Myocarditis

Myocarditis is inflammation of the myocardium, most commonly triggered by a viral infection or by the immune response that follows one, though the list of recognized triggers is genuinely broad — autoimmune and hypersensitivity reactions, specific drugs, and, of real current clinical importance, both mRNA COVID-19 vaccination and immune checkpoint inhibitor (ICI) cancer therapy.^[1] Clinical severity spans an enormous range: from an entirely subclinical finding, through mild chest pain and transient ECG changes that resolve without specific treatment, to fulminant cardiogenic shock, life-threatening ventricular arrhythmia, or sudden cardiac death as the very first presentation — sometimes in a previously healthy young person only days removed from what looked like an ordinary viral illness.^[1] This is precisely why this chapter leads with emergency recognition rather than treatment: the central clinical skill this condition demands is recognizing when apparent viral symptoms, chest pain, or fatigue are not "just a viral illness" but the leading edge of a process that can deteriorate within days.

The 2024 ACC Expert Consensus Decision Pathway organizes myocarditis into four stages that parallel the familiar heart-failure staging framework, and this chapter uses that same structure throughout: Stage A (exposure to a known myocarditis trigger — a viral illness, an mRNA vaccine dose, an ICI — without cardiac symptoms or abnormal testing), Stage B (asymptomatic but with objective evidence of myocardial injury or inflammation on testing), Stage C (symptomatic myocarditis — chest pain, dyspnea, palpitations, or overt heart failure), and Stage D (hemodynamic or electrical instability — cardiogenic shock, sustained ventricular arrhythmia, or high-grade heart block; this is fulminant myocarditis).^[1] Roughly half of patients have complete resolution within 2-4 weeks, but about a quarter go on to persistent cardiac dysfunction and 12-25% progress to end-stage heart failure or death — outcomes that are meaningfully worse with biventricular dysfunction, Stage D presentation at diagnosis, and the presence of late gadolinium enhancement on cardiac MRI.^[1]

There is no specific antiviral treatment for most viral myocarditis, which is why heart-failure-directed pharmacotherapy is the genuine backbone of management for the majority of patients with reduced left ventricular function. That backbone, however, is not the whole story: giant cell myocarditis and eosinophilic myocarditis require immunosuppression as first-line, disease-specific therapy rather than supportive care alone, and recognizing which pathway a patient is on — supportive versus immunosuppressive — is one of this chapter's central organizing decisions.^[2] A parallel decision applies to the two triggered forms this chapter specifically emphasizes: ICI-associated myocarditis, which carries a strikingly high mortality rate and demands immediately holding the ICI and starting corticosteroids at first suspicion, and mRNA-vaccine-associated myocarditis, which is usually mild and self-limited but still requires prompt recognition, supportive care, and specific guidance on future vaccine dosing.^[3][4] Finally, activity restriction — genuinely avoiding competitive sport and vigorous exercise for a defined period after diagnosis — is a specific, concrete counseling point running through this entire chapter, because vigorous exercise during active myocardial inflammation is a recognized trigger for malignant ventricular arrhythmia.^[5]

Epidemiology and etiology

The true incidence of myocarditis is difficult to pin down because so many cases are subclinical or never biopsied; it is likely substantially underdiagnosed. Viral infection is the most common identified trigger worldwide — historically coxsackievirus and other enteroviruses, with adenovirus, parvovirus B19, human herpesvirus 6, and, more recently, SARS-CoV-2 itself all well described. SARS-CoV-2 infection is, in fact, a meaningfully more common and more severe trigger of myocarditis than the mRNA vaccines used to prevent it — an important, genuinely reassuring point for patient counseling, and one addressed directly in Special Populations and Common Errors to Avoid.^[4] Beyond infection, recognized triggers include autoimmune and connective tissue disease, drug hypersensitivity reactions, hypereosinophilic states, and, of specific and growing current importance, mRNA COVID-19 vaccination and immune checkpoint inhibitor cancer therapy — see Risk Factors for the full list.^[1]

