Viral myocarditis (VM) is a disease caused by a variety of viruses with focal or diffuse myocardial cell degeneration and necrosis, interstitial inflammatory cell infiltration, fibrous exudate and other pathological changes that lead to myocardial damage, cardiac dysfunction and/or arrhythmias. The disease often causes inflammatory changes in the pericardium, endocardium, and other organs, so pericarditis and endocarditis can exist at the same time. The name “viral myocarditis” does not exist in Chinese medicine. From its pathogenetic characteristics and clinical manifestations, it seems to be included in the classical medical records of “heart disease”, “typhoid fever”, “warm disease”, “chest paralysis” and “palpitation”. “, “palpitations”, “palpitations”, “palpitation”, “deficiency labor”, “sudden death”, “heart water”, and “heart disease”. “heart water”, “sweating” and many other diseases. The basic etiology of this disease is the invasion of the heart body by external evil and toxins, causing the heart’s Qi, blood, yin and yang to be biased, and the resulting blood stasis and phlegm to be used for each other, which is always a deficiency of the root and the symptoms.
Viral myocarditis is a common disease in pediatrics. According to the survey on the incidence of pediatric myocarditis in nine provinces and cities in China, the incidence is 18.27/100,000 and the prevalence is 21.83/100,000; the gender is slightly more in boys, accounting for 54.4%; the age distribution is 17.2% for those less than 2 years old, 18.0% for those between 2 and 4 years old, and 64.8% for those between 4 and 14 years old; the disease can develop in spring, summer, autumn and winter, and the peak season is closely related to the epidemiological pattern of the causative virus. The peak season is closely related to the epidemiological pattern of the causative virus, generally in July, August and January to March. The clinical manifestations of the disease vary in severity. In mild cases, the disease may be detected by chance during physical examination without obvious conscious symptoms, or may have mild symptoms such as fatigue, excessive sweating, palpitations, dizziness, chest tightness, shortness of breath or wheezing, etc. The first heart sound in the apical region is low on auscultation, and premature beats and ST-T changes can be seen on electrocardiography. In more severe cases, the onset of the disease may be rapid, with significant weakness, palpitations, shortness of breath, precordial discomfort or pain, nausea, vomiting, abdominal pain, etc. On examination, the heart may be slightly enlarged, arrhythmia, gallop rhythm, and other signs of cardiac insufficiency. In extremely severe cases, heart failure and cardiogenic shock may occur within a few hours to 1 to 2 days after the onset of the disease, and death may occur if the patient is not rescued in time. If the disease is prolonged and develops into chronic myocarditis, there are recurrent episodes of heart failure or severe rhythm disturbances, the heart is progressively enlarged and can develop into dilated cardiomyopathy, which eventually leads to death without treatment. In view of the fact that there is no specific treatment for viral myocarditis, Chinese medicine therapy is still the most common treatment method used by Chinese and Western medicine in China.
Diagnosis of the disease]
I. Diagnostic criteria
(a) Western medical diagnostic criteria
Diagnostic criteria for pediatric viral myocarditis, revised by the National Pediatric Myocarditis and Cardiomyopathy Academic Conference held in Kunming in 1999 by the Cardiovascular Group of the Pediatric Branch of the Chinese Medical Association.
1. Clinical diagnostic basis
(1) Cardiac insufficiency, cardiogenic shock or cardio-cerebral syndrome.
(2) Heart enlargement (X-ray, echocardiography has one of the manifestations).
(3) Electrocardiographic changes: ST-T changes in 2 or more major leads (I, II, avF, V5) dominated by R waves for more than 4 days with dynamic changes, sinus atrioventricular block, atrioventricular block, complete right or left bundle branch block, paired or parallel premature beats, ectopic tachycardia due to non-atrial node and atrioventricular folding, low voltage (except in neonates ) and abnormal Q waves.
(4) Elevated CK-MB or positive cardiac troponin (cTnI or cTnT).
2. pathogenic diagnosis basis
(1) Confirmation index: From the endocardial, myocardial and pericardial (biopsy, pathology) or pericardial puncture fluid examination of the affected child, the diagnosis of myocarditis caused by virus can be confirmed if one of the following is found
①Virus was isolated.
② Viral nucleic acid was detected with a viral nucleic acid probe.
