Myocardial Disease. Cardiomyopathy, Dilated Hypertrophic Restrictive Endemic, etc. and Myocarditis
Myocardial disease refers to the disease with cardiomyopathy as the main manifestation. The disease can be divided into two categories: one is primary or idiopathic cardiomyopathy of unknown etiology, also known as cardiomyopathy. The other is secondary or specific cardiomyopathy with a clear etiology or associated with systemic disease. Primary cardiomyopathy is divided into three types. Dilated cardiomyopathy is the most common in the world, followed by hypertrophy and restricted type is rare. Specific cardiomyopathy includes inflammatory or non-inflammatory cardiomyopathy such as alcoholic cardiomyopathy and perinatal cardiomyopathy. Keshan disease is an endemic cardiomyopathy with a unique epidemiology and a special type of cardiomyopathy.
What is Cardiomyopathy?
Cardiomyopathy, also known as idiopathic cardiomyopathy, can be divided into three types, namely dilated cardiomyopathy (Dilated Cardiomyopathy), Hypertrophic cardiomyopathy and Restrictive cardiomyopathy.
The incidence of cardiomyopathy has a tendency to increase significantly. The annual incidence is about 50,000 per 100,000 people. The incidence varies from region to region, and may be related to the environment, culture, and living habits.
What is Dilated Cardiomyopathy?
Dilated cardiomyopathy, also known as congestive cardiomyopathy, is characterized by enlarged heart, heart failure, and arrhythmia.
What are the Causes of Dilated Cardiomyopathy?
The cause is unknown and may be related to the following factors:
1. Viral myocarditis: In recent years, viral myocardium has increased. In particular, Coxsackie B virus has an affinity for the myocardium. Myocardial fibrosis and myocardial hypertrophy eventually form cardiomyopathy.
Cambridge measured Coxsackie B virus neutralizing antibodies in 50 patients with dilated cardiomyopathy. He found that patients with dilated cardiomyopathy had more than 1024 neutralizing antibodies than the control group. And found that the course of disease is shorter than one year and the fever has a significantly higher neutralizing antibody. Wilson animal experiment, experimental Coxsachie B viral myocarditis, a few months later myocardial fibrosis and small focal inflammatory cell infiltration to form cardiomyopathy.
Burch found electron-like particles in the myocardium of myocardial disease patients with electron microscope, as explained above, some cardiomyopathy is Consequences of Myocarditis Development.
2. Allergic reactions: Some patients with this disease have increased antiviral antibodies. Suppression of T cell dysfunction often occurs, and the disease is believed to be caused by an allergic reaction to the virus after viral infection.
3. High blood pressure, about 10% of the blood pressure increased. However, the increase in blood pressure occurs in heart failure, and the blood pressure decreases with the control of heart failure. Therefore, the increase in blood pressure is not the main factor of the disease.
4. Malnutrition and portal cirrhosis are complicated by the disease, more than the general population, the higher incidence of poor residents suggests that the disease is related to nutrition, the lack of certain essential amino acids or trace elements in the body may be the cause of the disease One.
What is the Pathology and Pathophysiology of Dilated Cardiomyopathy?
Dilated cardiomyopathy often enlarges the heart, and the dilatation of the heart is most obvious in the bilateral ventricles. Therefore, it is called dilated cardiomyopathy. Those with less dilated cardiac chambers have slightly thickened ventricular walls, the development of lesions, the dilation increases, and the ventricular walls become relatively thin. Ventricular wall thickness is normal or slightly thickened.
Due to myocardial fibrosis, myocardial contraction is weak, ejection score is reduced, semi-lunar valve orifice may have functional stenosis, left and right ventricles expand, which can cause relative insufficiency of the atrioventricular valve opening, and repeated impact of blood flow causes slight increase in atrioventricular valve Myocardial lesions can expand into the endocardium, and increase in local pressure in the heart. Insufficient local blood supply can cause endocardial plaque fibrous thickening, with malignant thrombosis in about 60% of cases.
The coronary arteries are normal, or there are arteriosclerotic lesions that are suitable for the patient’s age. Myocardial cells with varying degrees of hypertrophy can be seen under the light microscope, the array can be enlarged, the nucleus is enlarged, and focal fibrosis can be seen in half of the cases. The nucleus of cardiomyocytes increased, the number of mitochondria increased, riboprotein, glycogen particles and myofibrils increased, suggesting that cardiomyocytes have strong anabolic metabolism.
Dilated cardiomyopathy: The heart cavity is significantly dilated, but the ventricular wall is not thickened, the ventricular wall is weak, the contraction is weak, the ejection score is decreased, the stroke volume is reduced, the residual blood volume in the heart chamber is increased, the end-ventricular pressure is increased, and the lung Obstructed blood return, pulmonary congestion, left heart failure.
About one third of this disease has left heart failure first, and some of them start with total heart failure. In the enlarged heart cavity, there is mural thrombosis, so arterial embolism is common. As the myocardial fibrosis can involve the pacing and conduction system, it is easy to cause arrhythmia.
What are the Clinical manifestations of Dilated Cardiomyopathy?
I. Symptoms Dilated cardiomyopathy is the most common type of primary cardiomyopathy. It is most common in 30-50 years of age. There are more men than women. The onset is slow. The asymptomatic heart can expand for many years, or it can show various types. Arrhythmia gradually develops and heart failure occurs.
