Acute Myocarditis

Etiology

Acute myocarditis can be broadly categorized into infectious and noninfectious causes. Viral infections are the most common identified etiology when a specific cause is determined.[6][7] However, in approximately 50% of cases, no definitive cause is identified, and the condition is classified as idiopathic.

Infectious Causes of Acute Myocarditis

• Viruses: Coxsackie and echoviruses are the most common cardiotropic viruses causing myocarditis. Other viral pathogens include HIV, adenovirus, hepatitis B and C, parvovirus B19, poliovirus, and Epstein-Barr virus.[8]
• Bacteria: Common bacterial causes include Legionella, Staphylococcus species, Salmonella, Shigella, Streptococcus species, Clostridium, and Mycobacterium tuberculosis. 
• Parasites: Notable parasitic causes include Trichinella spiralis (trichinosis) and Schistosoma species (schistosomiasis).
• Protozoa: The important protozoan pathogens include Trypanosoma cruzi (the causative agent of Chagas disease) and Toxoplasma gondii.
• Spirochetes: Borrelia burgdorferi, the causative agent of Lyme disease, can also lead to myocarditis.

Noninfectious Causes of Acute Myocarditis

Noninfectious causes of acute myocarditis encompass a broad spectrum of conditions and exposures. These include eosinophilic myocarditis and autoimmune disorders such as systemic lupus erythematosus, polymyositis, and dermatomyositis. Cardiotoxic drugs are also well-recognized contributors. Other noninfectious etiologies include systemic diseases such as sarcoidosis, inflammatory bowel disease, and giant cell arteritis. Additional causes include acute rheumatic fever, exposure to venoms or chemicals (eg, hydrocarbons), and cellular rejection following cardiac transplantation.[9]

Epidemiology

The true prevalence of acute myocarditis remains uncertain due to its variable clinical presentation and the challenges associated with diagnosis. The condition is frequently underdiagnosed, complicating efforts to determine its exact incidence and prevalence. Acute myocarditis occurs more commonly in younger adults and affects individuals across all sexes and racial groups. However, notable regional variations in incidence have been reported.[10][11]

According to the Global Burden of Disease Report (2019), the estimated incidence of acute myocarditis is approximately 6.1 cases per 100,000 individuals.[12] Other sources suggest a broader incidence range, from 10 to 22 cases per 100,000 population. In 2013, an estimated 1.5 million cases were reported globally.[13] Additionally, myocardial involvement is estimated to occur in up to 5% of patients with an acute viral illness. Among individuals presenting with angina-like chest pain, mildly elevated troponin I levels, and no evidence of CAD, cardiac magnetic resonance imaging (MRI) has identified myocarditis in approximately 13% of cases.[14]

Pathophysiology

Acute myocarditis is classified as an inflammatory cardiomyopathy. A triphasic model has been proposed to describe the pathophysiology of acute myocarditis.

• Phase I involves direct myocardial injury caused by infectious agents (viruses, bacteria, fungi, parasites), toxins, drugs, or autoimmune mechanisms.

• Phase II involves an immune-mediated response characterized by cytokine release, cellular infiltration, molecular mimicry, production of antimyocyte antibodies, and a T-cell response targeting cardiac self-antigens.

• Phase III represents either resolution or progression to chronic disease. Potential outcomes include complete resolution with full recovery, chronic inflammation, myocardial fibrosis, cardiomyopathy, or progression to dilated cardiomyopathy.[7]

Autoimmunity has a significant role in inflammatory myocarditis.[15] Autoantibodies against the cardiac myosin chain are detected in more than half of cases of inflammatory myocarditis. Additionally, environmental factors may interact with genetic predispositions to promote inflammatory responses.[6]

In viral myocarditis, the inflammatory process begins when the virus enters myocardial cells, triggering an innate immune response within the first week. This is followed by an adaptive immune response over the subsequent 1 to 4 weeks. In the chronic stage, chronic inflammation and remodelling of the myocardium can lead to myocardial dilation and the development of cardiomyopathy.[6][16] Viral-induced cell damage leads to the release of interleukins (ILs) and damage-associated molecular patterns, which facilitate the recruitment of inflammatory cells from the innate immune system.