(③) Positive specific viral antibodies.
(2) Reference basis: Myocarditis can be considered to be caused by a virus in the myocarditis series if one of the following is present in combination with clinical manifestations.
①Virus isolated from the child’s stool, pharyngeal test or blood, and the recovery period serum is the same antibody titer than a serum increased or decreased by more than 4 times.
②The child’s blood was positive for specific IgM antibodies early in the course of the disease.
(3) Viral nucleic acid was detected in the blood of the child with a viral nucleic acid probe.
3. basis for confirming the diagnosis
(1) The clinical diagnosis of myocarditis can be made if two clinical diagnostic bases are present. The diagnosis is supported by evidence of viral infection at the same time or 1 to 3 weeks before the onset of the disease.
(2)Those who have both one of the pathogenic confirmatory bases can be diagnosed as viral myocarditis, and those who have one of the pathogenic reference bases can be clinically diagnosed as viral myocarditis.
(3) Where no confirmatory basis is available, the necessary treatment or follow-up should be given to confirm or exclude myocarditis according to changes in the condition.
(4) Rheumatic myocarditis, toxic myocarditis, congenital heart disease, connective tissue disease and myocardial damage of metabolic diseases, hyperthyroidism, primary cardiomyopathy, primary endocardial elastosis, congenital atrioventricular block, cardiac autonomic abnormalities, beta-receptor hyperfunction and drug-induced electrocardiographic changes should be excluded.
4. Staging
(1) Acute stage: new onset, with obvious and variable symptoms and positive findings on examination, generally within six months of disease duration.
(2) Extended period: recurrent clinical symptoms, objective examination indexes are persistent, and the duration of disease is more than six months.
(3) Chronic phase: Progressive heart enlargement, recurrent heart failure or arrhythmia, sometimes mild and sometimes severe, and the duration of the disease is more than one year.
(B) Diagnosis of symptoms
1. Central symptoms
Viral myocarditis is characterized by cardiac manifestations as the central symptom. The clinical symptoms include fatigue, chest tightness, breathlessness, palpitations, shortness of breath, precordial discomfort or pain, dizziness, pale face, sweating, enlarged heart, and pulse generation.
2. Diagnosis of symptoms
(1) Evidence of deficiency
(1) Qi-Yin deficiency evidence Obvious weakness, dizziness and sweating, palpitation, dry mouth, pale or red tongue, little coating, thin and weak pulse.
(2) Qi-yang deficiency, pale face, cold limbs, palpitations, shortness of breath, weakness and spontaneous sweating, pale tongue, thin white fur, sluggish and feeble pulse or knotted generation.
(③) Heart yang deficiency evidence Sudden onset of pale or grayish face, restlessness, chest tightness and shortness of breath, blue lips, cold extremities, enlarged heart, mass under the right hypochondrium, swelling of the lower extremities, little urination, blue tongue or petechiae, and weak pulse.
The onset of the disease is rapid and violent, with sudden onset of pale or blue-gray face, cold extremities, profuse sweating, restlessness, or even coma, shortness of breath, little or no urination, blue lips and nails, skin blossoming, blood pressure dropping, and a weak pulse that wants to die.
⑤ Qi and blood deficiency, pale or yellowish face, palpitations and palpitations, weakness, dizziness, sweating and shortness of breath, pale tongue, thin coating, thin or knotted pulse, generation.
(6) Evidence of loss of both yin and yang pale face or zygomatic red, fatigue, palpitations and palpitations, spontaneous sweating and night sweating, chest tightness and shortness of breath, cardiothoracic pain, dizziness and tinnitus, waist and knees i soft, disturbed and dreamy, enlarged heart, progressive aggravation, even swollen face and limbs, shortness of breath when moving, cough when lying down, lump under the right side, pale, red or dark purple tongue, thin and dry moss or little moss, fat and tender tongue, sunken and weak pulse or weak and fast pulse or sluggish and knotty pulse.
(2) Standard evidence
(1) Heat toxicity evidence Low fever that does not subside, or repeated fever, red and swollen throat, cough, myalgia, skin rash, red tongue, thin moss, floating or slippery pulse.
②Dampness and toxicity evidence Fever rising and falling, sweating without relief, generalized pain, red and swollen throat, nausea and vomiting, abdominal pain, diarrhea, dullness, tiredness and fatigue, chest tightness and abdominal distension, red tongue with greasy coating, moist pulse or slow pulse.