Patient may first have left heart failure, flustered, shortness of breath, can not lie flat. Then there was right heart failure, hepatomegaly, edema and oliguria. It can also manifest as total heart failure. Chest pain or dull pain, typical angina pectoris is rare. Dizziness or headache, or even syncope may occur due to reduced stroke volume, insufficient blood supply to the brain.
Due to the thrombus in the wall of the heart, it can cause pulmonary, brain, kidney, and limb arterial embolism. Arrhythmias are more common, with ectopic rhythms, especially pre-ventricular contractions, atrial fibrillation incidence of about 10-30%, and various types of conduction blocks can also be available. Arrhythmia may be the only manifestation of the patient. Sudden death may occur due to arrhythmia or arterial embolism.
Signs: Heart enlargement is most common. The first heart sound of the apex is weakened. Due to relative mitral regurgitation, the apex often has systolic murmurs. Occasional murmurs can be heard at the apex of the heart. The murmur increases when heart failure worsens. The murmur weakens or disappears during the reduction, and about 75% of patients can hear the third or fourth heart sound. Increased blood pressure in 10% of patients may be related to increased catecholamine secretion and sodium retention during heart failure. After the control of heart failure, blood pressure returned to normal, and some patients with hypertension also coexisted.
What are the Laboratory and other inspections for Dilated Cardiomyopathy?
(A) X-ray examination: cardiac enlargement is prominent, with left ventricular enlargement and right ventricular enlargement, and left atrial and right atrial enlargement are also possible. The heart enlargement is obvious when the heart failure is controlled. After the heart failure is controlled, the heart enlargement is reduced. When the heart failure becomes worse, the heart enlarges again. “Accordion effect” is present. Cardiac pulsation is generally weakened, and segmental motion abnormalities may occur early in the lesion. The aorta was normal, the pulmonary artery was slightly dilated, and the pulmonary congestion was mild.
(B) ECG can have a variety of arrhythmias, the most common pre-ventricular contraction, followed by atrial fibrillation. Different degrees of atrioventricular block, right bundle branch block is common. Extensive ST-T changes, left ventricular hypertrophy, left atrial hypertrophy, pathological Q may occur due to myocardial fibrosis, and each lead has low voltage. .
(C) Echocardiography: The left ventricle is significantly enlarged, the left ventricular outflow tract is dilated, the ventricular septum and the left ventricular posterior wall pulse amplitude are weakened, and the sum of the pulse amplitudes of the two is less than 13mm. In the early stage of the lesion, there may be weakened segmental motion, and the amplitude of mitral valve anterior and posterior lobes weakened.
The mitral valve opening is small, and the mitral valve leaflets may be slightly thickened. Both the right ventricle and the double atria can be enlarged. During heart failure, the mitral valve can be changed like a city wall, and the bimodality can be restored after the heart failure is controlled.
(D) Isotopic examination: Isotope myocardial perfusion imaging mainly shows enlarged cardiac chambers, especially enlarged ventricles on both sides. Myocardial imaging is said to be diffuse sparse, but there are no localized defect areas, the amplitude of ventricular wall pulsation is reduced, ejection fraction is reduced, and isotope myocardium Perfusion imaging can be used not only for diagnosis but also for identification with ischemic cardiomyopathy.
(E) Endocardial myocardial biopsy: The clinical manifestations and auxiliary examination of dilated cardiomyopathy lack specificity. In recent years, endocardial myocardial biopsy has been carried out at home and abroad. The diagnosis of this disease has higher sensitivity and lower specificity.
What is the Diagnosis for Dilated Cardiomyopathy?
1. History of congestive heart failure.
2. Cardiac signs: enlarged heart, weakened first heart sounds, apical systolic murmurs, increased heart failure murmurs, and reduced or attenuated heart murmurs. There is often a pathological third heart sound.
3. X-ray, echocardiography, cardiogram, and isotope scan showed dilated heart without significant hypertrophy.
4. ECG shows ectopic rhythm, conduction block, extensive ST-T changes or abnormal Q waves
5. Arterial embolism
6. Rule out other heart disease, or secondary cardiomyopathy caused by other reasons. Due to the lack of specific diagnosis basis for this disease, the diagnosis is still mainly excluded, and the following diseases should be identified.
What is the Differential diagnosis for Dilated Cardiomyopathy?
I. Coronary heart disease: When there is chest pain, chest tightness, arrhythmia, ST-T changes of ECG and Q wave, it is difficult to distinguish between the two. Especially for patients over 40 years old, it is very easy to be mistaken for coronary heart disease. The following conditions are helpful for identification:
1. Age: Coronary heart disease occurs more than 40 years old, and cardiomyopathy occurs in middle-aged people.
2. History: Coronary heart disease often has a history of angina pectoris or myocardial infarction, while cardiomyopathy often has a history of heart failure, palpitation, shortness of breath, and lower limb edema. The chest may have tingling or chest tightness, and about 10% have typical angina.
3. Heart enlargement: Coronary heart disease causes heart enlargement after repeated heart failure. The heart enlargement is the main manifestation in cardiomyopathy, and the heart enlarges and the pulse is weak.
4. Echocardiography: In coronary heart disease, the enlargement of the heart is not obvious, and the heart shows a limited pulsation weakening, while the cardiomyopathy heart significantly expands, and the amplitude of the ventricular wall pulsation is generally weakened.