Typical presentation

• A preceding viral prodrome — fever, myalgias, upper respiratory or gastrointestinal symptoms — in the 1-3 weeks before cardiac symptoms begin, though this history is not always present or elicited.
• Chest pain, which can be pleuritic/positional (suggesting an accompanying pericardial component) or can closely mimic acute coronary syndrome, including troponin elevation and ST-segment changes — a genuine diagnostic trap addressed in Assessment & Diagnosis.
• Dyspnea, fatigue, and reduced exercise tolerance, from evolving left ventricular dysfunction.
• Palpitations, from atrial or ventricular ectopy, and, less commonly, sustained arrhythmia.
• Presyncope or syncope, which can reflect a life-threatening arrhythmia or high-grade AV block and is a genuine red flag (see Red Flags/Refer).
• In children, presentation is often less specific — vomiting, lethargy, poor feeding, or abdominal pain rather than classic chest pain — which is exactly why a high index of suspicion matters in this age group (see Special Populations).
• Tragically, sudden cardiac death or cardiogenic shock can be the first presentation, particularly in young people and especially during or immediately after vigorous exertion — the central reason this chapter treats activity restriction as a genuine safety issue rather than a routine convalescence recommendation.^[5]

The core distinction this chapter is organized around: supportive versus immunosuppression-first management

Endomyocardial biopsy in eosinophilic myocarditis: an extensive eosinophilic infiltrate involving the endocardium and myocardium (hematoxylin and eosin stain). This is the biopsy finding that distinguishes eosinophilic myocarditis from the more common lymphocytic pattern and identifies a patient who needs corticosteroids rather than supportive care alone. Image: Deb K, Djavidani B, Buchner S, Poschenrieder F, Heinicke N, Feuerbach S, Riegger G, Luchner A — CC BY 2.0, via Wikimedia Commons.

Two current, specifically important triggered forms

mRNA COVID-19 vaccine-associated myocarditis is uncommon (roughly 1.2 cases per 100,000 vaccine doses in Canada as of January 2024) but has a recognizable pattern: most often young males under 30, more common after the second dose, with symptom onset typically within 1-7 days (peaking days 1-3) of vaccination, and the great majority of cases mild and self-limited.^[4][7] ICI-associated myocarditis is rarer still but disproportionately dangerous, with reported mortality in the range of 25-50% despite its low overall incidence — early recognition and immediately holding the causative agent are genuinely time-critical.^[3] Both are covered in full in their own parts of Choose Initial Treatment and Special Populations, reflecting their real, current clinical importance.

Infectious and post-infectious triggers

• Viral infection — historically coxsackievirus B and other enteroviruses, adenovirus, parvovirus B19, human herpesvirus 6, influenza, and SARS-CoV-2, among others; a preceding viral illness in the 1-3 weeks before cardiac symptoms is the most commonly identifiable trigger.^[1]
• Less commonly, bacterial (including Lyme carditis and diphtheria), fungal, or parasitic infection (e.g., Chagas disease, more relevant with a relevant travel/exposure history), and, in immunocompromised patients, opportunistic organisms such as cytomegalovirus (see Special Populations).

Immune-mediated and hypersensitivity triggers

• Autoimmune and connective tissue disease — systemic lupus erythematosus, systemic sclerosis, sarcoidosis (cardiac sarcoidosis is a distinct, granulomatous form with its own specialist-directed pathway), and inflammatory myopathy.
• Drug hypersensitivity reactions, including DRESS (drug reaction with eosinophilia and systemic symptoms) — a recognized trigger specifically for eosinophilic myocarditis; identifying and stopping the causative drug is itself a core part of treatment (see Choose Initial Treatment).
• Hypereosinophilic syndrome and eosinophilic granulomatosis with polyangiitis (EGPA/Churg-Strauss) as underlying drivers of eosinophilic myocarditis when no drug trigger is identified.
• An association with thymoma, myasthenia gravis, and inflammatory bowel disease is recognized in giant cell myocarditis, though many cases have no identified associated condition.^[2]

