Symptoms in eosinophilc myocarditis are highly variable. They tend to reflect the many underlying disorders causing eosinophil dysfunction as well as the widely differing progression rates of cardiac damage. Before cardiac symptoms are detected, some 66% of cases have symptoms of a common cold and 33% have symptoms of asthma, rhinitis, urticarial, or other allergic disorder. Cardiac manifestations of eosinophilic myocarditis range from none to life-threatening conditions such as cardiogenic shock or sudden death due to abnormal heart rhythms. More commonly the presenting cardiac symptoms of the disorder are the same as those seen in other forms of heart disease: chest pain, shortness of breath, fatigue, chest palpitations, light headedness, and syncope. In its most extreme form, however, eosinophilic myocarditis can present as acute necrotizing eosinophilic myocarditis, i.e. with symptoms of chaotic and potentially lethal heart failure and heart arrhythmias. This rarest form of the disorder reflects a rapidly progressive and extensive eosinophilic infiltration of the heart that is accompanied by massive myocardial cell necrosis.

Hypereosinophilia (i.e. blood eosinophil counts at or above 1,500 per microliter) or, less commonly, eosinophilia (counts above 500 but below 1,500 per microliter) are found in the vast majority of cases of eosinophilic myocarditis and are valuable clues that point to this rather than other types of myocarditis or myocardial injuries. However, elevated blood eosinophil counts may not occur during the early phase of the disorder. Other, less specific laboratory findings implicate a cardiac disorder but not necessarily eosinophilic myocarditis. These include elevations in blood markers for systemic inflammation (e.g. C reactive protein, erythrocyte sedimentation rate), elevations in blood markers for cardiac injury (e.g. creatine kinase, troponins); and abnormal electrocardiograms ( mostly ST segment-T wave abnormalities).

Eosinophilic coronary periarteritis is a heart disorder caused by extensive eosinophilic infiltration of the adventitia and periadventitia, i.e. the soft tissues, surrounding the coronary arteries. The intima, tunica media, and tunica intima layers of these arteries remain intact and are generally unaffected. Thus, this disorder is characterized by episodes of angina, particularly Prinzmetal's angina, and sudden death due to heart dysfunction. The disorder is considered distinct from eosinophilic myocarditis.

Among the signs of subacute bacterial endocarditis are:

- Malaise

- Weakness

- Excessive sweat

- Fever

Eosinophilic states that may occur in association with Loeffler endocarditis include hypereosinophilic syndrome, eosinophilic leukemia, carcinoma, lymphoma, drug reactions or parasites, as reported in multiple case series. Hypereosinophilia can be caused by a worm (helminth) that invokes the chronic persistence of these eosinophils, resulting in a condition known as hypereosinophilic syndrome.

The eosinophilia and eosinophilic penetration of the cardiac myocytes leads to a fibrotic thickening of portions of the heart (similar to that of endomyocardial fibrosis). Commonly the heart will develop large mural thrombi (thrombi which lay against ventricle walls) due to the deterioration of left ventricular wall muscle. Symptoms include edema and breathlessness. The disease is commonly contracted in temperate climates (due to the favorable conditions for parasites), and is rapidly fatal.

Endocarditis is an inflammation of the inner layer of the heart, the endocardium. It usually involves the heart valves. Other structures that may be involved include the interventricular septum, the chordae tendineae, the mural endocardium, or the surfaces of intracardiac devices. Endocarditis is characterized by lesions, known as "vegetations", which is a mass of platelets, fibrin, microcolonies of microorganisms, and scant inflammatory cells. In the subacute form of infective endocarditis, the vegetation may also include a center of granulomatous tissue, which may fibrose or calcify.

There are several ways to classify endocarditis. The simplest classification is based on cause: either "infective" or "non-infective", depending on whether a microorganism is the source of the inflammation or not. Regardless, the diagnosis of endocarditis is based on clinical features, investigations such as an echocardiogram, and blood cultures demonstrating the presence of endocarditis-causing microorganisms. Signs and symptoms include fever, chills, sweating, malaise, weakness, anorexia, weight loss, splenomegaly, flu-like feeling, cardiac murmur, heart failure, petechia of anterior trunk, Janeway's lesions, etc.

Infective endocarditis may also be classified as "culture-positive" or "culture-negative". By far the most common cause of a "culture-negative" endocarditis is prior administration of antibiotics.

Sometimes microorganisms can take a longer period of time to grow in the culture media, such organisms are said to be "fastidious" because they have demanding growth requirements. Some examples include pathogens like "Aspergillus" species, "Brucella" species, "Coxiella burnetii", "Chlamydia" species, and HACEK bacteria. Due to delay in growth and identification in these cases, patients may be erroneously classified as "culture-negative" endocarditis.

Historically, infective endocarditis has been clinically divided into "acute" and "subacute" presentations (because untreated patients tended to live longer with the subacute as opposed to the acute form). This classifies both the rate of progression and severity of disease.