5. Coronary heart disease susceptible factors, such as hypertension, hyperlipidemia, hyperglycemia, and cardiomyopathy are rare.
6. Isotope examination: Isotope myocardial perfusion imaging, cardiomyopathy mostly bilateral ventricular enlargement, while coronary disease is mainly left ventricular enlargement, right ventricular enlargement is less.
7. Coronary angiography: It is the most reliable condition to distinguish the two. In dilated cardiomyopathy, there is no> 50% stenosis of the coronary arteries.
II. Blood pressure may be normal, low or elevated during hypertensive heart disease and cardiomyopathy
i. In cardiomyopathy heart failure, due to water and sodium retention, blood volume increases, tissue hypoxia, arterial spasm, and increased catecholamine secretion can cause temporary blood pressure Sexual increase, mainly diastolic blood pressure, after the correction of heart failure, blood pressure fell to normal within a few days. But cardiomyopathy can also coexist with high heart disease.
The identification of cardiomyopathy with hypertension and hypertension is mainly based on the course of hypertension. In addition to aggressive hypertension, the development of hypertension to hypertension with heart disease and heart failure often takes several years.
ii. Severity of high blood pressure. When high blood pressure causes high heart disease and heart failure, there is often a severe increase in blood pressure.
iii. Left ventricular hypertrophy and dilated aorta during high heart disease.
iv. In hypertension, there are often changes in the fundus and kidneys of hypertension.
III. Rheumatic heart disease and cardiomyopathy Due to the expansion of the left ventricle, relative mitral regurgitation occurs, and systolic murmurs can occur, and a few have diastolic murmurs. X-ray examination often enlarges the left atrium, left ventricle and right ventricle, and is often misdiagnosed as rheumatic mitral valve disease. Identification points:
i. In cardiomyopathy, murmurs appear or increase during heart failure, and murmurs weaken or disappear after heart failure is corrected. Rheumatic mitral valve disease, murmur increases after heart failure is corrected.
ii. X-ray shows that the heart of the cardiomyopathy is generally enlarged, the pulse is generally weakened, and the degree of pulmonary congestion is mild. Rheumatic mitral valve disease, prominent pulmonary artery segment, severe pulmonary congestion.
iii. Extensive ST-T changes in ECG cardiomyopathy and pathological Q waves of left bundle branch block. Wind heart disease is rare.
iv. Echocardiography; the heart cavity is generally enlarged during cardiomyopathy, the wall pulsation is weak, the mitral valve opening is small, and the tricuspid valve changes like a city wall during heart failure. After the heart failure is corrected, the bimodal shape is restored. The cuspid wall-like changes are different.
IV. Pericardial effusion, the heart generally expands during cardiomyopathy, and the pulsation is very easy to be mistaken for pericardial effusion. It can be identified according to the following conditions:
i. The heart is enlarged, the pulsation is weakened, and the disease duration is more than six months.
ii. X-ray examination, left ventricular enlargement, suggesting cardiomyopathy.
iii. Echocardiography, the heart is significantly enlarged without liquid dark areas, supporting cardiomyopathy.
iv. ECG: left ventricular high voltage, left ventricular hypertrophy, bundle branch block, abnormal Q wave, ventricular arrhythmia, etc. suggest cardiomyopathy.
v. During the contraction time, PEP is prolonged, LVET is shortened, and the PEP / LVET ratio is increased, which supports cardiomyopathy.
V. Keshan disease is an endemic cardiomyopathy, and there is a certain endemic area. Preschool children and women of childbearing period are more common. Dilated cardiomyopathy is sporadic, mostly in middle-aged men.
What is the treatment for Dilated Cardiomyopathy?
The etiology of this disease is unknown, and there is no specific therapy. Those who have not developed heart failure should prevent infection, prevent overwork, quit smoking and alcohol to prevent heart failure. Heart failure, diuretics can be used, such as systolic blood pressure is not less than 12.7kpa (95mmHg) can be used vasodilators.
Due to myocardial degeneration, necrosis, fibrosis, and poor tolerance to digoxin, low-dose maintenance therapy should be used. Patients with arrhythmia can choose medication according to different arrhythmias.
Those with low blood pressure can intravenously inject dopamine 5ug / min. Patients with clinical symptoms that do not improve and biopsy confirmed myocarditis may try a course of immunosuppressive drugs. Short duration, fever onset, can also try hormone therapy. The myocardial β-receptor density is down-regulated in patients with this disease, and the decline is more pronounced as the degree of heart failure increases. In order to increase myocardial beta receptor density and improve myocardial responsiveness, it can be treated with beta receptor blockers.
For those with a systolic blood pressure of not less than 12.2kpa (90mmmHg), metoprolol can be used at 6.25mg, 3 times a day, and the dose can be increased once every 3-5 days. Combined use for 3-6 months can improve cardiac function, but each person’s tolerance is different. Attention should be paid to changes in blood pressure and cardiac work. In severe cases, drug treatment can not consider heart transplantation.
What is the Prognosis for Dilated Cardiomyopathy?
Once heart failure occurs, the prognosis is poor, with a 5-year mortality rate of 35% and a 10-year mortality rate of 70%.
What is Hypertrophic Cardiomyopathy?