Drug- and therapy-triggered forms — the two current forms this chapter emphasizes

• Immune checkpoint inhibitor (ICI) therapy — anti-PD-1/PD-L1 and anti-CTLA-4 agents used in cancer treatment. Risk is substantially higher with combination ICI therapy (dual checkpoint blockade) than with monotherapy, onset is typically early — a median of around 30 days after starting therapy and often within the first few doses — and concurrent immune-related myositis and/or myasthenia gravis (an overlap syndrome) carries a markedly higher mortality than isolated myocarditis.^[3]
• mRNA COVID-19 vaccination — age under 30, male sex, and the second dose of the primary series are the most consistent risk factors identified; onset is typically within 1-7 days of vaccination.^[4][7]

Other recognized risk factors

• Cardiotoxin exposure — cocaine, excessive alcohol use, and certain other drugs.
• A family history of cardiomyopathy or unexplained sudden cardiac death, reflecting a genetic predisposition component in some patients that is increasingly recognized as clinically relevant — genetic counselling and testing is now a specific 2024 ACC recommendation where feasible (see Non-Pharmacologic Treatment).^[1]
• Young age and male sex are epidemiologic associations across several of this chapter's triggered forms (viral myocarditis generally, vaccine-associated myocarditis, and the sudden-cardiac-death-in-athletes literature specifically).

Initial testing — every patient with suspected myocarditis

ECG, cardiac troponin, and transthoracic echocardiography are the core initial tests and carry real prognostic value, but a normal result on any of them does not exclude myocarditis when clinical suspicion remains — do not let reassuring initial testing close the diagnostic question prematurely.^[1] ECG findings are nonspecific and varied: diffuse ST-segment and T-wave changes (which can mimic pericarditis when a pericardial component coexists), sinus tachycardia, ectopy, or frank conduction block. Troponin is elevated in most patients with active myocarditis and can be markedly elevated — occasionally above 10,000 ng/L in mRNA-vaccine-associated cases — though the degree of elevation does not reliably predict severity on its own.^[7] BNP or NT-proBNP tracks the degree of hemodynamic/heart-failure involvement. Echocardiography assesses left and right ventricular function (wall-motion abnormalities in myocarditis are often more global than the territorial pattern of an acute coronary occlusion, though regional patterns do occur and are not reassuring on their own) and any pericardial effusion.

Cardiac MRI — the cornerstone noninvasive diagnostic tool

Cardiac MRI is central to modern myocarditis diagnosis, characterizing myocardial edema, hyperemia, necrosis/fibrosis (via late gadolinium enhancement), pericardial inflammation, and LV function in a single noninvasive study.^[1] The updated (2018) Lake Louise diagnostic criteria require at least one T2-based marker of myocardial edema (T2-weighted imaging or T2 mapping) and at least one T1-based marker of non-edematous injury (late gadolinium enhancement, T1 mapping, or extracellular volume), with pericardial effusion and systolic dysfunction as supportive additional findings. Late gadolinium enhancement in particular carries independent prognostic weight — its presence is associated with a worse long-term trajectory — which is why CMR findings feed directly into the follow-up risk-stratification described in Monitoring & Follow-Up.^[1]

Endomyocardial biopsy — reserved, not routine, but genuinely decision-changing in specific scenarios

Endomyocardial biopsy (EMB) remains the reference standard for identifying a specific, etiology-directed diagnosis (most importantly, distinguishing giant cell and eosinophilic myocarditis from the far more common lymphocytic/viral pattern) and for excluding mimics, but it is not recommended routinely given its procedural risk and imperfect sensitivity from sampling error.^[1] The classic case-definition indications, still in current use, are:

^[6] Outside these and a small number of other specific scenarios (e.g., suspected cardiac sarcoidosis, or unexplained cardiomyopathy where the result would change management), EMB adds procedural risk without changing the treatment plan for the large majority of hemodynamically stable, non-progressive presentations — see Common Errors to Avoid.