Blood stasis, dark face, blue lips, tingling in the heart, palpitations and palpitations, weakness and night sweating, tightness in the chest, enlarged heart, vague green tongue or petechiae, thin coating, astringent or thin pulse or knotted promotion.
④ phlegm-dampness evidence chest tightness and breath-holding or long outgassing, palpitation and shortness of breath, dizziness, little food and dullness, chest pain, fat tongue, white and greasy coating, moist and smooth pulse or knotted generation.
Differential diagnosis
1. congenital heart disease including atrial septal defect, ventricular septal defect, patent ductus arteriosus, pulmonary orifice stenosis, aortic orifice stenosis, tetralogy of Fallot, large vessel misalignment, Eisenmenger syndrome, and tricuspid valve inferior displacement malformation. Clinically, some non-cyanotic and murmur-less congenital heart diseases are sometimes easily misdiagnosed as viral myocarditis, such as atrial septal defect and mild pulmonary orifice stenosis, which are often misdiagnosed due to the combination of incomplete right bundle branch block and degree I atrioventricular block. It is usually not difficult to differentiate from myocarditis using echocardiography, especially Doppler techniques.
Congenital cardiac conduction system abnormalities include congenital atrioventricular block, congenital pathological sinus node syndrome, congenital prolonged Q-T interval syndrome, and pre-excitation syndrome, whose electrocardiographic and clinical features are similar to those of viral myocarditis. In congenital atrioventricular block of degree II, a systolic murmur and mild enlargement of the heart may occur due to a decrease in the number of contractions and compensatory strengthening of the heart; preexcitation syndrome is prone to paroxysmal supraventricular tachycardia, etc., which is easily misdiagnosed as viral myocarditis in clinical practice. It is usually distinguished by in-depth examination, combined with medical history and family history.
Primary cardiomyopathy is a disease of unknown cause, with lesions mainly located in the myocardium, and the main clinical manifestations are slow progression, cardiac enlargement, arrhythmia and cardiac insufficiency. According to the pathophysiological changes, there are three types of cardiomyopathies: dilated, hypertrophic and restrictive (constricted), and the first two types are the most common. Clinically, this disease should be considered if the heart is enlarged and the X-ray shows spherical enlargement of the heart shadow without other causes; or congestive heart failure without other heart diseases; or the heart enlarges during fainting attack and the arterial embolism of body circulation and pulmonary circulation occurs without other causes. Echocardiography and endomyocardial biopsy can help in the diagnosis of this disease. The differential diagnosis between chronic viral myocarditis and primary cardiomyopathy is difficult, and the fact that some patients with viral myocarditis can develop cardiomyopathy has been confirmed by many studies. A history of acute myocarditis can provide clues to the diagnosis of chronic viral myocarditis. Patients with hypertrophic cardiomyopathy may have a family history.
4. rheumatic myocarditis, especially certain simple rheumatic myocarditis, has extremely striking similarities to viral myocarditis. Both types of myocarditis can present with fever, palpitations, dizziness, sweating, sore throat, arthralgia, heart murmurs, and arrhythmias. Viral myocarditis can also present with elevated AS0 titers and increased sedimentation, making it very easy to misdiagnose as rheumatic myocarditis. Some scholars believe that the Jones criteria for the diagnosis of rheumatic fever, revised by the American College of Cardiology in 1965, actually include certain viral myocarditis and some heart diseases with unknown original trapping. Most scholars now believe that cardiomyopathies without rheumatoid polyarthritis or chorea are often viral or of unknown origin. Clinically, the differentiation of the two types of myocarditis must be combined with medical history, epidemiology, physical examination, electrocardiogram, X-ray and other comprehensive analysis, and viral pathogenic testing can be performed for differentiation if available.
5. post-streptococcal syndrome Most often occurs in adolescents, the diagnosis of “tonsil-heart syndrome” was first proposed while differentiating rheumatic fever and rheumatic myocarditis, which was later changed to post-streptococcal syndrome after discussion. This disease is due to repeated streptococcal infections that cause the tonsils and pharyngeal isthmus to exist as chronic lesions, which constantly release streptococcal toxins and trigger a series of post-infection symptoms, such as arthralgia, palpitations, shortness of breath, etc. ST-T changes are less severe than in viral myocarditis, and there are no serious consequences, and the symptoms are sometimes mild and severe.
