What Is Keshan Disease?

Keshan disease, also known as endemic cardiomyopathy, was discovered in Keshan County, Heilongjiang Province, China in 1935, hence its name. According to data survey, the acute Keshan disease has basically disappeared in 1980. Patients present mainly with acute and chronic cardiac insufficiency, enlarged heart, arrhythmia, and embolization of organs such as the brain, lungs, and kidneys.

Basic Information

nickname

Endemic cardiomyopathy

English name

Keshan disease

Visiting department

Cardiology

Common symptoms

Pale complexion, cold limbs, weak pulses, temperature does not rise, mental weakness, cough, shortness of breath, etc.

Cause of Keshan disease

The cause is unknown. Keshan disease all occurred in low-selenium areas. The selenium in patients' hair and blood was significantly lower than that of residents in non-sick areas. Oral sodium selenite can prevent the occurrence of Keshan disease, indicating that selenium is related to the occurrence of Keshan disease. However, given that the ward is generally low in selenium, and the incidence is only a small part of the residents, and the lack of selenium cannot explain the annual and seasonal incidence of Keshan disease, it should also be considered that there are many types of Keshan disease besides low selenium Other factors may be involved, such as soil and nutrition factors, viral infections, etc.

Keshan disease clinical manifestations

It is mainly acute and chronic cardiac insufficiency, enlarged heart, arrhythmia, and embolization of organs such as brain, lung and kidney.

Acute Keshan disease

It can occur suddenly, or it can occur acutely on a latent or slow basis. In the north, the acute type mostly occurs in winter, and can often be caused by cold, overwork, infection, overeating, overeating, or childbirth. Sudden onset of illness. Severe cases can manifest as cardiogenic shock, acute pulmonary edema, and severe arrhythmia. At first, I often feel dizzy, nausea and vomiting repeatedly, and then irritable. Severe cases can die within hours or days. On physical examination, the patient was pale, the limbs were cold, the pulses were weak, the temperature did not rise, the blood pressure was lowered, and the breathing was shallow. The heart is generally slightly large and the heart sounds are weak, especially the weakening of the first heart sound. There may be diastolic gallops and mild systolic hair-like noises. Arrhythmias are common and are mainly premature ventricular contractions, paroxysmal tachycardia, and atrioventricular block. Snoring occurs in the lungs during acute heart failure. Hepatomegaly and lower limb edema are also common.

2. Subacute Keshan disease

Onset is not as acute as acute. The patients are mostly young children. Most of them occur in spring and summer. Cardiogenic shock or congestive heart failure can also occur. In the early stages of the onset of symptoms, the symptoms include malaise, cough, shortness of breath, loss of appetite, dull complexion, and general edema. There may also be enlarged heart, galloping horses and hepatomegaly.

3. Chronic Keshan disease

Onset is slow and can also be transformed from acute, subacute, or latent. The clinical manifestations are mainly chronic congestive heart failure, complaining of palpitations, shortness of breath, exacerbation after exertion, and oliguria, edema, and peritoneal effusion. The physical examination showed that the heart was enlarged to both sides, the heart sound was low, mild and moderate systolic murmurs and diastolic gallops were audible, and later signs of right heart failure such as jugular vein anger, hepatomegaly, and lower extremity edema. Severe cases may have pleural and abdominal effusions and cardiogenic cirrhosis. Arrhythmias are common, such as ventricular premature beats, tachycardia, conduction blocks, and atrial fibrillation.

4. Potential Keshan disease

Often asymptomatic, can work or work as usual, but found in the census, this is a stable potential. Those who change from other types may have symptoms such as palpitations, shortness of breath, dizziness, and fatigue. ECG may have ST-T changes, prolonged QT interval, and premature beats. Latent patients have a damaged heart, but the heart function is well compensated, and the heart is not enlarged or slightly enlarged.

