What is myocarditis?

Myocarditis is inflammation or degeneration of the heart muscle. Myocarditis may be a complication during or after various viral, bacterial, or parasitic infectious diseases, such as polio, influenza, rubella, or rheumatic fever. Myocarditis is often caused by various diseases such as syphilis, goiter, endocarditis, or hypertension, however, myocarditis may appear as a primary disease in adults or as a degenerative disease of old age.
Myocarditis may be associated with dilation (enlargement due to weakness of the heart muscle) or with hypertrophy (overgrowth of the muscle tissue). Individuals who smoke cigarettes have a higher mortality and risk of myocardial infarction than individuals who do not smoke.
In some cases of myocarditis may progress to congestive heart failure, requiring hospitalization, heart failure medications, or cardiac transplantation.

Cause of Myocarditis


Myocarditis is a caused by inflammation of the muscle of the heart. Although a variety of medical conditions can cause myocarditis, the most common cause is infection by viruses. Enteroviruses are recognized as the most common cause of myocarditis. Over many years, a chronic enterovirus heart infection and the body’s response to that infection in the heart can lead to irreversible heart muscle damage and heart failure.

Frequency

In United States

Frequency is difficult to ascertain, owing to the wide variation of clinical presentation. Incidence is usually estimated at 1-10 cases per 100,000 persons. Incidence of positive right ventricular biopsy findings in patients with suspected myocarditis is highly variable (ranging from 0-80%). According to estimates, as many as 1-5% of patients with acute viral infections may have involvement of the myocardium.

Diagnosis myocarditis

Laboratory Studies

• Complete blood count - Leukocytosis (may demonstrate eosinophilia)
• Elevated erythrocyte sedimentation rate (and other acute phase reactants such as C-reactive protein)
• Rheumatologic screening - To rule out systemic inflammatory diseases
• Elevated cardiac enzymes (creatine kinase or cardiac troponins)
  • These are an indicator for cardiac myonecrosis. Cardiac troponin (troponin I or T), in particular, is elevated in at least 50% of patients with biopsy-proven myocarditis. They may also help identify those with resolution of viral myocarditis.
  • The test has 89% specificity and 34% sensitivity and increases more frequently than creatine kinase MB subunits (elevated in only 5.7% of patients with biopsy-proven myocarditis).
• Serum viral antibody titers for viral myocarditis
  
  • Common viral antibody titers available for clinical evaluation include coxsackievirus group B, HIV, cytomegalovirus, Ebstein-Barr virus, hepatitis virus family, and influenza viruses. Titers increase 4-fold or more with gradual fall during convalescence (nonspecific), hence requiring serial testing.
  • Antibody titer test is rarely indicated in the diagnosis of viral myocarditis or any dilated cardiomyopathies, owing to its low specificity and the delay of rising viral titers, which would have no impact on therapeutic decisions.
  • The presence of viral genome in endomyocardial biopsy samples have been sought to be the criterion standard for viral persistence; however, it lacks specificity as the presence of viral genome can also be present in healthy controls. The most common viral genomes found include parvovirus and herpes simplex.

Imaging Studies

• Echocardiography: This is performed to exclude other causes of heart failure (eg, valvular, amyloidosis, congenital) and to evaluate the degree of cardiac dysfunction (usually diffuse hypokinesis and diastolic dysfunction). It also may allow gross localization of the extent of inflammation (ie, wall motion abnormalities, wall thickening, pericardial effusion). In addition, echocardiography may distinguish between fulminant and acute myocarditis by identifying near-normal left ventricular diastolic dimensions and increased septal thickness in fulminant myocarditis (versus increased left ventricular diastolic dimensions and normal septal thickness in acute myocarditis), with marked improvement in systolic function in time.
• Cardiac angiography: This is often indicated to rule out coronary ischemia as a cause of new-onset heart failure, especially when clinical presentation mimics acute myocardial infarction. It usually shows high filling pressures and reduced cardiac outputs.
• Gadolinium-enhanced magnetic resonance imaging (MRI): This imaging technique is used for assessment of the extent of inflammation and cellular edema, although it is still nonspecific. Delayed-enhanced MRI has also been used to quantify the amount of scarring that occurred following acute myocarditis.
• Nuclear imaging: Antimyosin scintigraphy (using antimyosin antibody injections) can identify myocardial inflammation with high sensitivity (91-100%) and negative predictive power (93-100%) but has low specificity (31-44%) and low positive predictive power (28-33%). In contrast, gallium scanning is used to reflect severe myocardial cellular infiltration and has a good negative predictive value, although specificity is low. Positron emission tomography (PET) scanning has been used in selected cases (eg, sarcoidosis) to assess the degree and location of inflammation.