6. non-viral myocarditis includes myocarditis caused by bacteria, fungi, rickettsia, spirochetes, mycoplasma, toxoplasma, etc., as well as myocarditis caused by toxins from various pathogens, the so-called toxic myocarditis. These pathogens cause disease, in addition to myocarditis, are almost always seen to have their own specific clinical manifestations such as lobar pneumonia, mycoplasma pneumonia, diphtheria, typhoid fever, etc., which are generally easy to identify.
7. connective tissue diseases The clinical manifestations of connective tissue diseases are extremely broad and can overlap with each other, all affecting joints, blood vessels, skin, mucous membranes, etc. Myocardial damage is only one manifestation of systemic diseases. Rheumatoid arthritis is a systemic connective tissue disease, and it has been reported that subcutaneous nodules may also appear in the pericardium, myocardium, and heart valves. SLE is more likely to invade the heart and cause lupus myocarditis, which can sometimes be misdiagnosed as viral myocarditis. These connective tissue diseases are all caused by autoimmune reactions and are often multisystemic, and are not difficult to distinguish clinically from viral myocarditis.
Metabolic diseases such as vitamin B1 deficiency (foot disease), diabetes mellitus, and type II glycogenosis can cause myocardial damage, but these diseases have their own specific history and clinical manifestations, and the diagnosis is not difficult to confirm through laboratory tests and response to treatment.
8. Hyperthyroidism is an endocrine disorder in which excessive production and release of thyroid hormones T4 and/or T3 cause an increase in metabolism, with enlargement of the thyroid gland, increased neuroexcitability, wasting and proptosis as the main clinical manifestations. Patients with this disease often present with palpitations, excessive sweating, fatigue and rapid heart rate due to increased basal metabolic rate, which are similar to the clinical symptoms of viral myocarditis, especially at the beginning of the disease and when the symptoms are atypical, they are more easily confused with viral myocarditis. If the condition is carefully observed and the necessary laboratory tests are performed, it is usually easy to differentiate.
9. Benign premature beats Referring to premature beats without pathological significance. The diagnosis is based on: (1) no history of heart disease, often found by chance; (2) no clinical conscious symptoms, activity as usual, small heart, no organic murmur; (3) premature beats are more frequent at night or at rest, heart rate increases after activity, and premature beats decrease or disappear significantly; (4) ECG shows premature beats of monogenic, paired type, no R waves falling on T waves, and no other ECG abnormalities. Benign premature beats can be caused by either fatigue, mental stress, or unstable vegetative nerve function, or by stimulation of left ventricular free tendon traction. The diagnosis of benign premature beats should be confirmed by systematic examination and comprehensive analysis in conjunction with clinical practice and, if necessary, by follow-up observation. Since premature beats are also one of the most common arrhythmias in viral myocarditis, it is important to make a good differential diagnosis between benign premature beats and pathological premature beats to avoid missed diagnosis or misdiagnosis.
10. β-receptor hyperactivity Most often seen in young women, with no clinical evidence of organic heart disease, palpitations, chest tightness, weakness and electrocardiogram ST-T changes, premature beats, etc. Sometimes it can be misdiagnosed as viral myocarditis. However, this disease has obvious sympathetic hypertension manifestations, such as insomnia, hyperhidrosis, agitation, high blood pressure, and hyperactive first heart sound, etc. The heart is not enlarged, and it is not related to viral infection, and the heart rate test is positive, so it is not difficult to differentiate it from viral myocarditis.
11. Vagal hypertonia can cause atrioventricular block of degree I or II type I. Clinically, it is easily misdiagnosed as viral myocarditis. It is characterized by no abnormal changes other than atrioventricular block and may be asymptomatic, or may have mild chest tightness, wheezing and fatigue. The conduction block is relieved or disappears during daytime activity and worsens at night when lying in bed. After applying atropine, the AV block disappears, and clinical attention should be paid to differentiation.