Additional testing and differential diagnosis

• Coronary angiography (or CT coronary angiography in appropriate lower-risk patients) to exclude obstructive coronary artery disease when the presentation mimics acute coronary syndrome — myocarditis is a diagnosis reached partly by exclusion in this scenario, and this should not be skipped out of an assumption that a young patient "can't have a heart attack."
• Inflammatory markers (CRP, ESR) are nonspecific but can support the overall clinical picture.
• Routine viral serology is generally low-yield and rarely changes management; targeted testing (e.g., HIV, Lyme serology, specific testing suggested by epidemiologic exposure or travel history) is more useful than a broad, undirected viral panel.
• A peripheral eosinophil count can support suspected eosinophilic myocarditis, though a normal count does not exclude it.
• Genetic counselling and testing, per the 2024 ACC pathway, for patients where a hereditary cardiomyopathy component is plausible (see Non-Pharmacologic Treatment).^[1]
• Differential diagnosis: acute coronary syndrome/myocardial infarction, Takotsubo (stress) cardiomyopathy, other forms of acute or chronic cardiomyopathy, and, in the ICI-therapy population specifically, other immune-related adverse events (myositis, pericarditis) that can coexist with or mimic myocarditis.

• Recognize the fulminant (Stage D) presentation early and escalate to a mechanical-circulatory-support-capable center without delay — this single decision has the largest effect on outcome of anything in this chapter.^[1]
• For the large majority of patients with reduced LV function: initiate and up-titrate heart-failure-directed pharmacotherapy, since no specific antiviral treatment exists for most viral myocarditis.^[8]
• Distinguish, through history, course, and — where indicated — endomyocardial biopsy, the patients who need immunosuppression as first-line therapy (giant cell myocarditis, eosinophilic myocarditis) from the majority who do not.^[2][6]
• For ICI-associated myocarditis: hold the causative agent immediately at first suspicion, regardless of severity grade, and start corticosteroids promptly given the disease's genuinely high mortality.^[3]
• For mRNA-vaccine-associated myocarditis: confirm the diagnosis, provide supportive care, and give clear guidance on future vaccine dosing per current national recommendations.^[4][7]
• Restrict competitive sport and vigorous exercise for a defined period during active inflammation, and reassess against objective criteria — not a calendar alone — before clearing return to play.^[5]
• Identify and manage life-threatening arrhythmia and high-grade conduction block promptly, including temporary or permanent pacing and defibrillator support where indicated.
• Where a hereditary component is plausible, offer genetic counselling/testing and consider first-degree-relative implications.^[1]

• Activity restriction is a genuine, specific counseling point, not a vague "take it easy" instruction — restrict competitive sport and vigorous/high-intensity exercise during active myocardial inflammation, since exercise in this setting is a recognized trigger for malignant ventricular arrhythmia; see Special Populations/Athletes and the Clinical Decision Algorithm for the specific, EF-stratified duration and clearance criteria.^[5]
• Mechanical circulatory support — intra-aortic balloon pump, percutaneous ventricular assist device, or VA-ECMO — for fulminant myocarditis with cardiogenic shock or refractory arrhythmia; this is genuinely first-line supportive therapy in this scenario, not a last resort, and early escalation (rather than prolonged high-dose inotrope/vasopressor use alone) is the safer strategy for a myocardium that may substantially recover.^[1]
• A wearable cardioverter-defibrillator is a reasonable bridge for patients with a significantly reduced LVEF early after diagnosis, given the real possibility of meaningful LV recovery over weeks to months — avoiding a premature permanent ICD decision in a cardiomyopathy that, unlike many others, can genuinely reverse.
• Standard heart-failure supportive measures (sodium/fluid moderation as appropriate, structured follow-up) for patients with reduced LV function, alongside the pharmacologic backbone.
• Genetic counselling and testing, where feasible, for patients in whom a hereditary cardiomyopathy component is plausible (a suggestive family history, an atypical or recurrent course) — a specific 2024 ACC recommendation reflecting growing recognition of a genetic-predisposition component in some myocarditis presentations.^[1]
• Avoid alcohol during the acute recovery period, consistent with general cardiomyopathy precautions.
• For confirmed or suspected mRNA-vaccine-associated cases: report to public health as an AEFI, and provide clear, written guidance on future dosing before discharge rather than leaving it to be sorted out later (see Choose Initial Treatment).^[7]
• For ICI myocarditis: coordinate closely and continuously with the treating oncology team — decisions about future cancer therapy (an alternative regimen, or the rare, carefully considered ICI rechallenge) are made jointly by cardio-oncology and oncology, not by cardiology alone.

