Myocarditis (myocarditis)
Myocarditis is a disease caused by infection or other causes of diffuse or focal inflammatory cell infiltration in the interstitial myocardium and its proximal myocardial fiber necrosis or degeneration, resulting in varying degrees of cardiac dysfunction and other systemic damage. Viruses are the main cause of myocarditis, but other agents such as bacteria, mycoplasma, protozoa, mycobacteria, chlamydia, and poisoning and allergies can cause the disease. Most viral causes are asymptomatic, but a very small number of severe cases can be fatal due to fulminant myocarditis. Most patients with acute viral myocarditis have normal heart anatomy and no previous history of heart disease. Yang Xiaodong, Department of Cardiology, Shanghai Children’s Hospital In the past, the clinical diagnosis of myocarditis was very irregular and often amplified due to problems of awareness and lack of definitive diagnostic tools. It was not until 1932, when myocarditis was objectively described in the book “Cardiology” by Thomas Lewis and Paul White, that the international medical community took a rigorous approach to the diagnosis of myocarditis. If the heart function is normal and there is pre-term contraction alone, then myocarditis cannot be diagnosed and no treatment is needed.
[Epidemiology].
Myocarditis is a rare disease in clinical practice; the cardiology department of Texas Children’s Hospital had 14,322 cardiac hospitalizations from 1954 to 1977, with myocarditis accounting for only 0.3%, and the statistics of the cardiology department of Toronto Children’s Hospital from 1951 to 1964 were similar to those of Texas. The British Wood (1968) in his book “Heart and Circulatory Diseases” said that out of about 10,000 new cardiac patients he met, only about 30 were diagnosed with myocarditis; another report said that during the 14 years from 1978 to 1992, 33 cases of myocarditis were diagnosed at Texas Children’s Hospital, 12 cases at Children’s Hospital of Pittsburgh and only 6 cases at Montsana Medical Center during the same period. In Hong Kong, there are 5,000 to 7,000 people hospitalized in the pediatric department of Prince of Wales Hospital each year, and no more than 2 people aged 1 to 15 years with myocarditis. As seen above, myocarditis is not a common disease. Viral in all myocarditis accounts for about 0, 38%, many viral infections for systemic diseases, mostly with manifestations of the primary major disease, while myocarditis is often a secondary lesion involved. It is known that more than 20 viral families cause myocarditis, and their species are mainly enteric and respiratory viruses, most of which are small RNA viruses, the most common of which are adenovirus and coxsackievirus. crist and Bell statistics 385 cases of myocarditis, about half of which are coxsackie group B (CVB), according to statistics in CVB viral infections, about 4% have cardiovascular damage, and severe cases are seen mostly in However, we cannot ignore the importance of enteroviral infections. For rotavirus, the main pathogen causing autumn diarrhea in children, studies have reported that it can cause myocarditis and even lead to cardiogenic shock or sudden death. Therefore, it needs to be given high priority in clinical practice.
A series of epidemiologic investigations have been conducted on the current cases of children with sudden death. In a study published in 2003, a group of studies from Australia showed that 1,24 out of 100,000 children younger than 10 years had dilated cardiomyopathy, and 25 out of 187 children with dilated cardiomyopathy (14%) were due to acute viral myocarditis; another group of studies from the United States showed that 1,13 out of 100,000 people aged 1-18 years had sudden death. Another study from the United States showed that 1,13 out of 10,000 people in the local population aged 1-18 years had dilated cardiomyopathy, and 21 of 239 children with confirmed dilated cardiomyopathy had acute viral myocarditis, accounting for 9% of the cases. Combining a large amount of information, it is believed that more than 10% of children with heart failure and dilated cardiomyopathy have a viral cause, but this number is not accurate due to the lack of a clear autopsy basis, and there are still many subclinical cases that have not been clearly diagnosed.
The causative viral types of acute myocarditis in children etiology morbidity evaluation genetic susceptibility, common adenovirus 55-60% can be detected by PCR method endotracheal aspiration plus has been identified.
It is often associated with mild or suspected myocarditis.
Myocardium containing coxsackie-adenovirus receptors is susceptible and may have a hereditary family history.
Coxsackievirus 30-35% was previously thought to be the most common virus causing myocarditis.
Later this virus can persist in patients with cardiomyopathy.