Additionally, stressors such as pain or anxiety activate medullary cells, triggering monocytopoiesis and the release of myeloid progenitor cells. The spleen is also activated to replenish proinflammatory cells, which then mobilize to the damaged myocardium. There, the release of interferon-gamma (IFN-γ) further enhances the recruitment of inflammatory cells. This exaggerated inflammatory response to viral-induced myocardial damage contributes to chronic inflammation, myocardial remodeling, and eventual ventricular dysfunction.[6]

In the innate immune response, macrophages, dendritic cells, and neutrophils are the first to infiltrate the myocardium. Toll-like receptors on these immune cells recognize viral components, amplifying the inflammatory response. Natural killer cells are crucial in eliminating infected cells, setting the stage for the adaptive immune phase. In the adaptive immune phase, CD8+ cytotoxic T cells target viral peptides on infected myocytes, thereby inducing cell death. CD4+ helper T cells enhance the immune response by producing cytokines such as IL-2 and IFN-γ.

B cells produce antibodies against viral antigens but can also generate autoantibodies targeting self-antigens through a process known as molecular mimicry. This phenomenon occurs when viral antigens closely resemble cardiac proteins, such as myosin, leading to autoimmune myocarditis. In the chronic phase, even after viral clearance, immune cells may continue to attack the heart due to the persistence of autoantigens. This prolonged inflammation causes myocyte necrosis, followed by fibrosis, and ultimately results in dilated cardiomyopathy.[7]

History and Physical

The clinical presentation of acute myocarditis is highly variable, ranging from asymptomatic or mild viral illness to fulminant heart failure, cardiogenic shock, or sudden cardiac death. The onset can be acute or insidious, and there are no pathognomonic symptoms specific to the condition. The classic triad includes chest pain, arrhythmias, and signs of heart failure or cardiogenic shock. Common symptoms may include fever, malaise, fatigue, palpitations, chest pain, dyspnea, orthopnea, presyncope, and syncope.

Chest pain may either mimic pericarditis—particularly in cases of myopericarditis, which occurs in at least 35% of patients—or resemble the central, severe discomfort characteristic of acute coronary syndrome. A preceding acute febrile illness, often respiratory or gastrointestinal in origin, is reported in approximately 60% of cases. Clinicians should also inquire about a history of prior myocarditis, autoimmune disorders, family history of cardiomyopathy or sudden cardiac death, and recent exposure to cardiotoxic agents.

Fulminant presentations may resemble acute decompensated heart failure, characterized by respiratory distress, orthopnea, palpitations, syncope, hemodynamic instability, and potentially life-threatening ventricular arrhythmias. In a study involving patients with clinically suspected myocarditis, approximately 25% exhibited reduced left ventricular ejection fraction (LVEF), sustained ventricular arrhythmias, or symptoms of low cardiac output.

On physical examination, findings typically correlate with the degree of cardiac dysfunction. In patients with decompensated heart failure, signs may include an S3 gallop, pulmonary rales, jugular venous distension, and peripheral edema. A pericardial friction rub may be heard in cases with pericardial involvement. A pansystolic murmur suggestive of mitral regurgitation may be present in patients with ventricular dilation. Additional findings may point toward systemic disease, depending on the underlying etiology. For example, lymphadenopathy may indicate sarcoidosis; a maculopapular rash may suggest eosinophilic myocarditis; and features such as erythema marginatum, polyarthralgia, chorea, and subcutaneous nodules are characteristic of acute rheumatic fever. Dysphagia may be observed in Chagas disease, while diphtheritic myocarditis can be associated with neurologic manifestations.

Evaluation

The ACC recommends a structured 5-step approach for evaluating and diagnosing acute myocarditis. This framework integrates clinical judgment with targeted diagnostic tools to ensure a comprehensive and systematic assessment.

• Step 1—Initial evaluation: When acute myocarditis is clinically suspected, the first step involves obtaining a complete blood count (CBC) with differential, cardiac biomarkers, an electrocardiogram (ECG), and a transthoracic echocardiogram. Evaluation should also aim to identify or rule out underlying CAD when clinically indicated.

• Step 2—Clinical triage: Patients should be triaged based on hemodynamic stability and symptom severity to determine the need for hospitalization, urgent referral to an advanced heart failure center, immediate arrhythmia management, or mechanical circulatory support.

• Step 3—Definitive diagnostics: Cardiac MRI with T1 and T2 mapping is the key diagnostic tool essential for evaluating myocardial inflammation and injury. Endomyocardial biopsy (EMB) should be considered in selected cases, particularly when the diagnosis is unclear or when specific histopathological subtypes are suspected.