Pediatrics

Children with myocarditis often present less specifically than adults — vomiting, lethargy, poor feeding, or abdominal pain rather than classic chest pain — which is exactly why a high index of suspicion matters in this age group; a sick-looking infant or child with unexplained tachycardia, hepatomegaly, or poor perfusion deserves cardiac consideration.^[7] For mRNA-vaccine-associated cases specifically, the Canadian Paediatric Society recommends NSAID dosing of ibuprofen 10 mg/kg/dose every 8 hours for a week (maximum 400 mg/dose, maximum 40 mg/kg/day up to 1200 mg/day), stepping down to 5 mg/kg/dose every 8 hours for a further week, with corticosteroids avoided as first-line pericarditis therapy given an association with higher recurrence risk.^[7] Activity modification for at least 1 month, or longer per specialist direction, is recommended for pediatric vaccine-associated myocarditis specifically; broader pediatric myocarditis activity restriction follows the same general principles as the adult pathway in the Clinical Decision Algorithm, individualized by a pediatric cardiologist. IVIG has been used empirically in some severe pediatric presentations at individual centers, but evidence supporting routine use is limited and inconsistent; it is not a standard, guideline-endorsed therapy and should be considered only in consultation with pediatric cardiology.

Athletes and the activity-restriction/return-to-play decision

Vigorous exercise during active myocardial inflammation can provoke malignant ventricular arrhythmia, which is why activity restriction is treated as a genuine safety intervention throughout this chapter rather than routine convalescence advice.^[5] Practice has genuinely evolved here: the older, still widely used standard calls for a flat 3-6 months of complete abstinence from competitive sport and vigorous exercise, with resting echocardiography, ambulatory ECG monitoring, and exercise testing before clearance.^[1] The 2025 AHA/ACC scientific statement on competitive sports participation offers a more nuanced, criteria-based, EF-stratified approach: for myocarditis with preserved LV function, resumption may reasonably occur 4-6 weeks after complete symptom resolution, provided inflammation has resolved (typically confirmed by cardiac MRI) and no relevant arrhythmia is present on monitoring; for myocarditis with reduced LV function, the more conservative at least 3 months symptom-free threshold still applies, again with confirmed resolution of inflammation and normalized function.^[5] Both approaches remain defensible in current practice, and the decision should be individualized and specialist-directed rather than mechanically applying whichever number is more familiar — see the Clinical Decision Algorithm for the full pathway.

Pregnancy

Peripartum cardiomyopathy is an important differential/overlapping consideration in a pregnant or recently postpartum patient with new heart failure and should be considered alongside myocarditis. ACE inhibitors, ARBs, ARNIs, and mineralocorticoid receptor antagonists are contraindicated in pregnancy; a beta-blocker and, where needed, hydralazine/nitrates form the mainstay of heart-failure pharmacotherapy in this setting, with delivery planning and management coordinated jointly by cardiology and maternal-fetal medicine.

Immunocompromised patients

Broaden the infectious differential in immunocompromised patients (transplant recipients, patients on significant immunosuppression) — cytomegalovirus and other opportunistic organisms become more relevant causes of myocarditis in this population, and specialist infectious disease input is appropriate.