1. Coxsackie-adenovirus receptor-containing-heart susceptible
2, myasthenia gravis-deficient individuals uncommon microviruses 1-2% in all age groups can cause fulminant myocarditis and sudden death.
It is associated with the development of idiopathic left ventricular insufficiency in adults.
There may be a current trend toward elevated diagnoses in myocarditis-causing viral agents.
Influenza virus A/B <15% herpes simplex virus EBV cytomegalovirus
[Pathology].
The pathological changes of myocarditis caused by various pathogens are not specific, the heart cavity is enlarged, the left ventricle is particularly, the heart hypertrophy, weight gain, pale and soft myocardium; ventricular wall is often thin, the myocardium can be thickened when the disease is prolonged; pericardial surface often has bleeding spots, the pericardium can have the same inflammation, so the pericardial fluid can be blood-colored. The heart valves and endocardium are mostly free of lesions and may be paler in color. Some lesions may resemble subendocardial elastosis (ejection fibrillation), so many scholars suspect that ejection fibrillation is the result of viral myocarditis, and it is very likely that myocarditis infection was present in the fetus. Recken et al. reported ECHO9 myocarditis in a 5-month-old infant, and the pathological findings were similar to those of ejection. In the acute phase, focal or diffuse mononuclear cellular infiltrates, including lymphocytes, plasma cells, and eosinophils, are seen microscopically; neutrophilic polymorphonuclear leukocytes are rare, unless they are bacterial in origin. Viral particles are rarely seen on electron microscopy. In severe cases, there is diffuse necrosis of the myocardium with loss of myocardial fiber crossings, and sometimes perivascular accumulation of lymphocytes and plasma cells can be seen. Chronic phase: microscopically, cardiomyocytes are seen to be hypertrophic, morphologically disorganized, with uneven nuclear staining, lymphocyte infiltration and fibrin exudation in the interstitium, local scar formation, coexistence of old and new lesions, and a small amount of mononuclear cell infiltration in the endocardium.
Bacterial myocarditis is a localized small abscess, especially in Gram-positive bacteria; tuberculous myocarditis may be a caseous nodule; hemorrhagic spots and hemorrhage are seen in those due to meningococci, and mycobacteria may have fibrous caseous pustules, focal granulomas or redundancies. The larvae of Ascaris lumbricoides migrate viscerally in the myocardium and may occasionally have pus foci.
Pathophysiology
The pathological changes of viral myocarditis have been reported in the literature, and in the past, coxsackie-B virus was common, but current data show that adenovirus is more common, accounting for about 55-60% of cases. Most cases are not due to direct viral damage, and only a few fulminant myocarditis may be due to direct and extensive destruction of myocardial cells by the virus.
In the late course of myocarditis produced by Nakamura et al. in rats inoculated with the virus, the RNA genome of the virus was no longer found in the body, and myocarditis occurred even after transplantation of normal rat hearts, suggesting that autoimmunity is a clear evidence of the persistence of myocarditis. During different periods of myocarditis, the body produces different pathophysiological changes in response to the immune system.
The major histocompatibility complex (MHC) is an important molecule that enables the presentation of viral antigens to the immune system. Class I MHC (HLA-A, B, C) are present in small amounts in human cardiomyocytes, sensitize CD8+ T cells upon binding to viral antigens, and later become target cells for cytotoxic T lymphocytes. Class II MHC (HLA-DP,OQ and DR) molecules, together with processed antigens, stimulate CD4+ helper T cells. MHC are not present in normal fetal and adult cardiomyocytes and when there is cellular damage, including viral infection, the expression of these MHC antigens is enhanced so that the antigens on the surface of cells abnormally expressed after viral attack of the myocardium are recognized by immune cells.
Hemodynamics: If there are extensive inflammatory changes in the myocardium, the function of the myocardium is significantly diminished and is unable to pump out the return blood efficiently, resulting in increased end-diastolic volume and an enlarged heart. The decrease in cardiac output in turn causes a decrease in renal blood flow, resulting in increased sodium and water retention and increased preload; sympathetic nervous system excitation causes vasoconstriction to maintain blood pressure, but this in turn increases afterload; both preload and afterload of the ventricle increase, making cardiac insufficiency increasingly worse, increasing end-diastolic volume and pressure of the ventricle; left atrial pressure is then correspondingly increased to fill the ventricle, and subsequently causes pulmonary venous depression, causing pulmonary edema. This causes pulmonary edema, and after a long period of time, the right heart pressure also increases, and the venous return to the right heart is stagnant, causing liver enlargement and subcutaneous edema. Therefore, most cases of myocarditis are characterized by chronic congestive heart failure.