• Step 4—Therapeutic management: Management includes discontinuing the inciting agent, addressing the underlying cause, treating any arrhythmias or cardiogenic shock, and enforcing temporary restrictions on strenuous activity, including competitive sports.

• Step 5—Longitudinal surveillance: Follow-up involves serial monitoring with cardiac biomarkers, echocardiography, and cardiac MRI with tissue mapping. When indicated, genetic counseling and testing should be incorporated. A comprehensive reevaluation is essential before clearing patients for return to high-intensity physical activity or competitive sports.

According to the 2013 European Society of Cardiology (ESC) guidelines and subsequent updates, a diagnosis of acute myocarditis is suspected when at least 1 clinical presentation is accompanied by a diagnostic finding from noninvasive testing. In asymptomatic individuals, at least 2 diagnostic criteria are required to establish the diagnosis. Clinical presentations may include chest pain, symptoms of heart failure, arrhythmias, or cardiogenic shock.

Diagnostic findings include electrocardiographic abnormalities, such as ST-T wave changes or PR segment depression (resembling pericarditis), ventricular arrhythmias, elevated cardiac biomarkers (such as troponin-I or creatine kinase-MB [CK-MB]), and left ventricular dysfunction with regional wall motion abnormalities that are not consistent with a coronary artery distribution on the echocardiogram. Additional supportive findings include a cardiac MRI consistent with the updated Lake Louise criteria and increased patchy or diffuse fluorodeoxyglucose (FDG) uptake on positron emission tomography (PET), both of which are indicative of myocardial inflammation.[1]

Diagnostic Investigations for Myocarditis

The tests mentioned below are commonly used to evaluate patients with suspected myocarditis: 

Complete blood count

CBC may reveal leukocytosis; eosinophilia can be seen in cases of eosinophilic myocarditis.

Inflammatory reactants

Elevated levels of C-reactive protein (CRP), ILs, or IFNs, along with an increased erythrocyte sedimentation rate (ESR), may indicate systemic inflammation associated with myocarditis.

Cardiac markers

Over half of patients with biopsy-confirmed myocarditis exhibit elevated troponin I or T levels, which have good specificity but limited sensitivity. Elevated levels of pro–B-type natriuretic peptide may also be present.

Electrocardiogram

ECG findings in acute myocarditis are often nonspecific and may include ST-segment changes, PR segment depression, and low voltage. Additional features can include sinus tachycardia, ventricular or bradyarrhythmias, and intraventricular conduction delays, signifying diseased myocardium. ECG changes may also suggest an acute coronary syndrome. Atrioventricular blocks can be present, and conduction system involvement raises the possibility of Lyme disease, giant cell myocarditis, or cardiac sarcoidosis. Diffuse ST elevation may occur in the presence of pericarditis. The sensitivity of ECG for diagnosing acute myocarditis is 47%.

Chest radiograph

Although not sensitive or specific for myocarditis, chest radiographs may reveal indirect signs such as cardiomegaly, pulmonary vascular congestion, pulmonary edema, or pleural effusion.

Echocardiogram

Echocardiography is a widely accessible bedside tool used to assess myocardial function, determine the degree of myocardial damage, and detect coexisting conditions such as valvular heart disease or intracardiac thrombus. Key findings may include reduced left ventricular systolic function, ventricular dilatation, an increased sphericity index, diastolic dysfunction, and pericardial effusion when present. Global longitudinal strain is typically reduced, offering additional diagnostic value. In fulminant myocarditis, ventricular dimensions are often preserved while septal thickness increases, indicating myocardial edema. In contrast, acute myocarditis more commonly presents with normal septal thickness and enlarged ventricular dimensions.

Cardiac magnetic resonance imaging

Cardiac MRI has become the gold standard for the noninvasive evaluation of myocarditis, offering detailed insights into structural and functional cardiac changes. In acute myocarditis, MRI can detect hallmark features, including myocardial edema, increased vascular permeability, hyperemia, myocyte necrosis, fibrosis, and pericardial involvement. Key imaging findings are listed below. 

• Early gadolinium enhancement or EGE: This suggests the expansion of the extracellular space due to capillary leakage and hyperemia. 
• T1 mapping: This reveals increased T1 values, indicating cellular damage, edema, and inflammation.
• T2 mapping: This demonstrates increased T2 signal intensity, indicating myocardial edema.
• Late gadolinium enhancement or LGE: This identifies patchy fibrosis and necrosis, typically in a nonischemic distribution—most often subepicardial or midwall—and commonly affects the inferolateral wall. The lack of enhancement in a coronary artery distribution helps differentiate myocarditis from ischemic injury. 
• Extracellular volume or ECV: An increased ECV indicates expansion of the interstitial space caused by edema, inflammation, or fibrosis. This parameter is valuable in distinguishing active myocardial inflammation from chronic scarring. 