Other Tests

• Electrocardiogram - Often nonspecific (eg, sinus tachycardia, nonspecific ST or T-wave changes)
  • Occasionally, heart block (atrioventricular block or intraventricular conduction delay), ventricular arrhythmia, or injury patterns with ST- or T-wave changes mimicking myocardial ischemia or pericarditis (pseudoinfarction pattern) may indicate poorer prognosis.
  • Arrhythmia is common in Chagas heart disease. The following may be seen: right bundle-branch block with or without bifascicular block (50%), complete heart block (7-8%), atrial fibrillation (7-10%), and ventricular arrhythmia (39%).

Procedures

• Endomyocardial biopsy (EMB): This is the criterion standard for diagnosis of myocarditis, although it still has limited sensitivity and specificity, as inflammation can be diffuse or focal. Routine EMB in establishing diagnosis of myocarditis rarely is helpful clinically, however, since histologic diagnosis seldom has an impact on therapeutic strategies, unless giant cell myocarditis is suspected.The risk of adverse events approaches 6% (including complications with 2.7% on sheath insertion and 3.3% on the biopsy procedure), including 0.5% probability of perforation.
• Because of sampling technique, sensitivity may increase with multiple biopsies (50% for 1 biopsy, 90% for 7 biopsies). The standard is to obtain at least 4 or 5 biopsies, although false-negative rates still may be as high as 55%.
• False-positive rates are also high, owing to small numbers of normally occurring lymphocytes in the myocardium and the difficulty in distinguishing between lymphocytes and other cells (such as eosinophils in hypersensitive/eosinophilic myocarditis).
• Wide interobserver variability in histologic interpretations is also a factor.
• Noncaseating granulomas for sarcoid myocarditis are found in only 5% of cases by biopsies, and in as many as 27% in autopsy series.
• Persisting viral mRNA can be found in only 25-50% of patients with biopsy-proven acute myocarditis, and persistent viral mRNA often confers a poor prognosis. Recent epidemiological results from the European Study on the Epidemiology and Treatment of Cardiac Inflammatory Disease (ESETCID) database found that only 11.8% of patients with suspected acute or chronic myocarditis and reduced ejection fractions had detectable viral genomes in biopsy samples.

Histologic Findings

Biopsy specimens from EMB should reveal the simultaneous findings of lymphocyte infiltration and myocyte necrosis.

Staging

The Dallas classification (1987) and the World Health Organization (WHO) Marburg classification (1996) are commonly used.

• Cell types - Lymphocytic, eosinophilic, neutrophilic, giant cell, granulomatous, or mixed
• Amount - None (grade 0), mild (grade 1), moderate (grade 2), or severe (grade 3)
• Distribution - Focal (outside vessel lumen), confluent, diffuse, or reparative (in fibrotic areas)
• Dallas classification (1987)
  • Initial biopsy
    • Myocarditis - Myocardial necrosis, degeneration, or both, in the absence of significant coronary artery disease with adjacent inflammatory infiltrate with or without fibrosis
    • Borderline myocarditis - Inflammatory infiltrate too sparse or myocyte damage not apparent
    • No myocarditis
  • Subsequent biopsy
    • Ongoing (persistent) myocarditis with or without fibrosis
    • Resolving (healing) myocarditis with or without fibrosis
    • Resolved (healed) myocarditis with or without fibrosis
• WHO Marburg criteria (1996) defines myocarditis as a minimum of 14 infiltrating leukocytes/mm², preferably T cells (CD45RO), with as many as 4 macrophages possibly included.

Fight with myocarditis

There is no cure for myocarditis, although the heart muscle inflammation usually goes away on its own in time.

The goal of treatment is to support heart function and treat the underlying cause of the myocarditis. Most children with this condition are admitted to a hospital. Activity can strain the heart and therefore is often limited.

Treatment may include:

• Antibiotics to fight infection
• Anti-inflammatory medicines called steroids to control inflammation
• Intravenous immunoglobulin (IVIG), a medicine made of substances that the body produces to fight infection, to control the inflammatory process
• Medicines called diuretics to remove excess water from the body
• Medicines to treat heart failure and abnormal heart rhythms

Approximately 50% of the time, myocarditis is classified as idiopathic, although the aforementioned report by Klugman et al found that 82% of the pediatric cases studied were considered idiopathic.The investigators also determined that 3% of cases in the study had a known bacterial or viral etiology, and that 6% of cases were related to other diseases.