The presentation of mild and severe cases of myocarditis varies, from asymptomatic and unrecognizable in mild cases to fulminant cardiogenic shock with a high mortality rate in a few severe cases. Most have a history of episodic or other viral infections within 1-3 weeks prior to the onset of cardiac symptoms.
Myocarditis is less severe in infants than in neonates, but the mortality rate from diphtheria complicating myocarditis was high half a century ago. Myocarditis can be complicated by adenovirus, mumps virus, varicella, and cytomegalovirus; most children have upper respiratory tract infections with low-grade fever, irritability, and pallor, followed by cardiac respiratory manifestations, and older children may complain of abdominal pain. On examination, the child may be agitated, or drowsy and disoriented, pale or mildly cyanotic, with cold or florid skin, shortness of breath, or even moaning; blood pressure is normal or falling, with weak apical beats, fast heart rate, and soft heart sounds or gallop rhythm. The softness of the first sound does not necessarily reflect the presence of myocarditis, as the P-R interval can be prolonged by any infection, and the ventricles can be lighter because they have more time to fill and the atrioventricular valve has floated nearly closed before systole. Occasionally, there may be a mild systolic murmur, and sometimes there may be pre-systole, but the majority of these are of unknown cause and should not be used alone as a basis for the diagnosis of myocarditis; most of the other clinically seen arrhythmias are also unrelated to myocarditis. The liver is mostly enlarged, but peripheral edema is rare ECG: can be used as a circumstantial evidence for the diagnosis of myocarditis. In the acute phase there may be sinus tachycardia at quiet times that is not commensurate with body temperature. Low voltage, ST-segment and T-wave changes are common patterns in myocarditis. Total QRS amplitude on limb leads does not exceed 5 mm, T-wave is low and flat, Q-wave is often absent on V5 and V6, and low voltage can be present on chest leads, but is nonspecific. Various conduction blocks and chronic arrhythmias including ventricular or atrial tachycardia may have a basis in myocarditis. Abnormal Q waves and prolonged Q-T intervals may also indicate myocardial damage. In severe cases, myocardial infarction-like S-T segment may be too high. In addition, some cases of myocarditis may not show abnormalities on the ECG even in the acute phase.
Echocardiography: Enlarged heart chambers, mainly left ventricular enlargement; reduced ejection fraction and shortening fraction, and reduced cardiac output all suggest signs of cardiac decompensation. If no structural abnormalities are detected on ultrasound but the heart is enlarged and hypocapnia is present, the diagnosis of myocarditis may be suggested by the medical history. In patients with mild myocarditis, the ultrasound may be normal.
X-rays: In the acute phase, a weakened heart beat, downward stretching of the left ventricle, and reduced myocardial tone can be flask-shaped with loss of normal bowing are seen. In the chronic phase, the heart shadow may be significantly enlarged, with the left ventricle predominant. Severe cardiac insufficiency can be seen as pulmonary stasis or edema, and a few may be accompanied by pericardial effusion.
Diagnosis
The clinical diagnosis of myocarditis requires comprehensive consideration and careful conclusion. In recent years, endomyocardial biopsy has been used abroad to confirm the diagnosis. However, this disease should be considered as one of the differential diagnoses in pediatric patients with heart failure for which no cause can be found, and should be highly suspected if there has been a recent viral infection and fever.
Myocardial biopsy: The promotion of myocardial biopsy in recent years has been helpful in diagnosis, but the positive rate varies widely because of different diagnostic criteria among families. Myocardial biopsy provides a basis for the diagnosis of myocarditis through electron microscopy or immunoelectron microscopy by cardiac catheterization for pathologic analysis. However, there are limitations because we mostly use right heart catheterization, while myocarditis is heavily left ventricular, and the sample selection range is small, so the positive rate may not be high if the lesion is not diffuse, plus it is an invasive test, and patient compliance is also a limiting factor. They found that most acute myocarditis patients had edema on the surface, and the endothelial surface was light red or brown; chronic active patients had purplish red, and chronic inactive patients had yellow; this revealed lesions in the left ventricular wall and allowed selective sampling for biopsy. Regarding the histological definition and classification of myocarditis a meeting of cardiologists held in Dallas in 1984 defined myocarditis as follows: myocardial infiltration with inflammatory cells and necrosis and/or degenerative changes of nearby cardiomyocytes, but non-ischemic damage.