Renal and hepatic impairment

Adjust ACE inhibitor/ARNI, spironolactone, and SGLT2 inhibitor dosing for renal function per standard heart-failure references, and monitor potassium and creatinine closely, particularly when combining an ACE inhibitor or ARNI with an MRA. Cyclosporine requires trough-level-guided dosing that is further complicated by renal or hepatic impairment — manage this specifically with the transplant/immunosuppression specialist team rather than by extrapolation.

• Repeat echocardiography at 2-4 weeks for patients who presented with Stage C or D disease, then again at 6 months to distinguish a lower-risk group (normalized LVEF, no late gadolinium enhancement) from a higher-risk group who may need continued cardiac MRI surveillance and closer follow-up.^[1]
• Reassess for arrhythmia — ambulatory ECG monitoring and, where relevant, exercise testing — as part of both routine follow-up and specifically before any return-to-play decision (see Special Populations/Athletes).^[5]
• For patients on immunosuppression (giant cell myocarditis, eosinophilic myocarditis, ICI myocarditis): monitor CBC, renal and hepatic function, and infection risk per the specific regimen, and confirm cyclosporine trough levels are on target where applicable.
• For ICI myocarditis survivors: cardiology and oncology should jointly review before any consideration of ICI rechallenge, given the disease's high mortality and the limited evidence base for safely resuming ICI therapy after a myocarditis event.
• For mRNA-vaccine-associated myocarditis: follow-up with the primary care provider within about a week if symptoms are improving, with specialist follow-up determined by severity and course; confirm the revaccination/deferral plan is documented and understood before the patient leaves care.^[7]
• Patient education: teach patients to recognize and promptly report new or worsening chest pain, dyspnea, palpitations, or presyncope during the recovery period; reinforce the specific activity-restriction plan and the objective criteria (not just a calendar date) that will be used to clear return to exercise or sport; and, for ICI or vaccine-triggered cases, explain clearly why the causative agent is being held or a future dose deferred, since this is often a source of real patient anxiety and confusion.
• Where genetic testing was pursued, ensure results are reviewed and, if a pathogenic variant is identified, that first-degree-relative implications are discussed.

1. Reduced LV function not improving despite optimized heart-failure-directed pharmacotherapy: reassess adherence and titration first, then reconsider whether endomyocardial biopsy is now indicated (a new ventricular arrhythmia, new high-grade AV block, or failure to respond within 1-2 weeks are each, on their own, indications per the Class I criteria) rather than continuing to escalate GDMT alone indefinitely.^[6]
2. Cardiogenic shock refractory to inotropic/vasopressor support: escalate without delay to mechanical circulatory support and formal transplant evaluation at a capable center — do not persist with escalating catecholamine doses as a substitute for mechanical support.^[1]
3. Giant cell myocarditis not responding to first-line corticosteroid-plus-cyclosporine therapy: escalate to additional immunosuppression (anti-thymocyte globulin or alemtuzumab) and ensure the patient is already listed or actively being evaluated for transplant, given the disease's substantial residual mortality even with treatment.^[2]
4. ICI myocarditis not improving within 24-48 hours of corticosteroids: escalate promptly to second-line immunosuppression (anti-thymocyte globulin, abatacept, ruxolitinib, tocilizumab, IVIG, or plasmapheresis) as a multidisciplinary cardio-oncology decision — avoid infliximab specifically if concurrent heart failure or significantly reduced LVEF is present.^[3]
5. Persistent high-grade AV block or life-threatening arrhythmia despite treatment of the underlying myocarditis: manage per standard pacing/ICD indications, using a wearable cardioverter-defibrillator as a bridge where meaningful LV recovery still seems plausible rather than proceeding immediately to a permanent device.
6. Vaccine-associated myocarditis with a course that is more severe or more persistent than the typical mild, self-limited pattern: broaden the work-up (cardiac MRI if not already done, reconsider endomyocardial biopsy) rather than continuing to manage it as routine mild disease.^[7]

