Myocarditis can progress to inflammatory cardiomyopathy when there is associated ventricular remodeling and cardiac dysfunction due to chronic inflammation.

While myocarditis may develop over periods ranging from hours to months, patients typically present with signs and symptoms that resemble heart failure, including the following:[1][12] Since myocarditis is often due to a viral illness, many patients experience symptoms consistent with a recent viral infection including a fever, rash, loss of appetite, abdominal pain, vomiting, diarrhea, joint pains, and easily becoming tired.

[15] More specifically, fulminant myocarditis is characterized by a distinct, rapid onset of severe heart failure symptoms, such as shortness of breath and chest pain, that develop over the course of hours to days.

[18] Worldwide, however, the most common cause is Chagas disease, an illness endemic to Central and South America that results from infection with the protozoan Trypanosoma cruzi.

[19][20] Globally, Chagas disease is the leading cause of myocarditis, which results from infection with the protozoan Trypanosoma cruzi.

[31] Over approximately the next 1–7 days the virus replicates and causes inflammation leadings to necrosis and apoptosis of cardiac muscle cells (myocytes) and activation of the innate immune system.

[31] Over the next 1–4 weeks, viral replication continues with subsequent activation of the acquired immune system leading to T cell infiltration and the formation of antibodies, including possibly auto-antibodies.

[19] The mechanism by which coxsackie B viruses (CBVs) trigger inflammation is believed to be through the recognition of CBV virions by Toll-like receptors.

[19] The binding of many types of coronaviruses, including the SARS-CoV-2 virus, through ACE2 receptors present in heart muscle may be responsible for direct viral injury leading to myocarditis.

[25] In addition to direct cardiac myocyte (heart muscle cell) damage due to SARS-CoV-2 viral infiltration and inflammation, there are other suspected mechanisms that COVID-19 may indirectly cause myocarditis.

[38][39] Myocardial inflammation can be suspected on the basis of elevated inflammatory markers including C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), or an increased IgM (serology) against viruses known to affect the myocardium.

[31] The presence of Q waves, a widened QRS complex, prolongation of the QT interval, high degree AV nodal blockade, and ventricular tachyarrhythmias are associated with a poor prognosis when seen on ECG in people with myocarditis.

Endomyocardial biopsy samples are assessed for histopathology (how the tissue looks like under the microscope): myocardial interstitium may show abundant edema and inflammatory infiltrate, rich in lymphocytes and macrophages.

[citation needed] 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.

[41] Cardiac MRI is most sensitive when performed 2–3 weeks after the initial clinical presentation of myocarditis and may be repeated 6–12 months after onset to monitor the evolution of disease or response to treatment.

[31] Empiric IV glucocorticoids are indicated in acute myocarditis with cardiogenic shock, heart failure, ventricular arrhythmias or high degree AV block that is suspected due to auto-immune disease; but the European Society of Cardiology also recommends subsequent viral genome testing of endomyocardial biopsy specimens due to risk of viral activation, which may necessitate discontinuation of immunosuppression therapy.

[46] In a majority of cases, the main therapies are used to support patients and are dependent on the severity of symptoms and the time course across which myocarditis develops.

[45] Additionally, the order in which therapies are used depends on the degree of heart dysfunction, with stabilization of patient blood pressure and breathing taking highest priority when present.

[17] This can involve the use of inotropes, or medications that make the heart contract with greater force, as well as antiarrhythmic drugs such as adenosine or carvedilol.

[45] ACE inhibitors or Angiotensin Receptor Blockers (ARBs) can have a protective benefit to the heart, so either are typically used in any patient with symptomatic myocarditis.

Shortness of breath at rest and swelling can be relieved with diuretics such as furosemide, and the addition of aldosterone receptor blockers can augment the diuresis while preventing the excess loss of potassium.

[15] People that require additional support with their heart function can benefit from the use of ventricular assist devices like intra-aortic balloon pumps.

[49] An implantable cardioverter-defibrillator (ICD) is sometimes required in those with cardiomyopathy or heart failure caused by myocarditis due to the risk of fatal ventricular arrhythmias.

[50] Electrocardiogram findings of ST elevations with upward concavity and an early repolarization pattern, however, were associated with a better cardiovascular prognosis in general.

[53] Myocarditis has been reported to be a major cause of sudden cardiac death (SCD) in infants, adolescents, and young adults, but the reported rates show wide variation (1 to 14 percent) among young people depending on differences in SCD definition and classification/ definition of myocarditis post-mortem as well as heterogeneity of study populations.

[54] In fulminant myocarditis, in which an inflammatory cytokine storm occurs, cardiac functions decline rapidly and the death rate is high.

[56] If one tests positive for an acute viral infection, clinical developments have discovered that 1-5% of said population may show some form of myocarditis.

[12] Young males specifically have a higher incidence rate than any other population due to their testosterone levels creating a greater inflammatory response that increases the chance of cardiac pathologies.

[59] Myocarditis is the third most common cause of death among young adults with a cumulative incidence rate globally of 1.5 cases per 100,000 persons annually.

[57] Myocarditis accounts for approximately 20% of sudden cardiac death in a variety of populations, including adults under the age of 40, young athletes, United States Air Force recruits, and elite Swedish orienteers.