Myocarditis refers to an underlying process that causes inflammation and injury of the heart. It does not refer to inflammation of the heart as a consequence of some other insult. Many secondary causes, such as a heart attack, can lead to inflammation of the myocardium and therefore the diagnosis of myocarditis cannot be made by evidence of inflammation of the myocardium alone.

Myocardial inflammation can be suspected on the basis of electrocardiographic (ECG) results, elevated C-reactive protein (CRP) and/or erythrocyte sedimentation rate (ESR), and increased IgM (serology) against viruses known to affect the myocardium. Markers of myocardial damage (troponin or creatine kinase cardiac isoenzymes) are elevated.

The ECG findings most commonly seen in myocarditis are diffuse T wave inversions; saddle-shaped ST-segment elevations may be present (these are also seen in pericarditis).

The gold standard is still biopsy of the myocardium, in general done in the setting of angiography. A small tissue sample of the endocardium and myocardium is taken, and investigated by a pathologist by light microscopy and—if necessary—immunochemistry and special staining methods. Histopathological features are myocardial interstitium with abundant edema and inflammatory infiltrate, rich in lymphocytes and macrophages. Focal destruction of myocytes explains the myocardial pump failure.

Cardiac magnetic resonance imaging (cMRI or CMR) has been shown to be very useful in diagnosing myocarditis by visualizing markers for inflammation of the myocardium.

Recently, consensus criteria for the diagnosis of myocarditis by CMR have been published.

Studies have shown no benefit for the use of herbal medicine on all cause mortality in viral myocarditis.

Intensive cardiac care and immunosuppressives including corticosteroids are helpful in the acute stage of the disease. Chronic phase has, mainly debility control and supportive care options.

In eosinophilic myocarditis, echocardiography typically gives non-specific and only occasional findings of endocardium thickening, left ventricular hypertrophy, left ventricle dilation, and involvement of the mitral and/or tricuspid valves. However, in acute necrotizing eosinophilic myocarditis, echocardiography usually gives diagnostically helpful evidence of a non-enlarged heart with a thickened and poorly contracting left ventricle. Gadolinium-based cardiac magnetic resonance imaging is the most useful non-invasive procedure for diagnosing eosinophilic myocarditis. It supports this diagnosis if it shows at least two of the following abnormalities: a) an increased signal in T2-weighted images; b) an increased global myocardial early enhancement ratio between myocardial and skeletal muscle in enhanced T1 images and c) one or more focal enhancements distributed in a non-vascular pattern in late enhanced T1-weighted images. Additionally, and unlike in other forms of myocarditis, eosinophilic myocarditis may also show enhanced gadolinium uptake in the sub-endocardium. However, the only definitive test for eosinophilic myocarditis in cardiac muscle biopsy showing the presence of eosinophilic infiltration. Since the disorder may be patchy, multiple tissue samples taken during the procedure improve the chances of uncovering the pathology but in any case negative results do not exclude the diagnosis.

These depend on the amount of inflammation. These are covered in their relevant articles.

- Acute: Heart failure; pericardial effusion; etc.

- Chronic: Valve diseases as noted above; Reduced cardiac output; Exercise intolerance.

The prognosis of eosinophilic myocarditis is anywhere from rapidly fatal to extremely chronic or non-fatal. Progression at a moderate rate over many months to years is the most common prognosis. In addition to the speed of inflammation-based heart muscle injury, the prognosis of eosinophilc myocarditis may be dominated by that of its underlying cause. For example, an underlying malignant cause for the eosinophilia may be survival-limiting.

About 30% of people with viral pericarditis or pericarditis of an unknown cause have one or several recurrent episodes.

Depending on the time of presentation and duration, pericarditis is divided into "acute" and "chronic" forms. Acute pericarditis is more common than chronic pericarditis, and can occur as a complication of infections, immunologic conditions, or even as a result of a heart attack (myocardial infarction). Chronic pericarditis however is less common, a form of which is constrictive pericarditis. The following is the clinical classification of acute vs. chronic:

- "Clinically": Acute (6 months)

Screening ECGs (either at rest or with exercise) are not recommended in those without symptoms who are at low risk. This includes those who are young without risk factors. In those at higher risk the evidence for screening with ECGs is inconclusive.