Hypertrophic cardiomyopathy is characterized by myocardial hypertrophy. According to the obstruction of left ventricular outflow tract, it can be divided into obstructive and non-obstructive hypertrophic cardiomyopathy. Those with asymmetric ventricular septal hypertrophy and subaortic stenosis are called idiopathic hypertrophic main Subaortic stenosis (Idiopathic hypertrophic subaortic stenosis IHSS).
What is the Cause of Hypertrophic Cardiomyopathy?
Unknown, possible factors are:
1. Heredity: There may be multiple onsets in a family, suggesting that it is related to heredity. Matsumori found that the detection rate of HLADRW4 was as high as 73.3%, and that of the control group was extremely low. The HLADR system is one of the genetic genes and has a regulatory effect on the immune response, indicating that the disease is genetically related.
2. Endocrine disorders: Typhoid cell tumor patients coexist with hypertrophic cardiomyopathy, human intravenous infusion of a large amount of norepinephrine can cause myocardial necrosis. Animal experiments, intravenous infusion of catecholamines can cause myocardial hypertrophy. Therefore, some people think that hypertrophic cardiomyopathy is caused by endocrine disorders.
What is the Pathology for Hypertrophic Cardiomyopathy?
The main lesion is myocardial hypertrophy, especially the ventricular septum and papillary muscles in the lower part of the aortic valve. The ventricular cavity often shrinks into an S-shaped fissure, and the ratio of the thickness of the ventricular septum to the thickness of the left ventricular wall is greater than 1.5, which is called asymmetric ventricular septal hypertrophy. Myocardial hypertrophy is also prominent in the apex and other parts of the heart. Myocardial cells are hypertrophic and disorderly arranged, which is one of the pathological changes of the disease. When there is significant mitral regurgitation, secondary mitral leaflet thickening may occur.
What are the Clinical manifestations of Hypertrophic Cardiomyopathy?
I. Symptoms: There is a significant difference between men and women. Most of them show symptoms in their 30s and 40s. As they get older, the symptoms become more pronounced. The main symptoms are:
i. Dyspnea, exertional dyspnea, and severe side-by-side breathing or paroxysmal difficulty breathing at night is due to reduced compliance of the hypertrophic myocardium, increased left ventricular end-diastolic pressure, and increased left atrial pressure, resulting in pulmonary congestion.
Ii. Angina pectoris; typical angina pectoris, often after labor. Chest pain lasts for a long time, and nitroglycerinization is not only ineffective and exacerbated. The onset of angina pectoris may be due to insufficient blood supply to the myocardial hypertrophy of the thin coronary arteries, and increased aerobic myocardial hypertrophy.
iii. Syncope and dizziness; mostly occur during exertion, the mechanism is unknown, it may be due to the decrease of left ventricular compliance, the positive muscle effect of sympathetic nerves after fatigue is enhanced, resulting in worse left ventricular compliance and less dilated ventricular blood The left ventricular outflow tract obstruction is aggravated, and the stroke volume is reduced, resulting in insufficient cerebral blood supply. It may also be due to excessive stimulation of the left ventricular baroreceptor, which causes reflex vasodilation. Resulting in a drop in blood pressure, when tachycardia or bradycardia occurs, syncope and dizziness can also occur.
iv. Palpitation; the patient feels that the heart beats strongly, especially in the left lying position, which may be caused by arrhythmia or changes in heart function.
II. Common signs of Hypertrophic Cardiomyopathy
i. Apical systolic pulse, due to myocardial hypertrophy, increase in pulse can be seen. As left ventricular compliance decreases, atrial contraction increases, blood flow hits the left ventricular wall, and there may be pre-systolic impulses in the apex. After the first heart sound, there is a second systolic pulse, forming a double systolic pulse.
ii. Systolic fine tremor; mostly in the apex of the heart. With systolic fine tremor, the left ventricular outflow tract obstruction is more severe.
iii. Systolic murmurs: “rough hairy” systolic murmurs in the lower left margin of the sternum or inside the apex are due to obstruction of the left ventricular outflow tract. All factors that increase myocardial contractility or decrease arterial resistance can increase the pressure difference between the left ventricle and the aorta, and increase murmurs.
Any factor that can reduce myocardial contraction or increase arterial resistance can reduce the pressure step. Small and noisy.
When the amount of return blood increases, the murmur decreases. Rejuvenating blood volume reduces murmur enhancement.
iv. Apical systolic murmur: about 50% of the disease is accompanied by mitral regurgitation, so the apex has systolic middle and late murmurs, or total systolic murmurs.
v. The third heart sound and the fourth heart sound.
Laboratory and other inspections for Hypertrophic Cardiomyopathy
(1) X-ray examination: The heart size is normal or increased. The heart size is proportional to the pressure step between the heart and the left ventricular outflow tract. The larger the pressure step, the larger the heart. Cardiac left ventricular hypertrophy is predominant. The aorta is not widened. The pulmonary artery segment is mostly not prominent. The pulmonary congestion is mostly mild and mitral valve calcification is common.
(2) ECG Due to cardiac ischemia and abnormal myocardial repolarization, ST-T changes are common. Left ventricular hypertrophy and left bundle branch block are also common.
Q waves may appear due to ventricular septal hypertrophy and myocardial fibrosis. The disease often has various types of arrhythmias.