12. Electrolyte disorders can cause abnormal ECG changes. For example, in hypokalemia, T-wave widening, hypotonicity or inversion, U-wave, prolonged Q-T interval, decreased S-T segment, premature atrial or ventricular beats, and even ventricular or supraventricular tachycardia, ventricular fibrillation, and sometimes bradycardia and AV block can occur; in hyperkalemia, T-wave hypertonicity, P-wave hypotonicity and widening, prolonged P-R interval, decreased or elevated S-T segment, and even ventricular tachycardia, ventricular flutter or ventricular fibrillation can occur. In hyperkalemia, the S-T segment may be prolonged and the Q-T interval may be prolonged. Many of these abnormal ECG changes can be seen in viral myocarditis, but they can be easily differentiated based on the etiology of the electrolyte disorder and its clinical manifestations, combined with laboratory tests.
Etiology and pathogenesis
I. Etiology and pathogenesis in Chinese medicine
(I) Etiology
1. Internal causes
(1) Insufficient endowment There are differences between individuals with different innate endowments, and such differences can affect the strength of the body’s positive energy. If the congenital endowment is insufficient and the positive qi is weak, it is easy to contract evil and develop the disease.
(2) The inappropriateness of nourishment The appropriateness of nourishment is also a major factor affecting the strength of the body’s vital energy. If life is irregular, lack of physical exercise, poor diet and partiality, nutritional disorders, as well as repeatedly infected with other diseases or long-standing illnesses, can make the body weak positive qi, resistance to evil and disease.
2. External causes
(1) The main cause of the disease is the external infection of evil toxins. The so-called evil poison mainly refers to the six evil spirits belonging to the four seasons, including the highly contagious epidemic gas. The six evil spirits, led by wind, can lead to the occurrence of this disease, among which wind-heat evil poison is most common.
(2) Predisposing factors After the invasion of evil toxins into the heart body, factors such as exhaustion of qi by strain, injury to qi by seven emotions, injury to the spleen by food stagnation, and repeated exposure to external evil can all predispose to the disease or aggravate it or cause it to linger on.
(II) Pathogenesis
The onset of viral myocarditis is the result of external factors acting on internal factors. It is generally believed that the onset of the disease is based on the deficiency of positive energy and the internal invasion of evil toxins.
The location of the disease is mainly in the heart, but can also involve other internal organs such as the spleen, lungs and kidneys. 3.
3. the nature of the disease is always a deficiency of the root and the symptoms of the disease. The origin lies in the heart’s qi, blood, yin and yang, and the symptoms include evil toxins, blood stasis and phlegm.
The disease is generally not very acute. However, in the early stage of the disease, if the evil toxin is trapped in the body and the positive energy is not supported, and the positive energy is in decline, the disease will be rapid and violent, and death may occur within a short period of time. In the middle and late stages of the disease, if the body is deficient in qi, blood, yin and yang, and the pathological products such as blood stasis, phlegm and dampness interact with each other, forming a vicious circle, the disease will not be cured, or even progressive aggravation, which can be life-threatening.
The pathological transformation process is very complicated, the initial stage of the disease is mainly manifested by the pathological changes of evil and poison invading the heart, and evil and positive fighting with each other, while the later stage of the disease is characterized by the partial strength and weakness of the body’s qi, blood, yin and yang, as well as the interaction of the resulting pathological products such as blood stasis and phlegm-dampness, resulting in a mixed evidence of deficiency and deficiency in deficiency.
6. symptoms and mechanisms
(1) Evil toxins invade the heart and impair the vital energy
(1) The internal invasion of evil and poison, the right qi is injured wind-heat or damp-heat evil and poison invasion of the body, can be from the mouth, nose or skin and hair. The evil of wind-heat first attacks the lung and then enters the lung from the surface. The heart and lungs live together in the upper jiao, and the lungs are connected to the heart veins, so the lungs are easily affected by evil to the heart. Wind-heat enters the lungs and turns into heat and toxin, which burns heart yin and depletes heart energy.
The evil of dampness and heat often offends the spleen and stomach. Dampness is a yin evil and is most likely to damage yang energy. Dampness traps the spleen and damages the yang of the spleen and stomach, which then affects the heart, resulting in a lack of heart yang. If the body is Yang-rich, the evil of wind and dampness can turn into heat from Yang, and damp heat from the spleen attacks the heart, which also makes the heart and mind restless. Generally, the first symptoms are vicious cold, fever, heavy head and limbs, vomiting and diarrhea, loss of appetite, etc. There may also be fever with ups and downs, lingering, distention and fullness of the abdomen, nausea and vomiting, diarrhea, red tongue with yellowish coating, followed by palpitations, chest tightness, shortness of breath, moist and slow pulse, knotted generation, etc.