PCR: In situ polymerase chain reaction (PCR) can find the tissue where the viral genome is located, showing that the viral genome is present in certain cardiac myocytes. Inflammatory mediators such as cytokines and adhesion factors can be analyzed by PCR and other methods, and in some cases the viral genome can be amplified, especially in adenovirus. In recent years, apoptosis has been observed in myocarditis due to autoimmunity. In a study by Bowles et al, a PCR assay found that 20% of patients with dilated cardiomyopathy were genetically positive for viruses, 3/5 of which were adenoviruses.
In recent years, the application of magnetic resonance, radionuclide and serum troponin I tests can make a determination of myocarditis. Myocardial biopsy is invasive and is not always necessary. In infants it is also necessary to exclude malformations of the left coronary artery originating from the pulmonary artery, and ultrasound can make the diagnosis.
Radionuclide examination: Intravenous injection of labeled compounds such as 99mu, 201 thallium, 111 indium, and 67 gallium can reveal areas of myocardial necrosis through scanners and gamma cameras, as well as computer program calculations to understand cardiac pump function, myocardial perfusion, myocardial metabolism, and ventricular wall motion to detect local and underlying myocardial damage in myocarditis. The use of 67 gallium (Gallium-67 Ga-67) is now beginning to attract attention, as 67 gallium can concentrate in the myocarditis lesion and is useful in diagnosing the inflammatory response of the myocardium, but is not very sensitive to cellular necrosis. 111 Indium can be labeled with monoclonal anti-myosin (coagulation) antibodies for scanning, and myosin is the major protein in cardiac myocytes, such as plasma membrane intact If the plasma membrane is intact, antibodies cannot bind to myosin, and only when the plasma membrane is disrupted can these monoclonal anti-myosin antibodies bind to intracellular myosin, thus demonstrating that the cells are damaged and necrotic.
Biochemical “markers” (Markers) of myocarditis.
Creatine Kinase CK has three isoenzymes (MM, BB and MB) present at different sites on electrophoresis, MM mainly in skeletal muscle, BB in brain and kidney extracts, while MB and MM are more frequent in the myocardium. CK-MB can also be slightly higher after cardiac surgery and in pediatric congenital heart disease such as transposition of the great arteries, pulmonary artery or aortic stenosis and complete pulmonary vein ectopic drainage. However, its damage to cardiac myocytes is not specific and is susceptible to other non-cardiac factors such as skeletal muscle injury and renal lesions.
Troponin cTn, a component of the promyosin complex, regulates calcium regulation of actin and myosin in cardiac and skeletal muscle. Troponin I (cTnI) and T (cTnT) are present in both skeletal and cardiac muscle. Monoclonal antibodies can be used to separate cTnI in cardiac muscle from skeletal muscle, without cross-reactivity with cTnI in skeletal muscle, so that the determination of cTnI and cTnT is specific for damage to cardiac myocytes, with better specificity and longer duration than CK-MB. In the early stage of myocarditis, the increase of troponin is more obvious, mainly because the damage and necrosis of myocardial cells are in the early stage.
[Diagnostic criteria].
The diagnostic criteria of viral myocarditis were revised according to the discussion at the National Academic Conference on Pediatric Myocarditis and Cardiomyopathy held in Kunming in September 1999.
I. Clinical diagnostic basis
(A) cardiac insufficiency, cardiogenic shock or cardio-cerebral syndrome.
(B) heart enlargement (X-ray, echocardiography has one of the manifestations).
(c) ECG 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, premature beats in association, polymorphic, multiple sources, paired or parallel beats, ectopic tachycardia due to non-atrioventricular node and atrioventricular folding, low voltage (except in neonates) and abnormal Q waves. ) and abnormal Q waves.
(d) Elevated CK-MB or positive cardiac troponin (cTnI or cTnT).