The 2018 updated Lake Louise criteria are widely used for diagnosing myocarditis.[17] A diagnosis of acute myocarditis is considered probable when at least one T2-based criterion and one T1-based criterion are present. T1-based criteria include nonischemic LGE, increased native T1 values, or increased ECV. T2-based criteria include increased T2 values or increased myocardial T2 signal intensity. 

Endomyocardial biopsy

EMB remains the gold standard for the definitive diagnosis of myocarditis.

• According to the 2024 ACC ECDP, EMB is indicated in the following scenarios:
  • Stage B myocarditis in patients receiving immune checkpoint inhibitors (ICIs).
  • Stage C myocarditis in the presence of left ventricular dysfunction, heart failure, arrhythmias, or peripheral eosinophilia.
  • Patients who are unable to undergo cardiac MRI or have an uncertain diagnosis.
  • Stage D myocarditis patients. 
• A biopsy should not be performed in stage B patients who are not receiving ICIs, have normal ejection fraction, minimal or no LGE, or exhibit hemodynamic or electrical instability.[5] EMB is recommended only when the potential clinical benefit clearly outweighs the risks associated with the procedure.
• The rate of major complications—such as cardiac perforation, tamponade, pneumothorax, arrhythmias, embolism, and valvular injury—is less than 1% when the procedure is performed in experienced centers.
• The histopathology of acute myocarditis varies depending on the causative organism and the extent of myocardial damage, which can be either focal or diffuse. Necrosis involving the coronary vessels may also be observed. In chronic cases, fibrosis may become evident. EMB is not routinely performed in nonfatal cases. Patients with myocarditis may or may not show evidence of viral genomes through polymerase chain reaction (PCR).
• The Dallas criteria (1987) were the most widely adopted histopathological standards by pathologists for diagnosing myocarditis.[18] These criteria define "active myocarditis" as histological evidence of myocyte damage in a pattern that is not consistent with ischemic injury. This is characterized by mononuclear infiltrates, and in some cases, neutrophilic or eosinophilic infiltrates may also be present. If the mononuclear infiltrates are sparse, the condition is classified as "borderline myocarditis." The absence of these changes is classified as "no myocarditis." The Dallas criteria have a sensitivity of 60% and a specificity of 80%. In subsequent biopsies, the criteria further classify myocarditis as "persistent, healing, or healed," with or without the presence of fibrosis. 
• The World Health Organization (WHO) endorses a combination of histopathology and immunohistology for classifying myocarditis. According to the WHO Marburg criteria, acute (active) myocarditis is characterized by more than 14 leukocytes per square millimeter, along with evidence of degeneration or necrosis. Chronic myocarditis also shows more than 14 leukocytes per square millimeter; however, necrosis or degeneration is typically absent. A leukocyte count of fewer than 14 per square millimeter suggests no myocarditis.[6]

Nuclear perfusion imaging and fluorodeoxyglucose-positron emission tomography scan

• Acute myocarditis is characterized by inflammatory cell infiltration, with activated immune cells exhibiting increased glucose metabolism. This heightened metabolic activity results in increased FDG uptake on PET imaging, which can be used to assess the extent and severity of myocardial inflammation. The typical findings on FDG-PET include patchy, diffuse, or focal uptake patterns that generally do not align with coronary artery territories. These areas of FDG uptake often correlate with T2-weighted hyperintensity and LGE observed on cardiac MRI.
• Adequate patient preparation for FDG-PET imaging includes following a high-fat, low-carbohydrate diet for 12 to 24 hours before the scan to suppress normal myocardial glucose uptake. Additionally, a 12-hour fasting period is recommended before the FDG injection. In some cases, a heparin injection may be administered to further enhance myocardial fatty acid metabolism and improve image specificity.

Coronary angiography

This technique is considered the gold standard for ruling out CAD, particularly when the clinical presentation closely resembles that of acute coronary syndrome. In patients without conventional contraindications, CT coronary angiography may serve as an alternative diagnostic option.

Treatment / Management

Management of Acute Myocarditis by Disease Stage

The management of acute myocarditis is tailored to the stage of the disease, as mentioned below. 

