selenium content is low. And investigate, from a low soil selenium content in soil adjacent ward to a high selenium area, found elevated levels of selenium in food, the disease also declined.
years found that selenium deficiency cardiomyopathy can occur in some animals, and induced cell-mediated immunity and decreased immune function, manifested as reduced antibody production, reduced response to antigen, phagocytic reduced capacity. Amount of selenium on the selenium caused a significant protective effect of myocardial damage and antioxidant capacity. And can improve the body's resistance to infection. selenium is glutathione peroxidase (GSH-px) of a composition, the enzyme's primary role is to restore the lipid peroxides, scavenging oxygen free radicals thereby protecting the integrity of cell membranes, low-selenium gsh can -px activity decreased, resulting in myocardial membrane system damage. Recent studies have still found that vitamin e can protect this enzyme, suggesting that in addition to external nitrite too low selenium and vitamin e deficiency may be involved in Keshan disease areas. selenium deficiency in experimental animals myocardial samples for electron microscopy and cytochemical examination (cytochrome oxidase, acid phosphatase and Ca2 + ATP enzyme), indicating myocardial membranes showed different degrees of damage; myocardial oxidative phosphorylation disorders, oxygen utilization low, ATP synthesis to reduce the . according to ATP inside the cell there is abnormal functioning of the regulation of calcium, leading to contraction of organelles and components of a series of changes.
recent studies have reported low magnesium (Mg content in plasma and red blood cells significantly reduced), may also be one of the causes of this disease and proposed treatment of the disease and the heart rate of magnesium disorders of necessity.
some characteristics are consistent with biological factors infection characteristics, such as Keshan disease, myocardial tissue from separable to many strains of viruses, including Coxsackie B virus. serological studies also show that about 1 / 3 of the acute type and 67.9% of the sub-acute Keshan disease double Coxsackie B virus in serum antibodies was 4 double high
, with isolated Coxsackie B virus vaccine caused a low selenium rat myocardial disease, injury and disease detection rate was significantly higher than normal selenium group. Virus on myocardial injury in addition to direct viral cytolytic effects, and can induce cytotoxic T cells, B cells, T helper cell proliferation strong, so the biological cause of the disease that the incidence of Keshan disease may be the basic factors of low selenium, some cases in a Coxsackie B virus infection to disease, and autoimmune response triggered further increased myocardial damage.
(B) the pathogenesis
(1) biogeochemical causes: the theory that the cause of Keshan disease present in the soil among the ward, acting on the human body through the food chain through amino acids, vitamins and trace element deficiency or imbalance, causing myocardial damage and disease.
① low selenium and external environment: internal and external environment, low selenium and Keshan disease is closely related. A large number of studies have shown that Keshan disease occurred in low selenium areas, ward food selenium content was significantly lower than non-endemic area, hair and blood selenium levels were significantly lower than non-endemic area residents, both inside and outside the ward show lack of selenium in the environment . By Heilongjiang, Shaanxi, Sichuan, more than 10 million people in the prevention of Keshan disease, oral administration of sodium selenite experiment, found that selenium on the prevention of acute-and subacute Keshan disease incidence significant effect. In addition, Keshan presence to patients and ward populations with low selenium-centered metabolic changes, such as patients and ward populations in tissues and blood glutathione peroxidase (GPX) were significantly lower than non-endemic populations; plasma lipid peroxide (MDA), free fatty acid (FFA) and other ingredients was significantly higher than non-endemic area; free radicals in patients with red blood cells and hemoglobin oxidation was significantly higher than non-patients, ward children was also higher than non-endemic area children. However, selenium can not fully explain all the popular Keshan disease characteristics, such as not all regions with low selenium Keshan disease occurrence; Although the ward generally low selenium, but the incidence of only a small part of the residents; selenium does not ward Keshan disease, with annual and seasonal changes in the corresponding multiple; the same ward of sick children and non-sick child, hair, blood selenium and selenium no significant differences. Therefore, the current that selenium deficiency is Keshan disease is extremely important to regional factors, but not the only factor.