②Internal trapping of evil toxin, deficiency of positive qi The deficiency of positive qi in the body or the low ability of infants to resist evil, if infected with evil toxin, will easily lead to internal trapping of evil toxin and deficiency of positive qi, resulting in critical pathological changes such as deficiency of heart yang, violent loss of yang qi, deficiency of qi and blood.
If the heart yang is deficient, the veins and ligaments are stagnant, water and dampness are stagnant and overwhelm the heart and lungs, then the face will suddenly appear pale, lips are blue, breathing is difficult, irritability, palpitations, chest tightness, neck and veins are distended, lumps under the dorsum, pulse is sunken and weak or weak, nausea and vomiting, limb edema, etc.; if the heart and kidney are depleted of true yin, yin does not converge yang, deficient yang is removed, then the face will appear pale, sweating and limbs are cold, lips and nails are blue and purple, skin is flowery, blood pressure drops, breath is low and uneven. If yin and yang are depleted, blood is deficient and cold condenses, blood does not nourish the heart, and qi and blood are disordered, then dizziness and palpitations are seen, and movement is worse, the hands and feet are cold, the pulse is sluggish, and even coma and convulsions occur, which are all critical.
After the intense struggle between evil and positive, although the evil toxin has been reduced, the positive energy has also been damaged, so it is manifested as the evidence of positive deficiency and evil love, and the deficiency is accompanied by real. The symptoms include low fever that does not subside, red throat, swelling and pain, coughing, irritability and dry mouth, palpitations and palpitations, shortness of breath and weakness, red tongue with little coating, thin and weak pulse, etc. The symptoms include low fever that does not subside or fluctuating fever, fatigue, palpitations and chest tightness, pale face, cold limbs and sweating, greasy tongue with coating, moist and slow pulse or knotted generation, etc. etc.
(2) Qi, blood, yin and yang are in favor of decay
Since myocarditis is most common in patients with exogenous wind and heat, it is easy to consume qi and injure yin, so deficiency of qi and yin is the most common pathological change of the disease. The heart Qi deficiency is weak, the blood vessels are not filled, so palpitations, shortness of breath, weak pulse or knotted generation; heart Qi deficiency is not solid, the Ying and Wei is not in harmony, so easy sweating. Deficiency of heart yin leads to loss of nourishment of the heart, hence palpitations; deficiency of heart yin leads to internal disturbance of deficiency fire, hence heart agitation, dry mouth, night sweating, and fine pulse.
(2) Deficiency of qi and yang is mostly due to external dampness that damages yang. Heart Yang is not revitalized, it is unable to drum the heart pulse, so see the pulse to slow, limbs cold, chest tightness heart pain, face [white light] white; Heart Yang deficiency, the blood transport is not normal, down to the kidneys, the Yang deficiency water flood, so see the face pale and green, shallow breathing, false restlessness, hypochondriac mass, limb edema, nausea and vomiting, pulse weak and fast number; Heart Yang decay and violent off, Zong Qi, then see sweating profusely, the extremities are cold, the mouth and lips blue, weak respiration, pulse weak to be. The respiration is faint, the pulse is weak and desperate, and the mind is blurred or even comatose.
(3) Deficiency of qi and blood Wind-heat and evil toxins injure yin and consume blood, deficiency of yin and blood, deficiency of blood and weakness of qi, or damp-heat and evil toxins damage the spleen and stomach, causing lack of source of qi and blood biochemistry, all of which can lead to pathological changes of deficiency of both qi and blood. Qi deficiency and blood deficiency result in deficiency of the heart and blood vessels, so palpitations and palpitations, dizziness and weakness, yellow face, restless sleep at night, spontaneous sweating and night sweats, weak or knotted pulse, etc. If the deficiency is in favor of Yin and Blood, the Heart Vessel is not nourished, so we can see great movement in the heart, heart pain, thin pulse or knotted generation, dizziness, heart trouble, dry mouth, night sweating, etc.