• Stage A: Patients in stage A are at risk for developing myocarditis. Management includes close monitoring for disease progression, strict avoidance of repeat exposure to known or suspected offending agents (eg, cocaine), and patient counseling on risk factors and preventive measures.

• Stage B: In addition to the measures outlined in stage A, patients at stage B should undergo a timely reassessment of their symptoms. An ECG and high-sensitivity troponin I (hs-TnI) should be obtained if not already performed. Management includes addressing the underlying etiology, for example, initiating immunosuppressive therapy in patients receiving ICIs. Hospitalization may be warranted based on the severity of left ventricular dysfunction and the overall clinical context.

• Stage C: At stage C, guideline-directed medical therapy (GDMT) for heart failure is implemented, which includes pharmacotherapy tailored to the underlying etiology (eg, immunosuppression or steroid use). EMB may be considered in selected patients based on clinical indications. Referral to an advanced heart failure center with a specialized myocarditis team is recommended. Patients should be restricted from strenuous activity for at least 3 to 6 months, while avoiding excessive sedentary behavior. Hospitalization is advised unless the clinical presentation is considered low-risk.

• Stage D: Patients with stage D myocarditis require admission to the intensive care unit (ICU) and prompt referral to an advanced heart failure center with a dedicated myocarditis team. Management includes GDMT for heart failure, pharmacological treatment targeting the underlying etiology, and appropriate interventions for arrhythmias and cardiogenic shock, including supportive measures or mechanical circulatory support. Strenuous physical activity should be restricted for at least 6 months. In cases where there is no recovery, consideration should be given to the placement of a durable left ventricular assist device (LVAD) or heart transplantation.[5]
(B3)

General Supportive Management Strategies of Acute Myocarditis

The management of acute myocarditis is primarily supportive, focusing on addressing certain conditions, as mentioned below.

Heart failure management

The overall management of heart failure includes medications commonly used to treat heart failure, irrespective of its underlying cause. Key medications involve beta-blockers, renin-angiotensin-aldosterone system (RAAS) inhibitors, mineralocorticoid receptor antagonists, sodium-glucose cotransporter-2 inhibitors (SGLT-2 inhibitors), and diuretics. The treatment strategy depends on the severity and hemodynamic status of the patient. In cases of acute heart failure, beta-blockers are withheld. Depending on the patient’s volume status, diuretics may be administered. In hemodynamically stable patients with left ventricular dysfunction, early initiation of RAAS inhibitors is advised. Once the hemodynamic and clinical status is optimized, beta-blockers can be introduced. In severe cases, mechanical circulatory support—such as an intra-aortic balloon pump or a LVAD—may be necessary.[19] (B3)

Digoxin is generally avoided in the treatment of acute myocarditis due to the inflamed and irritable nature of the myocardium, which increases susceptibility to arrhythmias. Digoxin can elevate intracellular calcium levels and enhance myocardial excitability, potentially triggering or worsening ventricular arrhythmias. The risk of toxicity is heightened in these patients due to altered drug distribution, changes in renal function, and increased myocardial sensitivity.

Arrhythmia management

Acute myocarditis may be complicated by ventricular or atrial arrhythmias, as well as heart block. For patients with hemodynamically stable tachyarrhythmias and no signs of peripheral hypoperfusion, initiating a beta-blocker is recommended. Amiodarone and dofetilide may be considered for the treatment of sustained ventricular arrhythmias. If necessary, heart block is managed with a temporary pacemaker, followed by a permanent pacemaker if indicated. An implantable cardioverter defibrillator is indicated in the chronic stage, according to standard recommendations, once the acute illness has resolved. 

Immunosuppressive therapy

Immunosuppressive therapy is not indicated for all patients with acute myocarditis. This is reserved for specific conditions, including eosinophilic myocarditis, giant cell myocarditis, granulomatous myocarditis (eg, sarcoidosis), and cases associated with autoimmune diseases or ICIs. Initial treatment typically begins with intravenous methylprednisolone (3–13 mg/kg/d boluses for 3 days), followed by oral prednisone (1 mg/kg) with a tapering schedule. Management of giant cell myocarditis requires a combination of high-dose intravenous steroids, a calcineurin inhibitor (eg, cyclosporine or tacrolimus), and azathioprine. Intravenous immunoglobulin may be considered in selected cases involving autoimmune, inflammatory, or antibody-mediated mechanisms. [5](B3)

Other therapies

Anticoagulation is indicated in patients with documented atrial or ventricular thrombus or those with atrial fibrillation, in accordance with standard clinical guidelines.