② vitamin e (VE) deficiency: discovered in recent years, VE of each component in the strongest antioxidant α-tocopherol (α-toco) in the ward Pay levels are generally lower than non-endemic area, and also confirmed that the ward population (including Keshan disease and healthy people) plasma α-toco and VE were significantly lower than the total amount of non-endemic healthy people, patients with red blood cells film in the α-toco and VE were significantly lower than the total amount of non-endemic normal, table Mountain mink disease patients are generally at low VE state. ward food in polyunsaturated fatty acids (PUFAs) levels were generally higher than the non-endemic area, α-toco (mg) and PUFAs (g) the ratio is generally lower than non-endemic area, and VE in vivo depends on the protection of PUFAs , suggesting that there may ward populations relative lack of α-toco to further reduce the body's antioxidant capacity.
③ protein and amino acids: ward resident animal and vegetable protein intake was significantly lower than non-endemic area; ward food than non-essential amino acids in the disease area. Sulfur-containing amino acids in plasma ward populations (S-AA) such as methionine deficiency, making the intake of selenium from dietary methionine substitution of methionine in protein synthesis, resulting in selenium can not play its proper physiological function. S-AA or a precursor of glutathione, its intake will lead to reduced glutathione synthesis, which is not only a GPX specific substrate reaction, and is itself a free radical scavenger. Thus, low selenium, S-AA intake and low VE can lead to decreased antioxidant capacity.
④ dietary potassium: Previous studies showed that the majority of low-selenium areas, external environment, there is a relatively high manganese phenomenon. Experiments showed that when the protein is in short supply, exogenous manganese can accumulate in the body, resulting in increased selenium excretion, tissue selenium content decreased, affecting the cells, especially red blood cells and myocardial antioxidant capacity. The poor-rich manganese combined with selenium, and mutual influence, can further reduce the myocardial antioxidant capacity, increased myocardial damage.
⑤ low-calcium diet: Dietary single ward, inadequate calcium intake is particularly evident. Animal studies found that calcium can increase the selenium-induced myocardial necrosis, so dietary calcium may also be combined in Keshan disease pathogenic factors play an important role. This may explain why Keshan disease occurred in the calcium needs of reproductive age women and a large growing children.
(2) biological cause:
① enteroviruses: Keshan disease from blood and myocardial tissue and the dead separable from other organs in a variety of viruses such as coxsackie virus A9, B1, B2, B3, B4, etc. type, echovirus type 12, adenovirus type 7 and so on. serological survey found Keshan disease and intestinal virus antibody positive rate is much higher than non-endemic control group, only the Coxsackie B virus and the antibody-positive rate as high as 68.6% to 90%, and found that about 1 / 3 of subacute, acute type patients was 4-fold antibody titer increase in serum in coxsackie virus igm positive rate 69.4%, indicating that most of Keshan disease has occurred in recent enterovirus infection. in situ hybridization with domestic and nested polymerase chain reaction technology, Keshan disease found in the myocardium enterovirus rna in both samples exist, the positive rates were 85.7% and 90%. These results suggest that attention should be paid enteroviruses, especially Coxsackie B virus infection in Keshan disease pathogenesis.
foreign animal studies have shown that, in the case of selenium and low VE in mice infected with coxsackie virus more easily. coxsackie virus infection in the low VE cardiac conditions, showing that the disease is more serious; not usually a benign strain of myocarditis caused by CVB3 / 0 mice also caused a low VE cardiomyopathy; also isolated from the myocardium virus, the cells were inoculated to a passage in mice have been added when the VE, can also cause significant myocardial injury, indicating that conditions in the low VE benign CVB3 / 0 phenotype changes may have occurred. selenium have a similar situation, such as separation from selenium derived from rat cardiomyocytes with benign CVB3 CVB3 / 0 for comparative analysis of nucleotide sequences and found that 6 (No. 234,788,2271,2438,3324,7334 bit) nucleotide mutation occurred, and these mutations with the known strain-induced myocarditis CVB3/20, CVB3/M1 consistent with the nucleotide sequence. In addition, selenium proteins, such as GPX, not only the synthesis of higher organisms, cells, CVB3 may also be encoded. The GPX part of CVB3 amino acid sequence homology with, and the capsid protein VP3 fusion protein can be formed. selenium or selenium above protease gene knockout CVB3 / 0 of the mutations have one in the area. Therefore, it was speculated that the mutant may also be pathogenic fusion protein with the function of this GPX inactivation.