- "Subacute bacterial endocarditis" (SBE) is often due to streptococci of low virulence (mainly viridans streptococci) and mild to moderate illness which progresses slowly over weeks and months (>2 weeks) and has low propensity to hematogenously seed extracardiac sites.

- "Acute bacterial endocarditis" (ABE) is a fulminant illness over days to weeks (<2 weeks), and is more likely due to "Staphylococcus aureus" which has much greater virulence, or disease-producing capacity and frequently causes metastatic infection.

This classification is now discouraged, because the ascribed associations (in terms of organism and prognosis) were not strong enough to be relied upon clinically. The terms "short incubation" (meaning less than about six weeks), and "long incubation" (greater than about six weeks) are preferred.

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

- Chest pain (often described as "stabbing" in character)

- Congestive heart failure (leading to swelling, shortness of breath and liver congestion)

- Palpitations (due to abnormal heart rhythms)

- 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 young children tend to be more nonspecific, with generalized malaise, poor appetite, abdominal pain, and chronic cough. Later stages of the illness will present with respiratory symptoms with increased work of breathing, and is often mistaken for asthma.

Since myocarditis is often due to a viral illness, many patients give a history of symptoms consistent with a recent viral infection, including fever, rash, diarrhea, joint pains, and easily becoming tired.

Myocarditis is often associated with pericarditis, and many people with myocarditis present with signs and symptoms that suggest myocarditis and pericarditis at the same time.

Nonbacterial thrombotic endocarditis (NBTE) is most commonly found on previously undamaged valves. As opposed to infective endocarditis, the vegetations in NBTE are small, sterile, and tend to aggregate along the edges of the valve or the cusps. Also unlike infective endocarditis, NBTE does not cause an inflammation response from the body. NBTE usually occurs during a hypercoagulable state such as system-wide bacterial infection, or pregnancy, though it is also sometimes seen in patients with venous catheters. NBTE may also occur in patients with cancers, particularly mucinous adenocarcinoma where Trousseau syndrome can be encountered. Typically NBTE does not cause many problems on its own, but parts of the vegetations may break off and embolize to the heart or brain, or they may serve as a focus where bacteria can lodge, thus causing infective endocarditis.

Another form of sterile endocarditis is termed Libman–Sacks endocarditis; this form occurs more often in patients with lupus erythematosus and is thought to be due to the deposition of immune complexes. Like NBTE, Libman-Sacks endocarditis involves small vegetations, while infective endocarditis is composed of large vegetations. These immune complexes precipitate an inflammation reaction, which helps to differentiate it from NBTE. Also unlike NBTE, Libman-Sacks endocarditis does not seem to have a preferred location of deposition and may form on the undersurfaces of the valves or even on the endocardium.

Subacute bacterial endocarditis (also called endocarditis lenta) is a type of endocarditis (more specifically, infective endocarditis). Subacute bacterial endocarditis can be considered a form of type III hypersensitivity.

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.

Myocarditis, also known as inflammatory cardiomyopathy, is inflammation of the heart muscle. Symptoms can include shortness of breath, chest pain, decreased ability to exercise, and an irregular heartbeat. The duration of problems can vary from hours to months. Complications may include heart failure due to dilated cardiomyopathy or cardiac arrest.

Myocarditis is most often due to a viral infection. Other causes include bacterial infections, certain medications, toxins, and autoimmune disorders. A diagnosis may be supported by an electrocardiogram (ECG), increased troponin, heart MRI, and occasionally a heart biopsy. An ultrasound of the heart is important to rule out other potential causes such as heart valve problems.

Treatment depends on both the severity and the cause. Medications such as ACE inhibitors, beta blockers, and diuretics are often used. A period of no exercise is typically recommended during recovery. Corticosteroids or intravenous immunoglobulin (IVIG) may be useful in certain cases. In severe cases an implantable cardiac defibrillator or heart transplant may be recommended.

In 2013, about 1.5 million cases of acute myocarditis occurred. While people of all ages are affected, the young are most often affected. It is slightly more common in males than females. Most cases are mild. In 2015 cardiomyopathy, including myocarditis, resulted in 354,000 deaths up from 294,000 in 1990. The initial descriptions of the condition are from the mid-1800s.

These are the typical mechanisms of autoimmunity. Autoantibodies or auto-toxic T-lymphocyte mediated tissue destruction. The process is aided by neutrophils, the complement system, tumor necrosis factor alpha, etc.

Aetiologically, these are most commonly seen in children with a history of sore throat caused by a streptococcal infection. This is similar to the post-streptococcal glomerulonephritis. Here, the anti-bacterial antibodies cross react with the heart antigens causing inflammation.

Inflammatory damage leads to the following:

- Pericarditis: Here the pericardium gets inflamed. Acutely, it can cause pericardial effusion leading to cardiac tamponade and death. After healing, there may be fibrosis and adhesion of the pericardium with the heart leading to constriction of the heart and reduced cardiac function.