Additionally echocardiography, myocardial perfusion imaging, and cardiac stress testing is not recommended in those at low risk who do not have symptoms.

Some biomarkers may add to conventional cardiovascular risk factors in predicting the risk of future cardiovascular disease; however, the clinical value of some biomarkers is questionable.

The NIH recommends lipid testing in children beginning at the age of 2 if there is a family history of heart disease or lipid problems. It is hoped that early testing will improve lifestyle factors in those at risk such as diet and exercise.

Screening and selection for primary prevention interventions has traditionally been done through absolute risk using a variety of scores (ex. Framingham or Reynolds risk scores). This stratification has separated people who receive the lifestyle interventions (generally lower and intermediate risk) from the medication (higher risk). The number and variety of risk scores available for use has multiplied, but their efficacy according to a 2016 review was unclear due to lack of external validation or impact analysis. Risk stratification models often lack sensitivity for population groups and do not account for the large number of negative events among the intermediate and low risk groups. As a result, future preventative screening appears to shift toward applying prevention according to randomized trial results of each intervention rather than large-scale risk assessment.

About 10% of people who present a clinical picture of infectious mononucleosis do not have an acute Epstein–Barr-virus infection. A differential diagnosis of acute infectious mononucleosis needs to take into consideration acute cytomegalovirus infection and "Toxoplasma gondii" infections. Because their management is much the same, it is not always helpful, or possible, to distinguish between Epstein–Barr-virus mononucleosis and cytomegalovirus infection. However, in pregnant women, differentiation of mononucleosis from toxoplasmosis is important, since it is associated with significant consequences for the fetus.

Acute HIV infection can mimic signs similar to those of infectious mononucleosis, and tests should be performed for pregnant women for the same reason as toxoplasmosis.

People with infectious mononucleosis are sometimes misdiagnosed with a streptococcal pharyngitis (because of the symptoms of fever, pharyngitis and adenopathy) and are given antibiotics such as ampicillin or amoxicillin as treatment.

Other conditions from which to distinguish infectious mononucleosis include leukemia, tonsillitis, diphtheria, common cold and influenza (flu).

The heterophile antibody test works by agglutination of red blood cells from guinea pig, sheep and horse. This test is specific but not particularly sensitive (with a false-negative rate of as high as 25% in the first week, 5–10% in the second, and 5% in the third). About 90% of patients have heterophile antibodies by week 3, disappearing in under a year. The antibodies involved in the test do not interact with the Epstein–Barr virus or any of its antigens.

The monospot test is not recommended for general use by the CDC due to its poor accuracy.

Diagnosis is usually based on serology (looking for an antibody response) rather than looking for the organism itself. Serology allows the detection of chronic infection by the appearance of high levels of the antibody against the virulent form of the bacterium. Molecular detection of bacterial DNA is increasingly used. Culture is technically difficult and not routinely available in most microbiology laboratories.

Q fever can cause endocarditis (infection of the heart valves) which may require transoesophageal echocardiography to diagnose. Q fever hepatitis manifests as an elevation of alanine transaminase and aspartate transaminase, but a definitive diagnosis is only possible on liver biopsy, which shows the characteristic fibrin ring granulomas.

Mortality in HIV-infected patients with cardiomyopathy is increased independently of CD4 count, age, sex, and HIV risk group.

The therapy is similar to therapy for non-ischemic cardiomyopathy: after medical therapy is begun, serial echocardiographic studies should be performed at 4-months intervals. If function continues to worsen or the clinical course deteriorates, a biopsy should be considered.

HAART has reduced the incidence of myocarditis thus reducing the prevalence of HIV-associated cardiomyopathy by about 30% in developed countries. However, the prevalence in developing countries is 32% and increasing as HAART is scarce – not to mention the effects of other risk factors such as high cholesterol and lipid diet. IVIGs can also help patients with HIV-associated myocarditis as mentioned earlier.

On infection the microorganism can be found in blood and cerebrospinal fluid (CSF) for the first 7 to 10 days (invoking serologically identifiable reactions) and then moving to the kidneys. After 7 to 10 days the microorganism can be found in fresh urine. Hence, early diagnostic efforts include testing a serum or blood sample serologically with a panel of different strains.