Exercise limitation

In cases of acute myocarditis, it is recommended to restrict activity. Patients should refrain from participating in competitive sports for at least 3 to 6 months following an episode of acute myocarditis.[20] Further recommendations will depend on ongoing clinical assessments, echocardiograms, and Holter monitoring.[21][22](B3)

Alcohol restriction

Alcohol consumption should be restricted to 1 drink per day, which is approximately 14 to 15 grams.

Differential Diagnosis

The differential diagnoses for acute myocarditis include:

• Acute coronary syndrome
• Pericarditis 
• Coronary vasospasm
• Stress cardiomyopathy
• Drug-induced myocardial injury (eg, cocaine and chemotherapy)
• Thyrotoxic cardiomyopathy
• Infective endocarditis with septic coronary emboli

Staging

The 2024 ACC ECDP outlines a 4-tier staging system for myocarditis, as mentioned below, which is modeled after the heart failure classification system.[5]

• Stage A (at risk): Individuals in this stage are exposed to risk factors for myocarditis but show no clinical symptoms or structural, biochemical, imaging, or histopathological evidence of disease. Examples include patients receiving cardiotoxic medications, those with recent viral infections or autoimmune disorders, and individuals with a genetic predisposition or a personal history of myocarditis.

• Stage B (asymptomatic): Patients with evidence of myocardial inflammation, detected through imaging modalities such as cardiac MRI, elevated high-sensitivity cardiac troponin, or histopathological findings, but who remain asymptomatic.

• Stage C (symptomatic): Patients presenting with symptoms attributable to myocarditis, such as heart failure, arrhythmias, or chest pain, along with histopathological evidence of myocarditis, cardiac MRI findings based on the 2018 updated Lake Louise criteria, or elevated high-sensitivity cardiac troponin, supported by additional evidence.

• Stage D (advanced): Patients who meet the criteria for Stage C myocarditis and exhibit hemodynamic instability or severe arrhythmias requiring interventions such as mechanical circulatory support or evaluation for heart transplantation.

Prognosis

Given the wide variability in clinical presentation, disease severity, and underlying etiology, the prognosis of acute myocarditis is equally heterogeneous. Adverse cardiovascular outcomes are more likely in patients presenting with acute decompensated heart failure, sustained arrhythmias, a LVEF below 50%, or those requiring inotropes, vasopressors, or mechanical circulatory support. Nonetheless, patients who survive the acute phase often have favorable outcomes.[23] Long-term follow-up indicates that at least 50% of patients develop cardiomyopathy. The 1-year mortality rate for acute myocarditis is approximately 20%, increasing to 56% by 4 years. Please see StatPearls' companion resource, "Viral Myocarditis," for more information.

Fulminant myocarditis is associated with significantly higher mortality rates and reduced transplant-free survival.[24] Persistent detection of viral genomes on serial EMBs is a poor prognostic indicator and may signal a diminished response to therapy.[25] The prognosis is also particularly unfavorable in cases of eosinophilic and giant cell myocarditis. Biomarkers can also provide prognostic insights—the presence of soluble Fas ligand at presentation suggests more favorable outcomes, whereas the presence of antimyosin autoantibodies is associated with a worse prognosis.[21][26]

According to the 2024 ECDP, key risk factors for adverse outcomes in myocarditis include:

• Clinical presentation: Heart failure, cardiogenic shock, or electrical instability, such as recurrent ventricular tachycardia or advanced atrioventricular block.
• Echocardiography: Evidence of biventricular dysfunction.
• Cardiac MRI: Presence of biventricular dysfunction and LGE.
• Endomyocardial biopsy: Histopathological diagnosis of giant cell myocarditis.[5]

Complications

Acute complications of myocarditis include:

• Left ventricular dysfunction and heart failure.
• Cardiogenic shock.
• Ventricular tachycardia or ventricular fibrillation: This increases the risk of sudden cardiac death.
• Bradyarrhythmias: High-grade atrioventricular block necessitating intervention. 
• Atrial arrhythmias: Atrial tachycardia or atrial fibrillation/flutter.
• Thromboembolic events: These events include stroke or systemic embolism due to left ventricular dysfunction.

Subacute and chronic or long-term complications include:

• Dilated cardiomyopathy and chronic heart failure. 
• Recurrent episodes of myocarditis.
• Increased risk of sudden cardiac death.
• Myocardial fibrosis and scarring.