Classification of myocarditis and ICMP is not stabilized so far and develops with increasing knowledge about aetiology and pathogenesis of the disease. There are several classifications which may be combined.

The most commonly used classification is so-called clinical-pathological evaluation combining histopathological findings with the clinical course of the disease. According to the duration, myocarditis is usually classified in acute and chronic form, however, some authors replaced term chronic myocarditis with the term ICMP

Perimyocarditis is a term used for myocarditis connected with the inflammation of the pericardium.

ICMP itself does not have any specific classification. It is mostly classified on the grounds of the EMB results, thus according to the presence or absence of the agent and inflammation



It is an uncommon form of myocarditis which is characterized by a fast progression of the disease. Patients present with acute heart failure and sometimes even with cardiogenic shock and a rapid decrease of the left ventricular ejection fraction may be observed.

Acute myocarditis is a “classical” form of myocarditis which differs from fulminant myocarditis in the milder initial course of the disease and often in the slower manifestation of symptoms. The myocarditis itself usually manifests according to the resources with heart failure, arrhythmias or chest pain mimicking acute coronary syndrome

It is a long-term damage to the myocardium with inflammatory processes. In the case that this process is connected with the systolic dysfunction and dilatation of the left ventricle, it is called ICMP.



Eosinophilic myocarditis is a rare type of myocarditis usually caused by a hypersensitive or allergic reaction.

Aetiology of eosinophilic myocarditis includes various agents – antibiotics (penicillin, sulfonamides, cephalosporine etc.), antipsychotics (clozapine), non-steroidal anti-inflammatory drugs (indomethacin), diuretics, some ACE-inhibitors (captopril and enalapril), digoxin, dobutamine, small-pox vaccine and others. Non-pharmacological causes of the eosinophilic heart impairment are parasitic infections, some systematic disorders (primarily Churg Strauss syndrome) and hematological diseases, various malignant diseases and idiopathic hypereosinophilic syndromes.

The most important therapeutic measure in patients with eosinophilic myocarditis is the removal of the agent if it is known. In most of the patients with non-infectious type of this myocarditis, immunosuppressive therapy consisting primarily from corticosteroids is indicated.



Giant-cell myocarditis (GCM) is a rare form of myocarditis mostly with a dramatic course and life-threatening complications. GCM is characterized by the histopathological finding of giant multinuclear cells, infiltration with eosinophils and T lymphocytes and necrosis of cardiomyocytes. GCM is definitively confirmed just with EMB.

It is often a fatal disease presenting in fulminant form and even with a transition to the cardiogenic shock.

Combined immunosuppressive therapy includes according to the resources usually the combination of corticosteroids with azathioprine or mycophenolate and cyclosporine. In the most of patients, ICD is indicated because of a high risk of death due to malignant arrhythmias. There are also many patients where the heart transplant is the only therapeutic option.



Sarcoidosis is a multiorgan granulomatous inflammatory disease. The histological finding of cardiac sarcoidosis is in some respects similar to GCM like the presence of giant cells, however in cardiac sarcoidosis greater extent of fibrous changes and primarily smaller presence of the myocardial necrosis and the presence of well-bordered granulomas may be observed.

Clinical manifestation of cardiac sarcoidosis is varied. It presents with heart failure under the picture of dilated or restrictive cardiomyopathy and with arrhythmias.

CMRI has an important role in the diagnosis of cardiac sarcoidosis and PET examination is also used when inflammatory activity is detected by 18F-FDG.

Like in eosinophilic and giant-cell myocarditis, even in cardiac sarcoidosis, the main therapeutic method is immunosuppressive therapy. This treatment is usually administered in monotherapy or in combination with other immunosuppressive drugs, primarily methotrexate. In the treatment of arrhythmias and prevention of sudden cardiac death, implantation of a permanent pacemaker or ICD is considered.



Cardiac impairment in HIV positive patients is a very frequent complication which is observed in 25 to 75 % of patients. Aetiology of myocarditis in HIV positive patients is unclear.

Manifestation and clinical picture of HIV positive patients with myocarditis are similar to other myocarditis types and also include a wide spectrum from asymptomatic individuals to cases presenting as a sudden death.

Treatment of myocarditis in HIV positive individuals is still not standardized including heart failure management, however, still, standard heart failure therapy is recommended.

Prognosis of patients is generally unclear and often unfavorable.



Myocarditis is connected with a considerable amount of autoimmune diseases (see chapter Aetiology). Some of them are already mentioned in the chapter Eosinophilic myocarditis (Churg Strauss syndrome and HES). Considering their great amount, this chapter introduces just SLE, ulcerative colitis, Crohn´s disease, coeliac disease and rheumatic fever.

Cardiac manifestation in SLE is present in 50 % of patients and myocarditis specifically in approximately 10 %.

Sizeable prevalence of coeliac disease was detected in both myocarditis (4,4 %,) and idiopathic DCMP (5,7 %).



Chagas disease is a parasitic disease caused by an infection with Trypanosoma cruzi. It is mostly found in the area of Central and South America [26]. According to WHO, 8 million people are infected worldwide.

The parasite is transferred by biting insect from Reduviidae family. Afterward, it infects primarily muscle cells (of the myocardium, smooth and skeletal muscles) and ganglionic cells. In case of chronic cardiovascular impairment, the disease progresses in so-called Chagas cardiomyopathy.

The clinical picture of patients is very variable. Therapy consists primarily of anti-parasitic treatment and therapy of heart failure and of thromboembolism. Prognosis is variable and is based on the extent of cardiovascular damage, which is the main cause of mortality in infected patients.