- Myocarditis: Here the muscle bulk of the heart gets inflamed. Inflamed muscles have reduced functional capacity. This may be fatal, if left untreated as is in a case of pancarditis. On healing, there will be fibrosis and reduced functional capacity.

- Endocarditis: Here the inner lining of the heart is inflamed, including the heart valves. This may cause a valve prolapse, adhesion of the adjacent cusps of these valves and occlusion of the flow tracts of blood through the heart causing diseases called valve stenosis.

Loeffler endocarditis is a form of restrictive cardiomyopathy which affects the endocardium and occurs with white blood cell proliferation, specifically of eosinophils. Restrictive cardiomyopathy is defined as a disease of the heart muscle which results in impaired filling of the heart ventricles during diastole.

The vegetations are small and formed from strands of fibrin, neutrophils, lymphocytes, and histiocytes. The mitral valve is typically affected, and the vegetations occur on the ventricular and atrial surface of the valve. Libman–Sacks lesions rarely produce significant valve dysfunction and the lesions only rarely embolize. However, there is data to suggest an association between Libman–Sacks endocarditis and a higher risk for embolic cerebrovascular disease in people with systemic lupus erythematosus (SLE).

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

Libman–Sacks endocarditis (often misspelled Libmann–Sachs) is a form of nonbacterial endocarditis that is seen in association with systemic lupus erythematosus. It is one of the most common heart-related manifestations of lupus (the most common being pericarditis - inflammation of the fibrous sac surrounding the heart).

It was first described by Emanuel Libman and Benjamin Sacks at Mount Sinai Hospital in New York City in 1924. The association between Libman–Sacks endocarditis and antiphospholipid syndrome was first noted in 1985.

The disease affects the valves with the following predilection: mitral valve > aortic valve > tricuspid valve > pulmonary valve

Grossly, vegetations form along lines of valve closure and are generally symmetric with a smooth or verrucoid (warty) texture. Histologically, lesions are composed of fibrin (eosinophilic) and platelets but, unlike bacterial etiologies, contain little evidence of PMNs, microorganisms or inflammation.

Löffler's syndrome or Loeffler's syndrome is a disease in which eosinophils accumulate in the lung in response to a parasitic infection.

It was first described in 1932 by Wilhelm Löffler in cases of eosinophilic pneumonia caused by the parasites "Ascaris lumbricoides", "Strongyloides stercoralis" and the hookworms "Ancylostoma duodenale" and "Necator americanus".

Although Löffler only described eosinophilic pneumonia in the context of infection, many authors give the term "Löffler's syndrome" to any form of acute onset pulmonary eosinophilia no matter what the underlying cause. If the cause is unknown, it is specified and called "simple pulmonary eosinophilia". Cardiac damage caused by the damaging effects of eosinophil granule proteins (ex. major basic protein) is known as Loeffler endocarditis and can be caused by idiopathic eosinophilia or eosinophilia in response to parasitic infection.

Some clinical examples:

Other examples are:

- Subacute bacterial endocarditis

- Symptoms of malaria

Possible symptoms include:

- General symptoms: Fever, weight loss

- Skin: Palpable purpura, livedo reticularis

- Muscles and joints: Myalgia or myositis, arthralgia or arthritis

- Nervous system: Mononeuritis multiplex, headache, stroke, tinnitus, reduced visual acuity, acute visual loss

- Heart and arteries: Myocardial infarction, hypertension, gangrene

- Respiratory tract: Nose bleeds, bloody cough, lung infiltrates

- GI tract: Abdominal pain, bloody stool, perforations

- Kidneys: Glomerulonephritis

Eosinophilia is a condition in which the eosinophil count in the peripheral blood exceeds . Eosinophils usually account for less than 7% of the circulating leukocytes. A marked increase in non-blood tissue eosinophil count noticed upon histopathologic examination is diagnostic for tissue eosinophilia. Several causes are known, with the most common being some form of allergic reaction or parasitic infection. Diagnosis of eosinophilia is via a complete blood count (CBC), but diagnostic procedures directed at the underlying cause vary depending on the suspected condition(s). An absolute eosinophil count is not generally needed if the CBC shows marked eosinophilia. The location of the causal factor can be used to classify eosinophilia into two general types: extrinsic, in which the factor lies outside the eosinophil cell lineage; and intrinsic eosinophilia, which denotes etiologies within the eosiniphil cell line. Specific treatments are dictated by the causative condition, though in idiopathic eosinophilia, the disease may be controlled with corticosteroids. Eosinophilia is not a disorder (rather, only a sign) unless it is idiopathic.

Type III hypersensitivity occurs when there is accumulation of immune complexes (antigen-antibody complexes) that have not been adequately cleared by innate immune cells, giving rise to an inflammatory response and attraction of leukocytes. Such reactions progressing to the point of disease produce immune complex diseases.

Bilateral hilar lymphadenopathy is a bilateral enlargement of the lymph nodes of pulmonary hila. It is a radiographic term that describes the enlargement of mediastinal lymph nodes and is most commonly identified by a chest x-ray.