In idiopathic cases, a viral etiology is often suspected but unproved, even with sophisticated immunohistochemical and genomic studies. Studies on patients with idiopathic dilated cardiomyopathy found evidence of viral particles in endomyocardial biopsy specimens in up to two thirds of the patients. 

• Viral - Enterovirus coxsackie B, adenovirus, influenza, cytomegalovirus, poliomyelitis, Epstein-Barr virus, HIV-1, viral hepatitis, mumps, rubeola, varicella, variola/vaccinia, arbovirus, respiratory syncytial virus, herpes simplex virus, yellow fever virus, rabies, parvovirus
• Rickettsial - Scrub typhus, Rocky Mountain spotted fever, Q fever
• Bacterial - Diphtheria, tuberculosis, streptococci, meningococci, brucellosis, clostridia, staphylococci, melioidosis, Mycoplasma pneumoniae, psittacosis
• Spirochetal - Syphilis, leptospirosis/Weil disease, relapsing fever/Borrelia, Lyme disease
• Fungal - Candidiasis, aspergillosis, cryptococcosis, histoplasmosis, actinomycosis, blastomycosis, coccidioidomycosis, mucormycosis
• Protozoal - Chagas disease, toxoplasmosis, trypanosomiasis, malaria, leishmaniasis, balantidiasis, sarcosporidiosis
• Helminthic - Trichinosis, echinococcosis, schistosomiasis, heterophyiasis, cysticercosis, visceral larva migrans, filariasis
• Bites/stings - Scorpion venom, snake venom, black widow spider venom, wasp venom, tick paralysis
• Drugs (usually causing hypersensitivity myocarditis)
  • Chemotherapeutic drugs - Doxorubicin and anthracyclines, streptomycin, cyclophosphamide, interleukin-2, anti-HER-2 receptor antibody/Herceptin
  • Antibiotics - Penicillin, chloramphenicol, sulfonamides
  • Antihypertensive drugs - Methyldopa, spironolactone
  • Antiseizure drugs - Phenytoin, carbamazepine
  • Amphetamines, cocaine, catecholamines
• Chemicals - Hydrocarbons, carbon monoxide, arsenic, lead, phosphorus, mercury, cobalt
• Physical agents (radiation, heatstroke, hypothermia)
• Acute rheumatic fever
• Systemic inflammatory disease - Giant cell myocarditis, sarcoidosis, Kawasaki disease, Crohn disease, systemic lupus erythematosus, ulcerative colitis, Wegener granulomatosis, thyrotoxicosis, scleroderma, rheumatoid arthritis
• Peripartum cardiomyopathy
• Posttransplant cellular rejection

What is myocarditis?

Hi there, i want to talk here about myocarditis. What is that? How can we fight with it... You can find a lot of information about myocarditis in my blog. Let's Go.

In medicine (cardiology), myocarditis is inflammation of heart muscle (myocardium). It resembles a heart attack but coronary arteries are not blocked.

Myocarditis is most often due to infection by common viruses, such as parvovirus B19, less commonly non-viral pathogens such as Borrelia burgdorferi (Lyme disease) or Trypanosoma cruzi, or as a hypersensitivity response to drugs.


The consequences of myocarditis thus also vary widely. It can cause a mild disease without any symptoms that resolves itself, or it may cause chest pain, heart failure, or sudden death. An acute myocardial infarction-like syndrome with normal coronary arteries has a good prognosis. Heart failure, even with dilated left ventricle, may have a good prognosis. Ventricular arrhythmias and high-degree heart block have a poor prognosis. Loss of right ventricular function is a strong predictor of death.




Let's talk about singns and symptoms 


The signs and symptoms associated with myocarditis are varied, and relate either to the actual inflammation of the myocardium, or the weakness of the heart muscle that is secondary to the inflammation. Signs and symptoms of myocarditis include:

• Chest pain (often described as "stabbing" in character)
• Congestive heart failure (leading to edema, breathlessness and hepatic congestion)
• Palpitations (due to arrhythmias)
• Sudden death (in young adults, myocarditis causes up to 20% of all cases of sudden death)
• Fever (especially when infectious, e.g. in rheumatic fever)

Symptoms in infants and toddlers tend to be more non-specific with generalized malaise, poor appetite, abdominal pain, chronic cough. Later stages of the illness will present with respiratory symptoms with increased work of breathing and is often mistaken for asthma.

Ok, it's my first post so see you next time.