Second, the pathogenic diagnosis based on
(a) Confirmation of diagnosis: The diagnosis of myocarditis caused by virus can be confirmed by finding one of the following in the endocardium, myocardium, pericardium (biopsy, pathology) or pericardial puncture fluid examination of the child.
1.Virus was isolated.
2. Viral nucleic acid is detected with a viral nucleic acid probe.
3. Positive antibodies to the specific virus.
(B) Reference basis: Myocarditis can be considered to be caused by a virus if one of the following is present in combination with clinical manifestations.
1.Virus isolated from stool, pharyngeal swab or blood of the child, and the recovery period serum isotype antibody titer increased or decreased by more than 4 times compared with the first serum.
2. Positive specific IgM antibodies in the blood of the child early in the course of the disease.
3. Viral nucleic acid is detected in the blood of the child with a viral nucleic acid probe.
3. Confirmation of diagnosis
(a) If two clinical diagnostic bases are available, the clinical diagnosis of myocarditis can be made. If there is evidence of viral infection at the same time or 1~3 weeks before the onset of the disease to support the diagnosis.
(B) at the same time with one of the pathogenic confirmation basis, can be diagnosed as viral myocarditis, with one of the pathogenic reference basis, can be clinically diagnosed as viral myocarditis.
(c) Where the diagnosis is not confirmed, 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.
IV. Staging
(A) Acute stage: new onset, obvious and variable symptoms and positive findings, generally within six months.
(B) Extended period: recurrent clinical symptoms, objective examination indexes do not heal, and the duration of the disease is more than six months.
(3) Chronic phase: progressive heart enlargement, recurrent heart failure or arrhythmia, the disease is sometimes mild and severe, and the duration of the disease is more than one year.
Treatment
If the disease is to be diagnosed, clinical progress and signs of heart failure should be observed.
(a) Rest Bed rest can reduce the burden on the heart and prevent accelerated viral replication in the myocardium. At least 8 weeks of bed rest in the acute phase; at least 6 months of half-day bed rest in the recovery phase; for those with severe cardiac insufficiency, strict bed rest is required until cardiac function is restored and cardiac examination improves before light activity.
(B) drug treatment of heart failure, although there is no special effect, but it is important to maintain adequate cardiac output; if there is heart failure, small doses of digoxin can still be applied, 0, 03mg/kg can be used as a total amount of maundyrification half amount of immediate oral, after two doses every 8 hours, the maintenance amount is about 1/5-1/10 of the total amount.
Diuretics are applied when there is congestive heart failure, heart and liver enlargement, which can excrete excessive extracellular fluid to enhance the function of each organ, but excessive diuretics can cause dehydration and even shock, and excessive K+ loss can easily lead to maundiflora poisoning. Furosemide (tachyphylaxis) 1mg/kg per dose is sufficient, not more than 2mg/kg per day; spironolactone (antiseptic) can also be added.
Neonates may exhibit shock with reduced cardiac output, and attention should be paid to inadequate perfusion of the peripheral circulation, such as heart rate, urine output and microvascular refill time. Dopamine can also be used in combination with dobutamine to support blood pressure and dilate the renal vasculature; if the dose is over 20ug/kg per minute, the alpha-adrenergic effect is enhanced, which can increase the peripheral circulatory resistance and is detrimental to treatment, so the dose should not exceed 15ug/kg per minute. The latter can excite β1, β2 and α receptors at a dose of 10ug/kg per minute each.
Vasodilators such as captopril (Captopril) can reduce afterload and are considered to be the drug of choice (Rezkalla), along with digoxin and diuretics, for congestive heart failure. In addition, people are increasingly focusing on the role of neuroendocrine mechanisms associated with heart failure, and some new drugs such as natriuretic peptides, angiotensin receptor blockers, aldosterone antagonists, beta-blockers, calcium sensitizers, endothelin receptor antagonists, vasopressin, etc. are being used.
Recently, it has been found in rats that if the lesions are mediated by CD4+ T cells, the efficacy is good; if the lesions are mediated by CD8+ T cells, hormones are ineffective. In contrast, early application of gammaglobulin has been suggested to be effective, but its effectiveness has yet to be further verified.
If there is no sign of bacterial infection, antibiotics are not necessary.