(3) Echocardiography is an important non-invasive diagnostic method.
i. The main manifestations are abnormal thickening of the ventricular septum, and the thickness of the ventricular septum at the end of diastole is greater than 15mm.
ii. The amplitude of ventricular septal motion is significantly reduced, generally ≤5mm.
iii. The ratio of interventricular septal thickness / left ventricular posterior wall thickness can reach 1.5-2.5: 1, and it is generally considered that the ratio> 1.5: 1 has diagnostic significance.
iv. The inner diameter of the left ventricle is smaller than that of a normal person.
v. The distance between the ventricular septum and the anterior leaflet of the mitral valve is often significantly reduced at the time of systole.
vi. Mitral valve systolic forward motion, close to the ventricular septum, and terminate before the second heart sound. The closing of the aorta in the middle stage of contraction may be due to the rapid blood flow velocity in the early contraction period and the sudden decrease in blood flow velocity due to the increase in obstruction in the later period of contraction, resulting in the attraction effect.
The above items should be comprehensively analyzed before they can draw the correct conclusions. Attention should be paid to hypertension and hypothyroidism, which can cause similar performance.
(4) Cardiac catheterization and cardiovascular angiography: Cardiac catheterization showed a pressure step between the left ventricle and the left ventricular outflow tract. The left ventricular end-diastolic pressure increased.
The pressure step was positively correlated with the left ventricular outflow tract obstruction.
n cardiovascular angiography, when the ventricular septal muscle hypertrophy is obvious, it can be seen that the ventricular cavity has a narrow slit-like change, which is meaningful for diagnosis.
What is the diagnosis for Hypertrophic Cardiomyopathy?
Youth middle-aged with labor angina, nitroglycerin cannot be relieved, and those with a family history of sudden death should think of the possibility of this disease.
Combining physical signs, electrocardiogram, X-ray and two-dimensional echocardiography can often provide a basis for diagnosis.
Cardiac catheterization has a pressure step between the left ventricle and the left ventricular outflow tract. Cardiovascular angiography is a reliable condition for the diagnosis of this disease. It shows that the papillary muscles and the ventricular septum are characteristically hypertrophic, usually a triangular ventricular cavity with a narrow fissure like change.
The ventricular space at the end of ventricular contraction usually shows complete or almost complete disappearance, and angiography can also confirm mitral regurgitation.
What is the Differential diagnosis for Hypertrophic Cardiomyopathy?
This disease should be distinguished from the following:
I. Coronary atherosclerotic heart disease, hypertrophic cardiomyopathy and coronary heart disease have angina pectoris. The electrocardiogram ST-T changes, and abnormal Q affects left ventricular hypertrophy. Therefore, the two diseases are more likely to be misdiagnosed.
i. Murmur: Hypertrophic obstructive cardiomyopathy can be heard in the lower left margin of the sternum or the inside of the apex, jet systolic murmur. Freak’s movements increase the noise, and raising the legs raises the noise. May be accompanied by fine contractions. There may also be systolic murmurs in coronary heart disease with ventricular septal perforation or with papillary muscle insufficiency. But it is reflux noise.
ii. Angina pectoris of coronary heart disease, remission within 3 to 5 minutes. Hypertrophic cardiomyopathy angina pectoris, nitroglycerin is ineffective, or even exacerbated.
iii. Echocardiography, hypertrophic cardiomyopathy, ventricular septal thickness> 15mm, left ventricular posterior wall ratio> 1.5: 1. Coronary heart disease is mainly manifested by abnormal wall motion.
iv. Cardiac catheter examination and coronary angiography can confirm the diagnosis.
II. Aortic valve stenosis: The systolic murmur of aortic valve stenosis is mostly in the second intercostal space of the right margin of the sternum, and the murmur is transmitted to the neck, mostly accompanied by systolic fine tremor, and the second aortic heart sound weakens. X-ray examination of the ascending aorta with stenosis and expansion is not difficult to distinguish.
III. Ventricular septal defect murmur is also in the lower left margin of the sternum, but for reflux murmur, echocardiography and cardiac catheterization can be clearly identified.
What is the Treatment of Hypertrophic Cardiomyopathy?
Hypertrophic cardiomyopathy develops slowly and has a good prognosis, but due to arrhythmia, it can cause sudden death. Care should be taken to avoid overwork and prevent excessive mental stress. Beta blockers and propranolol can reduce myocardial contractility and relieve left Ventricular outflow obstruction improves left ventricular wall compliance and left ventricular filling, and also has an antiarrhythmic effect.
Dosage: 10mg, orally, 3 times a day. It can be gradually increased up to 480mg / day. Can also be used calcium channel blockers, verapamil 40mg orally 3 times a day, nifedipine 10mg, orally, 3 times a day. Can improve ventricular diastolic function, should pay attention to observe blood pressure to prevent blood drops too low.
Surgical treatment: If the pressure step is greater than 60mmHg, those who fail to respond to medication can be treated surgically. Feasible hypertrophic muscle resection. Patients with severe mitral valve insufficiency may perform mitral valve replacement.
What is Restrictive Cardiomyopathy?
The disease includes endomyocardial fibrosis, which mostly occurs in the tropics, and Löffler’s Cardiomyopathy, which mostly occurs in the temperate zone. This disease is very rare in Asia and Africa.
What is the Cause of Restrictive Cardiomyopathy?