Kidney function tests (blood urea nitrogen and creatinine) as well as blood tests for liver functions are performed. The latter reveal a moderate elevation of transaminases. Brief elevations of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and gamma-glutamyltransferase (GGT) levels are relatively mild. These levels may be normal, even in children with jaundice.

Diagnosis of leptospirosis is confirmed with tests such as enzyme-linked immunosorbent assay (ELISA) and polymerase chain reaction (PCR). The MAT (microscopic agglutination test), a serological test, is considered the gold standard in diagnosing leptospirosis. As a large panel of different leptospira must be subcultured frequently, which is both laborious and expensive, it is underused, especially in developing countries.

Differential diagnosis list for leptospirosis is very large due to diverse symptoms. For forms with middle to high severity, the list includes dengue fever and other hemorrhagic fevers, hepatitis of various causes, viral meningitis, malaria, and typhoid fever. Light forms should be distinguished from influenza and other related viral diseases. Specific tests are a must for proper diagnosis of leptospirosis.

Under circumstances of limited access (e.g., developing countries) to specific diagnostic means, close attention must be paid to the medical history of the patient. Factors such as certain dwelling areas, seasonality, contact with stagnant contaminated water (bathing, swimming, working on flooded meadows, etc.) or rodents in the medical history support the leptospirosis hypothesis and serve as indications for specific tests (if available).

"Leptospira" can be cultured in Ellinghausen-McCullough-Johnson-Harris medium (EMJH), which is incubated at 28 to 30 °C. The median time to positivity is three weeks with a maximum of three months. This makes culture techniques useless for diagnostic purposes but is commonly used in research.

A physical examination will demonstrate many of the features listed above.

Blood tests

- Complete blood count may reveal normocytic anemia and eventually thrombocytosis.

- Erythrocyte sedimentation rate will be elevated.

- C-reactive protein will be elevated.

- Liver function tests may show evidence of hepatic inflammation and low serum albumin levels.

Other optional tests include:

- Electrocardiogram may show evidence of ventricular dysfunction or, occasionally, arrhythmia due to myocarditis.

- Echocardiogram may show subtle coronary artery changes or, later, true aneurysms.

- Ultrasound or computerized tomography may show hydrops (enlargement) of the gallbladder.

- Urinalysis may show white blood cells and protein in the urine (pyuria and proteinuria) without evidence of bacterial growth.

- Lumbar puncture may show evidence of aseptic meningitis.

- Angiography was historically used to detect coronary artery aneurysms, and remains the gold standard for their detection, but is rarely used today unless coronary artery aneurysms have already been detected by echocardiography.

- Temporal artery biopsy

Carditis is the inflammation of the heart or its surroundings. The plural of carditis is carditides.

It is usually studied and treated by specifying it as:

- Pericarditis is the inflammation of the pericardium

- Myocarditis is the inflammation of the heart muscle

- Endocarditis is the inflammation of the endocardium

- Pancarditis is the inflammation of the entire heart: the epicardium, the myocardium and the endocardium

- Reflux carditis refers to a possible outcome of esophageal reflux (also known as GERD), and involves inflammation of the esophagus/stomach mucosa

Blood tests routinely performed include electrolytes (sodium, potassium), measures of kidney function, liver function tests, thyroid function tests, a complete blood count, and often C-reactive protein if infection is suspected. An elevated B-type natriuretic peptide (BNP) is a specific test indicative of heart failure. Additionally, BNP can be used to differentiate between causes of dyspnea due to heart failure from other causes of dyspnea. If myocardial infarction is suspected, various cardiac markers may be used.

According to a meta-analysis comparing BNP and N-terminal pro-BNP (NTproBNP) in the diagnosis of heart failure, BNP is a better indicator for heart failure and left ventricular systolic dysfunction. In groups of symptomatic patients, a diagnostic odds ratio of 27 for BNP compares with a sensitivity of 85% and specificity of 84% in detecting heart failure.

Many cases of croup have been prevented by immunization for influenza and diphtheria. At one time, croup referred to a diphtherial disease, but with vaccination, diphtheria is now rare in the developed world.