• Dismissing chest pain, fatigue, or dyspnea following a recent viral illness in a young, otherwise healthy patient as "just the virus" without considering myocarditis and screening for red flags.
• Underestimating how quickly a seemingly mild presentation can progress — missing the fulminant trajectory by not reassessing hemodynamic status closely enough in the first hours to days.^[1]
• Ordering endomyocardial biopsy routinely in hemodynamically stable, non-progressive myocarditis where it adds procedural risk without changing management — versus the opposite, and arguably more consequential, error of not obtaining an urgent biopsy in the two specific Class I scenarios where the result genuinely changes treatment.^[6]
• Using NSAIDs in a patient with myocarditis and LV dysfunction or heart failure, rather than reserving them for pericarditic-type pain specifically in patients without LV dysfunction.^[1]
• Failing to hold an immune checkpoint inhibitor immediately at the first suspicion of myocarditis, including mild (grade 1) presentations — this is precisely the scenario where ICI myocarditis's disproportionate mortality makes early action non-negotiable.^[3]
• Reaching for infliximab as a familiar second-line immunosuppressant in ICI myocarditis without recognizing that TNF-alpha inhibitors can themselves worsen heart failure — avoid it specifically when concurrent heart failure or significantly reduced LVEF is present.^[3]
• Treating giant cell or eosinophilic myocarditis with the same supportive-care-only approach as typical viral myocarditis, rather than recognizing the need for immunosuppression as first-line, disease-specific therapy.^[2]
• Applying a rigid, one-size-fits-all activity-restriction rule without individualizing to LV function and objective recovery criteria — both the traditional 3-6-month approach and the newer EF-stratified, criteria-based approach are defensible, but neither should be applied mechanically without reassessment.^[5]
• Alarming patients about mRNA COVID-19 vaccination out of proportion to its actual risk — SARS-CoV-2 infection itself is a meaningfully more common and more severe trigger of myocarditis than the vaccines used to prevent it, and this context is worth proactively sharing with a concerned patient or parent.^[4]
• Forgetting to document and communicate a clear future-dosing/revaccination plan after a vaccine-associated myocarditis event, leaving the patient and their primary care provider without guidance at the next scheduled dose.^[7]
• Assuming a dramatic, fulminant presentation necessarily predicts a worse long-term outcome than a milder-looking one — the opposite is often true once the acute phase is survived with appropriate support.^[9]

How to use this table: Doses are adult doses and require patient-specific confirmation (renal/hepatic function, weight, allergy history). Pediatric dosing is weight-based per the current product monograph unless stated. Drug pricing is intentionally omitted. Select any drug name to open its complete Pharmasist Drug Database page.

Heart-Failure-Directed Pharmacotherapy — the Backbone of Management

For reduced LV function; there is no specific antiviral treatment for most viral myocarditis, so this is genuinely first-line care, following standard HFrEF titration principles.

Acute Hemodynamic Support — Fulminant Myocarditis

A bridge to mechanical circulatory support, not a substitute for it — early escalation to MCS is preferred over prolonged high-dose catecholamine exposure in a myocardium that may recover.

Anti-Inflammatory Analgesia — Pericarditic-Type Pain Only

Reserve for pericarditic-type chest pain in patients WITHOUT LV dysfunction; avoid when LV dysfunction or heart failure is present.

Giant Cell Myocarditis — Combination Immunosuppression

Start without delay once confirmed or strongly suspected; combined with parallel early transplant evaluation given substantial residual mortality even with treatment.

Eosinophilic Myocarditis

Corticosteroids are the mainstay; identifying and removing a causative trigger (e.g., a hypersensitivity/DRESS-associated drug) is just as important as the drug therapy itself.

Immune Checkpoint Inhibitor (ICI) Myocarditis — Corticosteroids and Steroid-Refractory Escalation

Hold the ICI immediately at any suspected grade before starting this pathway; escalate to second-line agents if not improving within 24-48 hours of corticosteroids.

Arrhythmia Management — a Specific Caution

Active myocardial inflammation heightens sensitivity to certain agents; prefer standard heart-failure-directed rate control where possible.