(iii) Arrhythmia control
If arrhythmias are present, supraventricular tachyarrhythmias can be controlled by digoxin. In recent years, amiodarone (acetaminophen iodofurone) has been used, with an initial dose of 5-10 mg/kg, divided into 1-2 mg/kg every few minutes, and then 5-10 mg/kg daily. -If there is complete atrioventricular block or rapid arrhythmia that cannot be controlled by drugs, esophageal atrial pacing or temporary pacemaker can be given.
Prognosis
The prognosis depends on the age of the disease, the severity of the myocardial lesion, the promptness of treatment, and adequate early rest. The prognosis for neonatal patients is poor, with the highest mortality rate in the first week and no sequelae in those who survive. The prognosis is slightly better in infants and children, with a mortality rate of about 10-25%, and most older children have a better prognosis. In the presence of conduction block or ventricular tachycardia, the mortality rate can be as high as 100%. Mild cases can gradually heal after six months with adequate rest; moderate cases can also be relieved to gradually heal after more than one year of treatment and rest; severe cases have a poor prognosis, often delayed for several years, and finally develop into cardiomyopathy leading to heart failure. Some patients with acute cardiogenic shock, if not rescued in time, can die quickly.
Fulminant myocarditis pediatric fulminant myocarditis is a life-threatening infectious disease of the myocardium, which is rare clinically and has a rapid onset and progression, with a high mortality rate of about 25%, especially in neonates up to 75%. The age of onset is mainly school-age children, and in small infants, myocarditis due to gastrointestinal diseases can occur as cardiogenic shock, which progresses rapidly and requires special attention. The main clinical manifestations of fulminant myocarditis are chest tightness, weakness, pallor, vomiting, abdominal pain, and malignant arrhythmias.
Treatment]
The treatment of fulminant myocarditis, which can occur within 24-48 hours of onset with acute cardiac insufficiency, As syndrome or severe arrhythmias, is a race to the bottom, and is currently based on a combination of anti-arrhythmic drugs and myocardial protection, as well as the reasonable use of adrenocorticotropic hormones. For children with congestive heart failure and pulmonary edema, causing respiratory distress and hypoxemia, prompt mechanical ventilation should be performed. The arrhythmia is supraventricular and can be controlled by digoxin; lidocaine is used in ventricular cases, with an initial dose of 1 mg/kg sedation and later reduced to maintain the blood concentration at 1-5 mg/ml, and amiodarone has been used in recent years, with 2,5-5 mg/kg sedation and a maintenance dose of 10-15 mg/kg, d, until it is converted to oral.
If pharmacological treatment is ineffective and severe arrhythmias such as sick sinus node syndrome, degree III AVB with alternating ventricular tachycardia and ventricular flutter still occur repeatedly, a temporary pacemaker should be installed in time to maintain the heart beat output and ensure effective blood circulation. Among 50 cases of fulminant myocarditis treated in 6 hospitals in Shanghai, 7 cases with temporary pacemakers survived and had a good prognosis, suggesting that the timely application of temporary pacemakers is an active, effective, and safe treatment method based on antiarrhythmia and myocardial protection.
For children with severe myocardial damage, left ventricular assist devices are now used internationally to maintain the pumping function of the heart and ensure adequate blood circulation, with good results.
[Prognosis].
The prognosis of fulminant myocarditis is closely related to the age of onset and the severity of myocardial damage, and the electrocardiogram is also suggestive: the mortality rate is higher in patients with extensive ST-T changes, ventricular tachycardia and ventricular fibrillation. Therefore, the principle of early diagnosis and timely treatment should be followed for these patients, especially in the presence of grade III AVB, a temporary pacemaker should be installed in time, which is very important to improve the prognosis of the children.
[Table] Diagnostic criteria for myocarditis in Dallas (USA)
1, general definition: non-ischemic resulting in myocardial cell damage with infiltration of inflammatory cells, and myocardial necrosis or degenerative changes.
2, Acute myocarditis: the presence of significant inflammatory cell infiltration (usually lymphocytes) and myocardial cell deformation necrosis, with or without fibrosis.
3, Suspected myocarditis: there is a significant cellular infiltrate, but it has not yet caused myocardial damage.
4. Recovering/post-recovery myocarditis: there is a clear basis for tissue repair and the inflammatory infiltrate is reduced or absent.