② fusarium streptozotocin: ward grain was extracted from fusarium streptozotocin and streptozotocin fusarium contaminated grain speculation as the cause of Keshan disease. However, fusarium moniliforme in Keshan disease endemic and non-endemic area were distributed, and not the dominant bacteria; bacteria contamination in different food types the difference between the ward and non-endemic area is greater than the difference between the same grain crops; The pollution distribution and Keshan disease in regional distribution is not consistent; fusarium and streptozotocin toxicity of selenium nutritional status of infected object is irrelevant; selenium or streptozotocin supplement VE on the toxicity of fusarium did not inhibit or reduce the effect, Keshan disease and selenium in prevention of the practice does not match; in fusarium streptozotocin-induced myocardial damage in Keshan disease, no similar enzymes and pathological changes. So, now that fusarium streptozotocin in the etiology of Keshan disease, the role to be further explored.
short, the current that Keshan disease is a complex disease induced by the endemic cardiomyopathy, the basic cause is due to biogeochemical factors and dietary factors superimposed , resulting in low selenium and closely related VE (α-tocopherol) intake is inadequate. Low selenium, low VE generally act on the ward population, usually caused by myocardial metabolism of subclinical or potential damage to cause rapid myocardial necrosis and clinical disease, but also a number of predisposing factors (condition factor) in the role. These factors do not exist significant regional differences, but can the clinical incidence of Keshan disease, multiple year, multiple play an important seasonal effects, such as coxsackie virus infection is an important condition factor.
2. pathologic autopsy confirmed a large number of China's northeast, north, northwest and southwest of the ward of the Keshan disease, the pathological characteristics are basically the same, based on mitochondrial damage based metabolic cardiomyopathy. eye view of the heart was myogenic expansion to both sides of the general expansion of the ventricle, severe spherical, often without ventricular wall thickening. See section have intertwined real myocardial degeneration, necrosis and fibrosis lesions. There are patchy endocardial thickening, 20% of patients with mural thrombus and lung, brain, kidney, spleen, mesenteric and peripheral vascular thrombosis. Heart valves and coronary arteries were normal. Light microscope, showing diffuse myocardial cell degeneration and focal necrosis to left ventricle and interventricular septum more common, and more severe, and mild right ventricle; ventricular than atrial weight; ventricle, the middle weight than the outer; acute type Keshan disease, subendocardial necrosis up to 95%, but children ventricle, the outer layer of endocardial lesions than weight. myocardial lesions and coronary artery branch closely related to the gradual, subacute in children were more obvious. myocardial cells showed granular degeneration, which can have varying sizes within the vacuolar degeneration, or fatty degeneration was lined due to myocardial necrosis. The same lesions, coagulation necrosis can be mixed and dissolved there, which type of severe acute coagulation necrosis with, and subacute necrosis solubility places, often accompanied by varying degrees of secondary inflammatory response. lesions may invade the conduction system, especially with bilateral bundle branch right bundle branch disease is more serious.
electron microscopy mainly visible swelling of mitochondria, proliferation, mitochondrial cristae damage, system damage and myocardial cell membrane capillary endothelial damage. Combined histochemical analysis shows that such pathological changes of myocardial cells, oxidation, reduction, metabolic system disorders. So some people think this disease is a kind of mitochondrial damage as the main feature of the primary metabolic cardiomyopathy (mitochondrial disease). Application of endomyocardial biopsy, the latent Keshan disease and cardiac-line electron microscopy found that the myocardial cell membrane system has obviously changed, endoplasmic reticulum, T tube, the expansion of intercalated disc, mitochondria hyperplasia, atypia, myogenic fiber hooks and tiny muscle and interstitial fibrosis dissolved.
application of molecular biology techniques in cardiac lesions are scattered around or apoptosis of myocardial cells, suggesting that cardiomyocyte apoptosis is also involved in the occurrence and development of myocardial damage.