(4) Loss of both yin and yang The kidney is the root of the innate nature, which sends true yin and true yang inside. If the heart disease is prolonged, the heart and kidney are poorly nourished, the yin and yang are lost, the qi and blood remain stagnant, and the phlegm and dampness stop gathering.
(3) Stasis of blood and phlegm-dampness blocking the heart vessels
(1) Blood stasis Blood stasis is both a pathological product of poor blood flow, which in turn can affect the flow of Qi and blood and become a new pathogenic factor. The pathological changes that lead to stagnant blood in myocarditis are mainly due to the following reasons: first, heat toxicity congestion in the heart, resulting in astringent blood flow; second, deficiency of heart qi, the inability to stimulate the blood vessels; third, deficiency of yin and blood, stagnant blood flow: fourth, the deficiency of yang qi, yin and cold, blood cold and stagnant. If blood stasis paralyzes the heart and blood does not run smoothly, palpitations and palpitations, chest pain and tightness, and sluggish or stagnant pulse are seen.
Like Blood stasis, Phlegm-Damp is both a pathological product and a new pathogenic factor. The pathological changes leading to phlegm and dampness are mainly due to the following reasons: First, the evil heat burns the fluids and produces phlegm; second, the deficiency of qi and dampness gather into phlegm, such as deficiency of lung qi, then the fluids are not distributed, spleen qi deficiency, then water and dampness are not controlled, etc., can form phlegm and dampness; third, the deficiency of yin and fire, decoction and phlegm: fourth, the deficiency of spleen and kidney yang, water floods as phlegm. If phlegm-dampness paralyzes the heart and yang, then chest pain and chest tightness, palpitations, dizziness; if phlegm-fire disturbs the heart and mind, then palpitations occur and stop, chest tightness and distress, insomnia and dreaminess, pulse protrusion or slippery count; if water-dampness stops inside and overrides the heart and lungs, then see palpitations and chest tightness, difficulty in breathing, coughing and vomiting blood, irritability, edema of the limbs, etc.; if phlegm-dampness is blocked inside and qi is stagnant, then see chest tightness, gasping for air, etc.
Western medicine etiology and pathology
(A) Causal viruses
So far it has been found that more than 20 kinds of viruses can cause myocarditis, pericarditis. Among them are mainly RNA viruses, such as small RNA virus family of enteroviruses (including coxsackie group B viruses 1 to 6, coxsackie group A viruses 1 to 24, echovirus 1 to 34, poliovirus 1 to 3 and new enterovirus 68 to 72) and rhinovirus, orthomyxovirus family of influenza viruses, paramyxoviruses in the parainfluenza virus, mumps virus, measles virus, respiratory tract syncytial viruses, encephalitis B virus, dengue fever virus, hemorrhagic fever virus, yellow fever virus, rubella virus, etc. of the family Phippoviridae, rabies virus of the family Popoviridae, etc. Some DNA viruses such as herpes simplex virus, varicella-zoster virus, cytomegalovirus, EBV, adenovirus, smallpox virus, and unclassified hepatitis viruses can also infect the human myocardium.
Different viral infections have different chances of causing myocarditis, with enterovirus and respiratory virus infections being the most likely causes. It is generally believed that coxsackie group B viruses are the main etiologic agent of myocarditis in infants, adolescents and adults, accounting for about 50% or more.
(II) Pathogenesis
It is very complex and has not been fully elucidated so far because of the infection characteristics of different viruses and the large differences in immunity and reactivity of different genotypes of the body, which are also influenced by various factors such as environment, nutrition, gender, exertion, and mental stimulation. However, at least two mechanisms have been recognized so far, the direct cytolytic effect of the virus and the myocardial cell injury caused by the virus-mediated cellular immune response. In addition, the role of mechanisms such as the free radical-lipid peroxidation chain reaction in the pathogenesis and evolution of viral myocarditis has received increasing attention, but remains controversial.
