1, myocarditis is a limited or diffuse acute or chronic inflammatory lesion of the myocardium. Including.
(1) Infectious: viral myocarditis caused by viral infection is predominant.
(2) Myocarditis caused by allergic, allergic reactions or rheumatic disease processes.
(3) Myocardial damage caused by physical and chemical factors. Viral myocarditis is an inflammation of the myocardium caused by cardiophilic viruses, especially coxsackieviruses are the most common. In normal life certain triggers such as bacterial infections, excessive fatigue, malnutrition, dramatic climate changes, pregnancy and hypoxia can cause the body’s immunity to decline and lead to viral infections. The incidence of the disease is higher in adolescents, and there is a trend of increasing incidence year by year. Most of the disease has a good prognosis after active treatment, but a few may develop serious myocardial damage, heart failure, cardiogenic shock, arrhythmia and life-threatening. Some of them may evolve into cardiomyopathy. Feng Baolin, Department of Cardiovascular Medicine, Second People’s Hospital of Neihuang, Henan Province
2. Diagnosis of viral myocarditis
Viral myocarditis is quite difficult to diagnose clinically because of the lack of typical clinical manifestations and the lack of specificity of most clinical ancillary tests. Due to the different degrees of extensiveness and severity of lesions, clinical symptoms can be asymptomatic, or severe arrhythmias, heart failure, cardiogenic shock and sudden death can occur.
Reference criteria for diagnosis of viral myocarditis
1) Medical history and signs
Cardiac manifestations such as post-infection weakness, chest tightness, dizziness (due to decreased cardiac output), decreased apical first heart sound, diastolic gallop rhythm, pericardial friction sound, heart enlargement, heart failure or A-Syndrome that cannot be explained by general causes appear within 3 weeks after viral infections such as upper whistle infection and diarrhea.
(2) The following arrhythmias or electrocardiographic changes newly appeared within 3 weeks after the above infection
(1) Sinus tachycardia, atrioventricular block, sinus block or bundle branch block.
(ii) Multiple, paired premature ventricular beats, voluntary or junctional tachycardia, paroxysmal or non-paroxysmal ventricular tachycardia, atrial or ventricular flutter or fibrillation.
(3) More than 2 leads with horizontal or downward oblique downward shift of S-T segment ≥0.05mv or abnormal elevation of S-T segment or abnormal Q wave.
(3) Reference indexes of myocardial injury
Serum troponin I or troponin T, CK-MB are significantly elevated. Echocardiography shows enlarged heart chambers or abnormal ventricular wall activity, and nuclear cardiac function tests confirm reduced left ventricular systolic or diastolic function.
(4) Pathogenetic basis
①Virus, viral gene fragment or viral protein antigen was detected from endocardium, myocardial pericardium or pericardial puncture fluid in the acute phase.
②Viral antibodies: the titer of homotypic viral antibodies in the second serum is 4 times higher than the first serum (2 sera should be more than 2 weeks apart) or primary antibody potency ≥ 640 is positive, and 320 is suspicious positive (there are different clinical laboratory standards).
(iii) Virus-specific IgM: those with ≥1:320 are considered positive. If there is also positive enterovirus nucleic acid in the blood, it is more supportive of a recent viral infection.
Severe viral myocarditis may be diagnosed if the patient has one or more manifestations of A-S syndrome attack, congestive heart failure, sustained ventricular tachycardia with hypotension, or pericarditis. If only a few premature beats or mild T-wave changes occur within 3 weeks after viral infection, the diagnosis of acute viral myocarditis should not be easily made.
For those who have difficulty in making a definitive diagnosis, long-term follow-up and endomyocardial biopsy for viral genetic testing and virological examination can be done when available. When considering the diagnosis of viral myocarditis, β-receptor hyperfunction, hyperthyroidism, mitral valve prolapse syndrome and other disorders affecting the myocardium, such as rheumatic myocarditis, toxic myocarditis, coronary artery disease, connective tissue disease, metabolic diseases and Keshan disease should be excluded.
3, common diagnostic misconceptions of viral myocarditis
There is no unified international diagnostic standard for viral myocarditis, and its misdiagnosis is very serious. The following are some of the common diseases that are easily misdiagnosed clinically with viral myocarditis.
1) Hyperthyroidism
It is not uncommon for hyperthyroidism to be misdiagnosed clinically as viral myocarditis. If there is a history of upper whistle infection just before the onset of the disease, it is more difficult to differentiate. Hyperthyroid patients have a fast heart rate, palpitations and chest tightness, but they are often sweaty and irritable, have weight loss, and have positive hand tremors. The diagnosis can be confirmed by clinical examination of thyroid function. Treatment as hyperthyroidism is effective. It is worth mentioning that hyperthyroidism is often associated with cardiac changes, which increases the rate of clinical misdiagnosis.
(2) Beta-receptor hyperfunction syndrome
Clinical misdiagnosis of β-hyperreceptor syndrome as viral myocarditis is most common, especially in primary care. The disease is more common in young women, who often present with palpitations, shortness of breath, paroxysmal chest tightness and chest pain, with a slightly faster heart rate than normal. Each episode lasts for several hours and is accompanied by sighing and other symptoms. There are no abnormal findings on echocardiography and the application of β-blockers is effective.