Keshan disease early symptoms?
, clinical symptoms
according to cardiac function, Keshan disease clinically divided into acute type, subacute type, slow type, and latent. The first three types of cardiac decompensation, which is compensatory type. Acute type manifestations of acute heart failure, often associated with cardiogenic shock and severe arrhythmia. subacute occurs primarily in children, with edema and congestive heart failure based. slow type mainly for chronic congestive heart failure, may occur gradually, but also by acute or subacute type of transition from. Latent heart function was good, no more symptoms, occasional arrhythmias and ecg changes.
1. acute type than in the winter of this type of disease, rapid-onset, rapidly changing, often in the cold, fatigue, cold, mental stimulation, eating and drinking, or women on maternity leave and other heart load under the effect of increasing the incidence of incentive. The most common manifestations of cardiogenic shock, severe acute type accounts for about 75% of Keshan disease. Patients often nausea, vomiting, dizziness as the main symptom, and often with dizziness, abdominal discomfort, chest tightness, palpitations, breathing difficulties chief complaint. Severe may die within a few hours. Examination 67% to 82% of patients with enlargement of the heart, may have gallop, pulmonary[Aftertreat]
Keshan disease ate?[Prevent]
Keshan disease should be how to prevent?
(a) comprehensive prevention measures pay attention to environmental sanitation and personal hygiene. Protection of water resources, improve water quality. improve nutrition, prevent the partial eclipse, especially for pregnant women, mothers and children should be strengthened to add protein, vitamins and essential trace elements, including magnesium, iodine, etc., and prevention of Kashin-Beck disease, endemic thyroid disease.
(b) of the endemic areas to promote the use of sodium selenate as a preventive medicine preventive medicine, after years of promotion, that can significantly reduce morbidity. Usually orally once every 10 days, 1 to 5 years old 1mg, 6 ~ 10 years old 2mg, 11 ~ 15 years old 3mg, 16 years old 4mg. incidence of the season can not stop taking three months. Eliminate poverty and improve people's living standard ward, are also important preventive measures.
researchers understand the composition of different foods, there are significant differences in prevalence. Keshan disease diet, beans, vegetables, animal food, etc low fat, vitamin A, vitamin b12 and selenium intake is particularly low, the calcium content of food is clearly inadequate. Observations confirm significantly improved diet in disease prevention. ward for change or improve dietary composition, reasonable arrangements for the supply of food, nutrition rationalization of residents will be able to control the occurrence of Keshan disease.
(c) the attention to rest and strengthen the management of patients with cardiac function according to limit or avoid physical and mental activities to promote patterns of life, work and rest. Rest can reduce the burden on the heart, promote recovery of myocardial injury. Prevent upper respiratory tract infection and mental stimulation. Unstable condition, should strengthen the follow-up.
(a) In addition to endemic areas, the disease occurred in my own country, Korea, Japan also has been reported. China mainly from the northeast to the southwest in a transition zone, namely, Heilongjiang, Jilin, Liaoning, Inner Mongolia, Hebei, Henan, Shandong, Shanxi, Shaanxi, Gansu, Ningxia, Sichuan, Yunnan, Tibet and other provinces and autonomous regions, mainly in the ward desolate hills, plateau and grassland areas of the countryside. Lower incidence in urban areas.
(b) Seasonal incidence of the disease has obvious multiple years and multiple seasons, the Northeast region and more acute type of onset in the cold winter, and Southwest zones, hot summer good disease season.