Keshan disease check

Blood test

The total number of white blood cells and neutrophils can be increased and the erythrocyte sedimentation rate can be increased in acute and subacute patients. The activity of serum aspartate aminotransferase (SGOT), creatine phosphokinase (CPK) and its isoenzymes, lactate dehydrogenase (LDH) and their isoenzymes can be increased to varying degrees in acute patients. It usually rises within a few hours after the onset, peaks in 1 to 3 days, and gradually returns to normal after 1 to 2 weeks. In recent years, heavy chain monoclonal antibodies against human myocardial myosin have also been successfully prepared, which also helps the diagnosis of early myocardial necrosis. The slow and latent types show low albumin, increased globulin, and increased serum a ₁ and a ₂ globulin. Enterovirus IgM was significantly increased in some patients, and enterovirus RNA could be positive in blood and myocardial specimens.

2. ECG examination

This disease can have a variety of ECG changes. Hypertrophy, myocardial damage, and arrhythmia are the most common.

(1) Myocardial damage The rise or depression of the ST segment can be seen, which is related to the damage of the epicardial or subendocardial myocardium, which is more common in the acute type. A small number of QS waves or Qr waves of myocardial myocardial infarction can be seen in limb leads or anterior cardiac leads, which are caused by myocardial necrosis or myocardial fibrosis. In addition, T wave is low flat, bi-phase or inverted, QT interval prolonged, low voltage, etc. are also common.

(2) Arrhythmias are divided into ectopic rhythms and conduction blocks. Ectopic rhythms are most commonly seen before ventricular contractions, often multi-source and frequent, followed by paroxysmal tachycardia and atrial fibrillation. Seen in patients over 40 years of age or children with significantly enlarged heart. Conductive block is most commonly seen in complete right bundle branch block, which can account for about 50% of abnormal ECG in adults, and is often the only potential ECG change; followed by atrioventricular block.

3.X-ray inspection

X-ray examination is an effective means to detect Keshan disease. It can be seen that the heart is enlarged, showing muscle-derived dilation, and impulse weakening. The slow and subacute types are the most obvious. Most of them are general and moderately enlarged. They can be spherical and generally enlarged, often accompanied by pulmonary congestion. The acute type is generally mild to moderately enlarged, and a few hearts are not enlarged. The enlarged transverse diameter of the heart moves downward, and the heart is triangular in weakness, and the pulsation weakens or disappears, which is called myogenic expansion; and the heart of a child patient is often enlarged spherically. Pulmonary blood vessels are mostly venous congestion or mixed congestion. In the early stage, the upper pulmonary vascular shadow is increased and widened. In acute patients, pulmonary vascular hypertension such as blurring of pulmonary blood vessel edges, enlarged hilars, and cloud-like shadows in the lung field can be seen. Sometimes manifestations of pulmonary embolism.

4. Echocardiography

Echocardiographic changes in this disease are very similar to dilated cardiomyopathy. Often manifested as dilated cardiomyopathy-like changes, the left atrium, left ventricle, and right ventricular cavity of the slow and subacute types are generally enlarged, the left and right ventricular outflow tracts are widened, the ventricular walls are thin, and diffuse ventricular activity is weakened, Segmental dyskinesia, decreased left ventricular ejection fraction, and sometimes mural thrombus. Acute ventricular cavity enlargement is more common. Doppler echocardiography revealed that mitral regurgitation was found in 49.2% of patients, and tricuspid regurgitation was also common. Valvular regurgitation could be reduced or even disappeared after heart failure was cured.

5. Endocardial myocardial biopsy

This is a biopsy combined with cardiac catheterization. Pathological examination of the endocardial myocardial tissue obtained will help diagnose the disease.

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 diagnosis of acute and chronic heart failure, enlarged heart, arrhythmia and other diagnosis is not difficult. In areas with northeast and northwestern areas of Kashin-Beck disease and endemic goiter disease, if patients have similar dilated cardiomyopathy, they should be considered chronic Keshan disease.