The cause is unknown. Some people think that it is an autoimmune disease caused by increased eosinophils and degeneration.
What is the Pathology and Pathophysiology of Restrictive Cardiomyopathy?
The main lesions are endocardial and subendocardial myocardial thickening with fibrous hyperplasia, and endocardial thickening can reach 10 times normal.
The papillary muscles can also be atrophied, shortened, the ventricular cavity shrinks, and the atrium enlarged. Thrombosis in the heart cavity.
Fibrotic lesions often involve the ventricular inflow tract and atrioventricular insufficiency occurs. Thickened and fibrotic endocardium and subendocardial myocardium have reduced compliance and impaired diastolic and systolic functions.
Due to limited ventricular diastole during diastole, atrial blood storage increased, atrial enlargement and hemodynamic changes similar to constrictive pericarditis.
What are the Clinical Manifestations of Restrictive Cardiomyopathy?
It is common in young adults and there is no obvious gender difference. Lesions can be confined to the left ventricle, right ventricle, or both ventricles. Due to the different lesions, there are different clinical manifestations.
1. Symptoms and signs caused by right ventricular disease: slow onset, abdominal distension and ascites.
Abdominal pain due to liver congestion or hepatomegaly or ascites caused by abdominal wall extension. Labor dyspnea and paroxysmal nocturnal dyspnea can be alleviated by ascites, indicating that dyspnea is mainly caused by ascites.
Discomfort in the anterior region of the heart, feeling weak due to decreased blood output, decreased labor force, and mild cough and expectoration in half.
Main signs: weakened apical pulsation and mild or moderate enlargement of the heart. The first heart sound weakened. Hairy systolic murmur on the left lower edge of the sternum. The third heart sound can be heard.
Lower extremity edema is not commensurate with ascites, the amount of ascites is large and the lower extremity is less edema.
After using diuretics, lower limb edema is reduced or disappeared, and ascites often persists, and jugular vein irritation is obvious.
2. The symptoms and signs caused by left ventricular lesions: palpitation, shortness of breath. Apical whistle-like systolic murmurs. A few apical parts have fine systolic tremors. When pulmonary vascular resistance increases, manifestations of pulmonary hypertension occur.
3. The symptoms and signs caused by bilateral ventricular lesions are manifested as syndromes of myocardial fibrosis in the right ventricle and left ventricle, but mainly show signs and symptoms of right ventricular lesions. A few patients show prominent arrhythmia, mostly atrial sexual arrhythmia can lead to extreme enlargement of the right atrium, even collapse, death, and some patients with chronic recurrent massive pericardial effusion as the main manifestation, often mistaken for simple pericardial disease.
What are the Laboratory and other inspections of Restrictive Cardiomyopathy?
(A) X-ray examination: The heart enlarges, and the right or left atrium enlarges significantly. When accompanied by pericardial effusion, the heart shadow increases significantly, and endocardial calcification can be seen.
(B) ECG: Due to the increased heart load, mitral valve type P waves, atrial fibrillation, atrioventricular block and bundle branch block can be seen.
(C) Cardiac catheter examination: Right ventricular endocardial myocardial fibrosis, due to reduced right ventricular compliance, right ventricular end-diastolic pressure increases, showing early diastolic depression, and diastolic plateau waves. Right atrial and vena cava pressures increased, left ventricle endocardium fibrosis, pulmonary circulation pressure increased, ventricular angiography showed that the ventricular cavity was reduced, and blood flow was slow.
What are the Diagnosis and Differential Diagnosis for Restrictive Cardiomyopathy?
The main manifestations of this disease are increased venous pressure, jugular vein irritation, hepatomegaly, ascites, and lower extremity edema. The heart is enlarged and pulsating, and signs of atrioventricular valve insufficiency are common. It should be distinguished from liver cirrhosis, constrictive pericarditis, and endocardial elastic fibrous hyperplasia.
What is the Treatment for Restrictive Cardiomyopathy?
1. To avoid fatigue and prevent infection, those with heart failure can use heart-strengthening, diuretics, and vasodilators, but the efficacy is poor and the prognosis is poor.
2. Surgical treatment: Endocardial dissection plus valve replacement is effective.
What is Myocarditis?
Myocarditis is often an inflammatory manifestation of systemic diseases on the myocardium. Due to the size and extent of myocardial disease, patients with mild disease may have no clinical symptoms, and severe death may cause sudden death. Those diagnosed promptly and properly treated can be completely cured and prolonged Those who do not heal can form chronic myocarditis or cause cardiomyopathy.
What is the Cause of Myocarditis?
Bacterial diphtheria, hemolytic streptococcus, pneumococcus, typhoid. Viruses such as coxsackie virus, acovirus, hepatitis virus, epidemic hemorrhagic fever virus, influenza virus, adenovirus, etc. Others such as fungi and protozoa can cause myocarditis. But viral myocarditis is more common.
What is the Pathogenesis for Myocarditis?