3) Mitral valve prolapse syndrome
Clinically, mitral valve prolapse syndrome may present with palpitations, chest tightness, chest pain, and even with various arrhythmias, and ST-T abnormalities on ECG, thus easily misdiagnosed as viral myocarditis. The heart murmur is more pronounced in this disease. Clinical echocardiography and markers of myocardial necrosis can help in the differential diagnosis.
4) Unexplained arrhythmias
Many clinical arrhythmias such as atrial asystole and ventricular asystole have no specific cause and are easily misdiagnosed as viral myocarditis if they occur just after an upper whistle infection. Such patients should be further observed by examining the ECG and markers of myocardial damage, and the diagnosis of viral myocarditis should not be made arbitrarily.
5) Coronary heart disease
Patients present with palpitations, chest tightness, paroxysmal chest pain, ST-T changes on ECG, and elevated cardiac enzymes. Viral myocarditis is considered in adolescents, and the diagnosis is easily confused if the patient is middle-aged or older and has a history of viral infection. However, coronary artery disease has its own dynamic evolution pattern in terms of ECG and cardiac enzymes, and coronary angiography is performed when necessary to clarify the diagnosis.
6）Rheumatic myocarditis
In addition to precordial discomfort, palpitations, chest tightness, chest pain and even dyspnea, the main manifestations of rheumatic myocarditis include cardiac inflammation, polyarthritis, chorea, annular erythema, subcutaneous nodules and fever. Anti-“O” may be increased, blood sedimentation is increased, serum C3 complement is increased, and streptococcal antigen test is positive.
4.Treatment of viral myocarditis
1）Rest
Viral myocarditis is mainly rest. Rest can reduce myocardial oxygen consumption and reduce the load on the heart. Rest as well as early diagnosis, early treatment has important significance for its prognosis. For those with obvious symptoms and obvious abnormalities in ECG and other auxiliary tests, bed rest should be given for 2-3 months during the acute phase. When the symptoms and signs are mild, appropriate indoor activities can be performed after improvement. Six months after the onset of the disease, those whose symptoms and signs and examinations are back to normal can work in half amount and adjust the rest time appropriately according to the patient’s cardiac function.
2）Anti-viral treatment
The peak of viraemia and lytic T lymphocyte damage to the myocardium at the onset of viral myocarditis has passed, but viral replication and the free radical damage caused by it continue in the myocardium. However, antiviral drugs are mostly unable to enter the interior of the cells, and in the acute phase the free radical scavenger vitamin C is used as the mainstay, supplemented by antiviral and immunotherapy. Ribavirin, acyclovir, transfer factor, interferon, and herbal cleansing and detoxification therapy can be used during viral infection as appropriate.
3）Targeting myocardial treatment
Normal myocardium produces many reactive oxygen radicals and many enzymes, which can remove oxygen radicals in time to protect myocardial cells from damage. The acute phase of myocarditis needs to be treated with free radical scavengers, vitamin C, coenzyme Q10, vitamin E, etc. Especially high-dose vitamin C is effective, the symptoms are eliminated quickly, commonly used amount of 150-200mg/(kg.d), intravenous drip, generally 4 weeks as a course of treatment. Also can be used Chinese medicine Astragalus injection 40mg once a day intravenous drip.
4）Improve cardiac function
Viral myocarditis can develop heart failure, which can be treated clinically with cardiotonic diuretics and vasodilators. Intractable heart failure can be treated with positive inotropic drugs such as dobutamine or dobutamine, and a small amount of morphine can be used for acute pulmonary edema. For cardiogenic shock high-dose vitamin C 100-200 mg (kg.d) intravenously, which can be repeated every 6 hours for low blood pressure, or in combination with dobutamine.
5）Anti-arrhythmic drug application
For sinus tachycardia without heart failure, β-blocker atenolol or calcium antagonist verapamil can be used for treatment. Methicillin or amiodarone is used for frequent ventricular precontractions. In the case of conduction block or bradycardia, drugs such as atropine should be used.
6) Antibiotics and hormone application
Bacterial infection is a condition factor of viral myocarditis. In order to prevent myocardial immune response caused by bacterial infection, antibiotic therapy is routinely used at the beginning of treatment to clear the foci of streptococcal infection or the carrier state. The hormonal treatment of viral myocarditis has been controversial, and most believe that glucocorticoid therapy can be tried for a short period of time when the treatment of heart failure, shock, and severe conduction block is not effective.
7）Other treatments
In addition to the above treatments, angiotensin-converting enzyme inhibitors (ACEI) can be used clinically to reduce the weight of the myocardium and inhibit the inflammatory response of the myocardium. To improve the immunity of the body can be used thymidine, gammaglobulin and other drugs.
There are no very effective preventive and curative measures for viral myocarditis, and clinical treatment is still based on comprehensive therapy. Therefore, we emphasize the importance of efforts to reduce the rate of clinical misdiagnosis and early treatment.