Keshan disease differential diagnosis

Acute Keshan disease needs to be distinguished from shock pneumonia, acute gastroenteritis, acute myocarditis, and acute myocardial infarction. Chronic Keshan disease needs to be distinguished from primary cardiomyopathy, rheumatic heart disease, and pericarditis.

Keshan disease treatment

This disease should be treated comprehensively. Rescue cardiogenic shock, control heart failure and correct arrhythmia.

Acute Keshan disease

As far as possible, "three early", early detection, early diagnosis and early treatment.

(1) Intravenous injection of high-dose vitamin C can generally be applied for about a week. Drugs that improve myocardial metabolism, such as coenzyme A, coenzyme Q10, and adenosine triphosphate can be used.

(2) Hibernation Therapy is suitable for those who frequently vomit and are irritable. After the medication, the body's metabolic rate is reduced, and myocardial oxygen consumption is reduced, which is conducive to the recovery of cardiac function. Intramuscular or intravenous drip of chlorpromazine, promethazine, pethidine in adults. Metoclopramide can also be used in patients with frequent vomiting, and correct acid-base balance and electrolyte disorders. Diazepam can also be used.

(3) Application of vasoactive drugs In patients with hypotension or shock, when vitamin C and blood volume supplementation have not been recovered, vasoactive drugs such as dopamine, alamin, and noradrenaline can be applied. If hypotension and left heart failure occur at the same time, in addition to cardiotonic drugs, dopamine or dobutamine can be combined with sodium nitroprusside, and the drug concentration and drip rate can be adjusted according to blood pressure.

(4) Cardiotonic drugs For patients with acute or subacute heart failure, it is advisable to dilute it with rapid digitalis preparations such as lanatoside C or poisonous trilobatin K and inject it intravenously. For those with poor treatment results, dobutamine, amidolone, and nitridone are still available. In addition, vasodilators are effective in treating acute and chronic heart failure. Pulmonary edema can also be injected intravenously with fast diuretics such as furosemide or buturamine.

(5) Anti-arrhythmia occurs frequently with premature ventricular beats and ventricular tachycardia. Lidocaine and magnesium sulfate can be injected intravenously or instilled. After basic control, the following oral medications can be selected for maintenance, such as mexiletine and prolo Ketones, amiodarone, propidamine, quinidine, beta-blockers, etc. Supraventricular tachycardia or rapid atrial fibrillation can be injected intravenously. For patients with high or degree atrioventricular block with slow ventricular rate, adrenal corticosteroids, atropine, isoprenaline and other treatments can be selected. If necessary, artificial cardiac pacemaker is provided for treatment.

2. Chronic Keshan disease

Mainly control heart failure and arrhythmia, and prevent infection, overwork, cold and other incentives, so as not to increase the burden on the heart. Digoxin is generally taken orally, according to individual principles, and the dosage is adjusted according to the needs of the disease. Diuretics are suitable for those who have edema. Dihydrochlorothiazide, spironolactone, and furosemide can be taken intermittently or daily. Pay attention to water and electrolyte balance, and correct it at any time. Vasodilators can be used for those with poor therapeutic effects, especially for refractory heart failure. Isosorbide nitrate, prazosin, hydralazine, phentolamine, captopril, sodium nitroprusside, etc. can be selected. In addition, non-digitalis cardiotonics such as dopamine, dobutamine, amrinone can also be selected. Arrhythmia treatment is the same as acute Keshan disease.

3. Subacute Keshan disease

The treatment principle is the same as the slow type, and those with cardiogenic shock should be treated according to the acute type.

4. Potential Keshan disease

Prevent infection, overwork and pay attention to nutrition. Follow up regularly.

Keshan disease prognosis

Severe acute types can die within hours of onset. Patients with chronic and subacute heart enlarge significantly, and those with repeated heart failure have a poor prognosis.