Take the virus as an example. When the virus is infected, the virus passes from the blood through the capillaries and the periplasm of the blood vessels into the myocardial fibers through blood circulation. It reproduces and replicates in the inner membrane of myocardial cells, causing cardiomyocyte lysis, necrosis, edema, and monocytes. Inflammatory reactions such as infiltration. The late stage of the disease may be due to humoral and cellular immunity induced by the virus or myocardial antigen.
i. Excessive exercise and exercise can cause the virus to multiply and reproduce in the myocardium, aggravating myocardial inflammation and necrosis.
ii. Bacterial infection, when mixed infection of bacteria and virus, may play a cooperative pathogenic role.
iii. Pregnancy: Pregnancy can enhance the reproduction of the virus in the heart muscle. The so-called perinatal cardiomyopathy may be caused by a viral infection.
iv. Other malnutrition, high fever and cold, hypoxia, excessive drinking, etc. can all induce viral myocarditis.
What is the Pathology for Myocarditis?
The severity varies, which can be limited or diffuse. The light can not see the lesion under the naked eye and light microscope, but the virus can be isolated. In severe cases, myocardial paleness lacks elasticity and myocardial dilatation.
There are inflammatory reactions such as monocyte infiltration in the myocardial stroma and around the blood vessels.
The lighter can heal without scarring. Severe cardiomyocytes edema, lysis, and necrosis and the lesions can be limited to the myocardium.
It can also invade the pericardium and present inflammation and exudation, or spread to the endocardium and present pancarditis.
Invasion of the sinoatrial node, atrioventricular node and other conductive systems can cause a variety of arrhythmias. But this this can also spread to the coronary arteries and cause myocardial ischemic damage.
Chronic myocarditis, enlargement of the heart, myocardial interstitial inflammation and myocardial fibrosis can form cardiomyopathy.
What are the Clinical Manifestations of Myocarditis?
Young adults are more likely to develop symptoms of primary infection, such as fever, sore throat, cough, vomiting, diarrhea, and muscle soreness. Most of the symptoms of myocarditis occur 1 to 3 weeks after the virus infection. Due to the arrhythmia, the heart palpitations can feel weak due to the decreased blood output.
When the pericardium and pleura are involved, chest tightness, chest pain, and angina pectoris may also appear. Severe cardiac insufficiency.
A common sign is that sinus tachycardia is not parallel to body temperature. There may also be sinus bradycardia and various arrhythmias. One-third to one-half of the enlarged heart is found in severe myocarditis.
Due to the enlargement of the heart, mitral or tricuspid regurgitation may occur, and the apex or sternum left lower margin systolic murmur.
Patients with severe myocardial damage or heart failure can hear the diastolic galloping rhythm, the first heart sound weakens, and those with pericarditis can hear the pericardial friction sound.
Mild cases can be completely asymptomatic, severe cases of heart failure or sudden death. Disparate performance. According to the clinical manifestations, it can be divided into six types:
i. Asymptomatic infection: S-T changes appear on the electrocardiogram 1 to 4 weeks after the infection, asymptomatic.
ii. Arrhythmia type Shows various types of arrhythmia, pre-ventricular contractions are most common.
iii. Heart failure type, the symptoms and signs of heart failure appear.
iv. The clinical manifestation of myocardial necrosis type is similar to myocardial infarction.
v. Heart enlargement Heart enlargement, mitral and tricuspid systolic murmurs.
vi. Sudden death type No warning, sudden death.
What are the Laboratory and other inspections for Myocarditis?
1. ECG: The positive rate of ECG abnormalities is high, and it is an important basis for diagnosis. After the onset of ECG, the ECG can suddenly change from normal to abnormal, and disappear as the infection subsides.
The main manifestations are the downward shift of the ST segment, and the T wave being flat or inverted.
Sinus node, atrioventricular node, ventricular block. Ectopic rhythms are most commonly seen in pre-ventricular contractions.
Pre-ventricular contractions can be the only manifestation of myocarditis, supraventricular or ventricular tachycardia, atrial fibrillation, etc., and other low voltage, Q-T Intervals extended, Q waves, etc.
2. X-ray examination Due to the different scope and severity of lesions, there are also large differences in radiographic examinations. Approximately one-third to one-half of the heart is enlarged, and most of them are mildly to moderately enlarged. Those who are significantly enlarged are often accompanied by pericardial effusion. The heart shadow is spherical or flask-shaped, the heart beat is weakened, and those with limited myocarditis or mild lesions can have a completely normal heart.
3. Blood test White blood cell count in viral myocarditis can be normal, high or decreased, most of the erythrocyte sedimentation rate can also be slightly faster, C-reactive protein is mostly normal, GOT, GPT, LDH, CPK is normal or elevated, chronic myocarditis is mostly in normal range.
4. Those who have the conditions can do virus isolation or antibody detection.
What is the Diagnosis for Myocarditis?
i. The main indicators of clinical diagnosis are acute and chronic cardiac insufficiency or cardio-cerebral syndrome.
ii. Running horse rhythm or pericardial friction sound.
iii. The heart is enlarged.
iv. The electrocardiogram has severe arrhythmia or obvious ST-T changes, or a positive exercise test.
Secondary indicators include:
i. History of viral infections such as upper respiratory tract infection and diarrhea at the same time or before 1-3 weeks.
ii. There are at least two symptoms of obvious weakness, paleness, shortness of breath, sweating, palpitations, chest tightness, pain in the front of the heart, dizziness, cold hands and feet, and muscle aches.
iii. The first heart sound of the apex is significantly reduced, or tachycardia is present when quiet.
iv. The ECG has ST-T changes.
v. The serum creatine kinase, aspartate aminotransferase, and lactate dechlorinase can be increased early in the course of the disease, and the anti-cardiac antibody is positive during the course of the disease. Those who have the conditions can isolate the virus and diagnose the pathogen.