(c) the population distribution of the disease occurs mainly in the rural young women and children. Northeast, Northwest Territories, the young women significantly more than men. Sichuan, Yunnan, places for children aged 2 to 6 is more common. Number of people also have a family disease. according to popular area survey, more than farming population incidence, while the urban population are rarely sick.[Treat]
1. acute Keshan disease
(2) improve myocardial nutrition metabolism: clinical practice has proved that high-dose intravenous vitamin c can improve the heart, blood vessels and body metabolism, increasing myocardial glucose utilization and glucose the original synthesis, increased myocardial energy reserves, improve the redox processes within the organization. In improving the metabolism, the enhanced myocardial contractility, increased cardiac output, cardiogenic shock to be corrected. Usage: patients with severe acute type, the first application of vitamin c 5 ~ 10g (children 3 ~ 5g) alone or by adding 25% to 50% glucose 20ml intravenous injection. according to the disease every 2 to 4 hours, repeat 1, 24h total no more than 30g (children 10 ~ 15g). shock mitigation, arrhythmia corrected, daily intravenous 5g (pediatric 3g), once every 3 to 7 days. shock recurrence can be reused. improve myocardial metabolism of drugs, such as coenzyme A, Pan Kuei Lee ketone (coenzyme Q10), diphosphate (FDP), etc. can also be used.
(3) reduce the burden on the heart: first is to make the patient calm to reduce the burden on the heart. For irritability, frequent vomiting, can be used sub-hibernation therapy. Used chlorpromazine 25mg, promethazine 25mg, pethidine 50mg (children of all 0.5 ~ 1.0mg/kg) intramuscular injection or intravenous infusion; or diazepam (stability) 20mg (0.25 ~ 0.5mg each time children / kg) intravenously. If necessary, re-use, so that patients in the sub-hibernation state.
(4) the application of vasoactive drugs: type of emergency patients, often in no hurry to correct the low blood pressure. If the 2nd injection of vitamin c have not picked up after the blood pressure, shock, when no relief can be applied vasoactive drugs such as dopamine, alamin and norepinephrine. Such as low blood pressure while left ventricular cardiac failure in addition to available drugs, it can also be combined with dopamine or dobutamine and sodium nitroprusside, and blood pressure regulation under the drug concentration and infusion rate.
(5) correction of acute heart failure and cardiac arrhythmias: acute type, subacute with heart failure, digitalis preparations, such as suitably fast lanatoside c 0.4 mg or poisonous hairs spin Hanako glycosides K0.25mg diluted intravenous injection. The treatment effect in poor still use dobutamine, ammonia topiramate topiramate ketone ketone and a nitrile. Moreover, the vasodilator treatment of acute and chronic heart failure, better effect. Acute pulmonary edema by acute heart failure treatment (use diuretics, cardiac glycosides, vasodilators, morphine, etc.). Patients had acute type of arrhythmia, and more to improve myocardial metabolism, correct treatment of cardiogenic shock improved or disappeared within 4h after, if not corrected, according to arrhythmia type, choose the appropriate anti-arrhythmic drugs. Frequent ventricular premature beats, ventricular tachycardia, intravenous injection or infusion of lidocaine and magnesium sulfate, to be under control after oral medication used to maintain the following, such as mexiletine, propafenone, amiodarone, disopyramide, quinidine, β-blockers and so on. Supraventricular tachycardia or atrial fibrillation, intravenous injection lanatoside C. height or Ⅲ degree atrioventricular block heart rate slow, the choice of adrenocorticotropic hormone, atropine, isoproterenol treatment. If there is a high degree or third degree atrioventricular block, artificial pacemaker can be installed.
(6) to prevent acute type to slow type: acute Keshan disease disease control, life guidance should be strengthened. month not to participate in physical labor. review within 3 months 1, to prevent the slow type. If there is enlargement of the heart and other signs of congestive heart failure, that is by Keshan disease treatment.
2. subacute Keshan disease, subacute Keshan disease in clinical manifestations of congestive heart failure, but a few associated with cardiogenic shock. The treatment of congestive heart failure with slow type, according to the choice of sub-hibernation condition or sedative drugs. Cardiogenic shock and those who deliberately, according to emergency type treatment.