Chest X-rays are frequently used to aid in the diagnosis of CHF. In a person who is compensated, this may show cardiomegaly (visible enlargement of the heart), quantified as the cardiothoracic ratio (proportion of the heart size to the chest). In left ventricular failure, there may be evidence of vascular redistribution ("upper lobe blood diversion" or "cephalization"), Kerley lines, cuffing of the areas around the bronchi, and interstitial edema. Ultrasound of the lung may also be able to detect Kerley lines.

A wide variety of treatment modalities are currently recommended including Immunosuppressive agents, intravenous immunoglobulins (IVIG), and antiviral agents although the effectiveness of these treatments are not well established and no specific treatment is available.

Myopericarditis is a combination of both myocarditis and pericarditis appearing in a single individual, namely inflammation of both the pericardium and the heart muscle. It can involve the presence of fluid in the heart. Myopericarditis refers primarily to a pericarditis with lesser myocarditis, as opposed to a perimyocarditis, though the two terms are often used interchangeably. Both will be reflected on an ECG. Myo-pericarditis usually involves inflammation of the pericardium, or the sac covering the heart.

The ACAM2000 smallpox vaccine has been known to cause myopericarditis in some people.

Inflammation, or vasculitis of the arteries and veins occurs throughout the body. This is usually caused by increased production of the cells of the immune system to a pathogen, or autoimmunity. Systemic vasculitides may be classified according to the type of cells involved in the proliferation, as well as the specific type of tissue damage occurring within the vein or arterial walls. Under this classification scheme for systemic vasculitis, Kawasaki disease is considered to be a necrotizing vasculitis (also called necrotizing angiitis), which may be identified histologically by the occurrence of necrosis (tissue death), fibrosis, and proliferation of cells associated with inflammation in the inner layer of the vascular wall.

Other diseases featuring necrotizing vasculitis include polyarteritis nodosa, granulomatosis with polyangiitis (GPA), Henoch–Schönlein purpura and eosinophilic granulomatosis with polyangiitis (EGPA).

Kawasaki disease may be further classified as a medium-sized-vessel vasculitis, affecting medium- and small-sized blood vessels, such as the smaller cutaneous vasculature (veins and arteries in the skin) that range from 50 to 100 µm in diameter. Kawasaki disease is also considered to be a primary childhood vasculitis, a disorder associated with vasculitis that mainly affects children under the age of 18. A recent, consensus-based evaluation of vasculitides occurring primarily in children resulted in a classification scheme for these disorders, to distinguish them and suggest a more concrete set of diagnostic criteria for each. Within this classification of childhood vasculitides, Kawasaki disease is, again, a predominantly medium-sized vessel vasculitis.

It is also an autoimmune form of vasculitis, and is not associated with ANCA antibodies, unlike other vasculitic disorders associated with them (such as granulomatosis with polyangiitis, microscopic polyangiitis and eosinophilic granulomatosis with polyangiitis). This categorization is considered essential for appropriate treatment.

Protection is offered by Q-Vax, a whole-cell, inactivated vaccine developed by an Australian vaccine manufacturing company, CSL Limited. The intradermal vaccination is composed of killed "C. burnetii" organisms. Skin and blood tests should be done before vaccination to identify pre-existing immunity, because vaccinating people who already have an immunity can result in a severe local reaction. After a single dose of vaccine, protective immunity lasts for many years. Revaccination is not generally required. Annual screening is typically recommended.

In 2001, Australia introduced a national Q fever vaccination program for people working in “at risk” occupations. Vaccinated or previously exposed people may have their status recorded on the Australian Q Fever Register, which may be a condition of employment in the meat processing industry. An earlier killed vaccine had been developed in the Soviet Union, but its side effects prevented its licensing abroad.

Preliminary results suggest vaccination of animals may be a method of control. Published trials proved that use of a registered phase vaccine (Coxevac) on infected farms is a tool of major interest to manage or prevent early or late abortion, repeat breeding, anoestrus, silent oestrus, metritis, and decreases in milk yield when "C. burnetii" is the major cause of these problems.

The current clinical case definition of diphtheria used by the United States' Centers for Disease Control and Prevention is based on both laboratory and clinical criteria.

Among the diagnostic procedures done to determine a cardiomyopathy are:

- Physical exam

- Family history

- Blood test

- EKG

- Echocardiogram

- Stress test

- Genetic testing