What is the Treatment for Myocarditis?
You should rest in bed to reduce tissue damage and accelerate the recovery of lesions. With arrhythmia, rest in bed for 2-4 weeks, and then gradually increase the amount of activity.
Those with severe myocarditis and enlarged heart should rest for 6 months to one year until the clinical symptoms completely disappear and the heart size returns to normal.
Traditional Chinese medicine: clearing heat and detoxifying traditional Chinese medicines, some of which have antiviral effects, such as Daqingye, Banlangen, Polygonum cuspidatum, Caohejong, Forsythia, etc.
Chinese medicines for activating blood circulation and removing stasis can improve myocardial ischemia and myocardial metabolism.
Drugs to improve myocardial nutrition and metabolism, such as coenzyme A, adenosine triphosphate, cyclic adenosine and so on. All have been used for treatment, but the effect is still uncertain.
Experiments have shown that the traditional Chinese medicine Astragalus has a positive inotropic effect, can regulate immune function, and can be used to treat the disease.
Immunosuppressive agents: The use of hormones is still controversial, but severe myocarditis with atrioventricular block and cardiogenic shock and heart failure can be used with hormones.
Prednisone is commonly used, 40-60mg / day, and gradually reduced after the condition improves, a course of 6 weeks.
If necessary, hydrocortisone or dexamethasone can also be administered intravenously. Heart failure can be used to strengthen the heart, diuretic, vasodilators. Arrhythmias are treated as normal arrhythmias.
What is Keshan Disease?
Keshan disease, also known as endemic cardiomyopathy, was discovered in Keshan County, Heilongjiang Province, China in 1935, hence the name Keshan disease.
What is the Cause of Keshan Disease?
Unknown, the cause of the study is divided into two categories of biogeochemical and biological causes.
The biogeochemical etiology said that the lack of or loss of balance of trace elements selenium, molybdenum, magnesium or related nutrients in the soil and water in the ward resulted in metabolic disorders and myocardial damage. The biological etiology theory believes that it is caused by a viral infection or due to the combined effect of the two causes.
What is the Pathology for Keshan disease?
The main lesions are myocardial parenchymal degeneration, necrosis and fibrosis are intertwined, the heart is dilated, the ventricular wall is not thickened, mural thrombus is common, and myocardial degeneration and necrosis can be seen under light microscope. Electron microscopy showed swelling of the mitochondria, detachment and rupture of the palate.
What are the Clinical manifestations of Keshan disease?
Can be divided into four types:
- Urgent or Acute
Acute type: often onset in winter, often caused by cold, overeating, overeating, etc. Nausea, vomiting, dizziness, and severe cases died within hours. Cardiac active shock, various severe arrhythmias. The heart is enlarged and the diastolic horse runs. Those with signs of edema, hepatomegaly, etc. that have not subsided for more than three months after the onset of acute type have changed from acute type to slow type.
Subacute type is a type of pediatric Keshan disease, which has more incidence in spring and summer, loss of energy, decrease in appetite, dull complexion, edema of the whole body, enlarged heart to both sides, galloping in diastole, enlarged liver, three months without remission, has turned to slow type.
The slow type is congestive heart failure. The heart expands to both sides. There are apical systolic murmurs, liver enlargement and lower extremity edema. This is very similar to dilated cardiomyopathy.
The underlying type is after various types of treatment or early in Keshan disease change.
What are the Laboratory and other inspections for Keshan Disease?
1. Acute serum GOT, CPK, LDH activity was enhanced. The total number of white blood cells increases, and the erythrocyte sedimentation speeds up. GPT increases in the chronic type due to hepatic congestion.
2. ECG examination Almost all of this disease have ECG changes, mainly showing ST-T changes, low voltage, Q-T interval prolonged. Various types of arrhythmias, especially complete right bundle branch block are more common.
3. X-ray examination: The heart is generally enlarged, the pulse is weakened, and the congestion is light.
4. Echocardiography: The double ventricles are enlarged, the amplitude of the wall pulsations is generally weakened, and the wall is not significantly thickened. These changes are similar to dilated cardiomyopathy.
What is the Diagnosis for Keshan Disease?
Keshan disease has epidemiological characteristics, that is, the characteristics of the region, season and population, heart enlargement, arrhythmia, heart failure, galloping rhythm and heart function-related murmurs, and it is not difficult to diagnose in Keshan disease endemic area. It can be distinguished from dilated cardiomyopathy according to epidemiological characteristics.
What is the Treatment for Keshan Disease?
i. The emergency type can be given a large amount of vitamin C5-10g intravenously, which can be repeated once every two hours, and those with lower blood pressure can also be given intravenous dopamine.
ii. Slow type is treated according to general heart failure.
What is the Prevention for Keshan Disease?
Oral sodium selenite can prevent acute Keshan disease.
- Dosage is 1mg for 1-5 years old
- 2mg for 6-10 years old
- 3mg for 11-15 years old
- 4mg for 16 years old and above, taken orally every 10 days
This is often taken in multiple seasons, can be stopped for 3 months in non-onset season, and nutrition should be improved at the same time Improve physical fitness and prevent illness.