3. Keshan disease, mainly heart failure and arrhythmia control and prevent infection, fatigue, chills and other incentives, so as not to increase the burden on the heart. cardiac drug digoxin is generally used in oral, adult 0.125 ~ 0.25mg / d, according to the principle of individual and need to adjust the volume with the disease. diuretics for edema, could be intermittent or daily oral administration of Hydrochlorothiazide, spironolactone and furosemide, etc. Should be noted that water and electrolyte balance, and at any time be corrected. Vasodilator for the treatment ineffective, especially for refractory heart failure. Choice of isosorbide, prazosin, hydralazine, phentolamine, captopril, sodium nitroprusside and so on. In addition, dopamine can also use more horse phenol-butylamine, amrinone (Amrinone) and other non-cardiac stimulant digitalis. digitalis may be prudent long-term use. treatment of cardiac arrhythmias and acute Keshan disease with.
(b) the prognosis
acute type if a reasonable place for emergency treatment of early clinical cure rate of up to 85 %, of which about 20% can be converted to slow-type, and more for the cause of death, cardiogenic shock or sudden death.
slow type, subacute patients with severe cardiac arrhythmia significantly increased and poor prognosis. Two 5-year survival rate in the 1970s to about 40%, improved in recent years as treatment, 5-year survival was significantly prolonged, but 10-year survival rate is still low. About half of the patients died of refractory heart failure, followed by sudden death.
Keshan disease, which checks should be done?
(a) blood test acute type and subacute patients leukocytes and neutrophils can be increased, erythrocyte sedimentation rate can be faster. type of severe acute serum aspartate aminotransferase (SGOT), creatine phosphokinase (CPK) and its isoenzymes, lactate dehydrogenase (LDH) and its isoenzyme activity may have increased to varying degrees. More than a few hours after the onset of increase in peak 1 to 3 days, 1 to 2 weeks after getting back to normal. In recent years, people have anti-muscle myosin heavy chain monoclonal antibody success also goes to help the early diagnosis of myocardial necrosis. Slow-and albumin-visible side-generation potential, globulin, serum protein electrophoresis a1 and a2 globulin. Part of the enterovirus igm in serum was significantly higher, and myocardial blood and other samples can be positive for enterovirus RNA.
1. heart dirty up or damage visible ST-segment depression, this and epicardial or subendocardial damage related, more common in acute type. A small number of joint or limb can be seen like precordial heart muscle like the QS wave infarction or Qr wave, this is due to myocardial necrosis or myocardial fibrosis. In addition, t wave flat, biphasic, or inverted, QT interval prolongation, low voltage, are also common.
2. arrhythmia into ectopic rhythm, conduction block, ectopic rhythm to ventricular contraction the most common, often multi-source, frequently, followed by paroxysmal tachycardia and atrial fibrillation, which is more common in patients over 40 years of age or significant expansion of the heart for children. block with complete right bundle branch block the most common, can account for 50% of adults, abnormal ecg or so, often the only potential-type ecg changes; followed by atrioventricular block.
(3) x-ray X-ray examination in the rural areas of Keshan disease is found to be an effective tool. Visible enlargement of the heart, showed myogenic expansion, weakened pulse to slow-type and subacute the most obvious, and more moderate expansion for the universality of the general increase can be spherical, often accompanied by pulmonary congestion. The universality of acute mild to moderate type was expanded, there are a few heart do not expand. Diameter down to expand the heart, the heart was unable to form a triangle, pulse weakened or disappeared, called myogenic expansion; and children often has a spherical expansion of the patient's heart. pulmonary vascular congestion or mostly mixed venous congestion, the upper part shows the early increase in pulmonary vascular shadow, widened, acute pulmonary vascular type were still visible edge blur, hilar enlargement and lung field cloudy shadows pulmonary hypertension of the performance. Sometimes visible manifestations of pulmonary embolism.
(D) echocardiography Echocardiography change of the disease and dilated cardiomyopathy are very similar. Usually dilated cardiomyopathy-like changes, slow and subacute type of left atrium, left ventricle, right ventricular cavity mostly universal expansion, left ventricular outflow tract widening, ventricular wall thin, diffuse ventricular activity weakened, and a segmental movement disorders, left ventricular ejection fraction, sometimes you can see the mural thrombus. Acute left ventricular cavity to expand more common type. Doppler echocardiography can be found in 49.2% of the patients had mitral regurgitation, tricuspid regurgitation are common in heart failure, valvular regurgitation after cure reduce or even disappear.