1. Direct cytolytic effect of the virus
The main pathogenesis of viral myocarditis is the direct lysis of myocardial cells by the virus in the early stages of the disease, with the appearance of myocardial necrotic lesions. -It is generally believed that viruses invade the heart and first attach to viral receptors in the cell membrane. Different species or groups of viruses bind only to their corresponding receptors, and if there is no receptor for the virus on the cell membrane, the virus cannot cause myocarditis. Generally, the number of viruses that can enter the cell and cause infection does not exceed 5% of the number that bind to the receptor on the membrane. Inside the cell, the virus is able to inhibit the metabolism of cardiomyocyte biomolecules so that they cannot be translated into their own RNA, but does not affect the replication of viral RNA. As a result, on the one hand, a large number of viruses replicate and mature, and on the other hand, the synthesis and modification of enzymatic proteins and the synthesis and assembly of structural proteins in cardiomyocytes are severely impaired, which eventually leads to the lysis of cardiomyocytes and the escape of a large number of replication and assembly of mature viral particles, which can further infect neighboring cardiomyocytes and cause necrotic foci in the myocardium.
2. Cellular immune damage effects
(1) T cell-mediated immune damage One study found that a class of T lymphocytes was isolated from the spleen of CVB3-infected male Balb/C mice, and in vitro experiments confirmed that they could directly kill CVB3-infected Balb/C mammary mouse cardiomyocytes, which are called cytotoxic T lymphocytes (CTL) because of their cytotoxic effects. Further studies revealed that there are two different functions of CTL in the lymph node cells of CVB3-infected mice: one that can specifically kill virus-infected cardiomyocytes, called virus-specific CTL (VCTL); and the other that can kill uninfected cardiomyocytes, called auto-reactive CTL (ACTL). VCTL is a subpopulation of T suppressor cells, which only lyses infected cardiomyocytes because it recognizes the virus-altered antigens on the surface of infected cardiomyocytes, often resulting in only minor myocardial damage. Both ACTL and VCTL are thymus-dependent, and after removal of the thymus in mice, these reactions do not occur even if the same virus is reinfected.
(2) Killing effect of NK cells NK cells are one of the third group of cells in the immune lymphocyte lineage distinct from T cells and B cells. This cell has a two-fold meaningful role in the pathogenesis of viral myocarditis. On the one hand, as a line of defense of the body against viral immunity, they have the function of protecting the body from viral infection. The killing effect of NK cells has been suggested to be related to their expression of the cytolytic factor perforin. The release of perforin on the surface of cardiomyocytes can cause ring-like damage to the cell membrane, after which a cytotoxic response mediated by perforin occurs, causing myocardial injury.
(3) Killing and antigen presentation by mononuclear macrophages Mononuclear macrophages are immune helper cells, which are both highly phagocytic and a major antigen presenting cell. In addition. It is also involved in cytotoxic reactions and delayed metaplasia. One study found that the cells were detectable in myocardial specimens on day 4 of infection of mice with CVB3. These infiltrating mononuclear macrophages are tightly connected to cardiomyocytes and T cells, suggesting that they recognize and phagocytose virus-infected cardiomyocytes early in the infection, deliver antigenic information to T cells after digestion and processing, and activate T cells by secreting interleukin-1 (IL-1) to initiate a series of immune responses.
3. Damaging effects of free radical-lipid peroxidation reaction
The free radical-initiated lipid peroxidation chain reaction may have an important role in the pathogenesis of viral myocarditis. In viral myocarditis, large amounts of oxygen free radicals can be generated due to massive replication of virus into cells, degeneration and necrosis of myocardial cells, killing of infected or uninfected myocardial cells by CTL, ischemia and hypoxia of myocardial tissue, and myocardial interstitial edema and inflammatory cell infiltration. Oxygen free radicals (OFR) acting on polyunsaturated fatty acids in cell membranes and subcellular structure membranes can trigger lipid peroxidation reactions and produce lipid peroxides (LPO), causing damage to myocardial cell membranes, permeability changes, mitochondrial swelling, lysis, rupture, lysosomal enzyme release, enzyme activity inactivation, etc. Acting on nucleic acid, protein and sugar components, it can cause nucleic acid breakage, protein denaturation and polysaccharide depolymerization in cardiomyocytes. Although LPO is a product of cell damage, it is easy to re-form free radicals by breaking the weaker peroxide chemical bonds in its molecules, which can intensify the lipid peroxidation chain reaction, therefore, it is believed that the system of scavenging OFR and inhibiting OFR reaction in the body cannot scavenge free radicals if it encounters the lipid peroxidation chain reaction triggered by free radicals.