(e) systolic time period for this measure show PEP / LVET (left ventricular spurting spurting early time and time ratio) ratio higher than normal (normal 0.345 ± 0.036), reflecting the disease decreased myocardial contractility.
Keshan disease and the diseases easily confused?
the major manifestations of acute disease and chronic heart failure, enlarged heart, arrhythmia, and brain, lung and kidney and other organs of the embolism. The major clinical is to identify what type of Keshan, according to the 1982 national exchange of experience of Keshan disease control at the sub-type is as follows.
(a) a sudden acute onset type of healthy people, but also from potential based on the type or slow type of acute attacks. In the north, acute type occurred in the winter, often due to cold, fatigue, infection, binge drinking, overeating or childbirth and other incentives and disease. Rapid onset. Severe cases can be expressed as cardiogenic shock, acute pulmonary edema and severe arrhythmia. Initial often feel dizziness, chest discomfort, nausea, repeated vomiting, vomiting yellow water, followed by irritability. Severe cases may die within hours or days. physical examination of patients see pale limbs Jueleng, weak pulse, body temperature did not rise, blood pressure, rapid shallow breathing. Generally mild big heart, weak heart sounds, especially in the first heart sound is even less, may have mild diastolic gallop and systolic murmur hair samples. Common arrhythmia, mainly ventricular premature beats, paroxysmal tachycardia and atrioventricular block. acute heart failure occurs when the pulmonary rales, hepatomegaly, and lower extremity edema are also common.
(b) subacute onset of acute type than abrupt. Patients, mostly children, 2 to 5 years old accounted for 85%. In spring, summer onset of the majority. Cardiogenic shock may occur or congestive heart failure. Early stages showed listlessness, cough, shortness of breath, loss of appetite, pale gray, and generalized edema. Also have enlarged heart, gallop rhythm and hepatomegaly. Brain, lung, kidney, etc. embolization is not uncommon.
(c) slow-type slow onset, and more in the unconsciously disease, or by the acute type, subacute or latent transforming from. The main clinical manifestations of chronic congestive heart failure, complained of palpitations, shortness of breath, tiredness after the increase, and there is oliguria, edema, and ascites. cardiac examination showed obvious to both sides of the expansion of low heart sounds can be heard and mild to moderate systolic and diastolic gallop murmur, late may have signs of right heart failure such as jugular vein Shu Zhang, hepatomegaly, and lower extremity edema. Can have serious chest, abdominal effusion, cardiac cirrhosis performance. Common arrhythmias such as ventricular premature beats, tachycardia, conduction block, atrial fibrillation, and so on.
(d) potential type can occur in healthy people, but also for other type of improvement phase. The former is often asymptomatic, can be labor or work as usual, but was found in the census, the potential of this type is stable. Transformation comes from the other may have heart palpitations, shortness of breath, dizziness, fatigue and other symptoms. ecg ST-T changes may have, QT interval prolongation and premature beat. Although latent damage to the heart, but well compensated heart function. The heart does not increase or slightly increased.
also need this disease and other diseases, differential diagnosis
2. slow type to be with dilated cardiomyopathy, peripartum cardiomyopathy, coronary heart disease, chronic pericarditis, rheumatic heart disease and identification. In particular, to identify with dilated cardiomyopathy, some scholars believe that identification of the two diseases should be clinical and epidemiological, pathological data and life changes linked to a comprehensive analysis. The main differential diagnosis in table 1.
dehydration heat-related illness
more other symptoms
"frozen" phenomenon "three fears" (water, sound, light 21 - hydroxylase deficiency igm antibodies sm accumulation increased belching physical scars, insomnia, daytime sleepiness, nighttime leukocytosis leukopenia signs of leukemic cell infiltration in sepsis to maintain sleep disorder galactosemia lost hold of a passive position overeating addiction rage stolen or hypochondriacal paranoia delusions
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