Myocarditis

Myocarditis is a genuinely humbling diagnosis to approach by echocardiography alone — its appearance so often overlaps with dilated cardiomyopathy that the real diagnostic skill lies less in recognizing one characteristic pattern and more in knowing exactly what echo can and can’t tell you, and what has to come from elsewhere. See Introduction to Diseases of the Myocardium for how myocarditis fits into the broader diagnostic framework this page builds on. This page draws primarily on the dedicated 2025 ESC guideline for the management of myocarditis and pericarditis, the first guideline to formally unify these two conditions under a shared diagnostic framework.

What Myocarditis Is

Myocarditis is myocardial inflammation, infectious or non-infectious in origin, producing a clinical picture that ranges from entirely asymptomatic to fulminant cardiogenic shock. The 2025 ESC guideline introduces a unifying term worth knowing: inflammatory myopericardial syndrome (IMPS) — covering myocarditis, pericarditis, and their overlap (myopericarditis or perimyocarditis), recognizing that these conditions frequently coexist and share diagnostic machinery rather than existing as entirely separate entities.

Etiology

A genuinely broad range of causes converges on the same inflammatory endpoint:

Category	Examples
Viral	Coxsackievirus A and B, echovirus, influenza A and B, respiratory syncytial virus, HIV-1, parvovirus B19, adenovirus, cytomegalovirus, herpes simplex virus, HHV-6, Epstein-Barr virus
Bacterial, spirochetal, protozoal	Haemophilus influenzae, mycobacteria, Borrelia and Leptospira species, Trypanosoma cruzi (Chagas disease)
Drugs and toxins	Immune checkpoint inhibitors, anthracyclines, fluorouracil, catecholamines, interleukin-2, trastuzumab, cyclophosphamide, copper, iron, lead, scorpion and wasp stings, snake and spider bites, radiation
Immune-mediated	Lymphocytic and giant cell myocarditis, systemic lupus erythematosus, rheumatoid arthritis, Churg-Strauss syndrome, Kawasaki disease, hypereosinophilic syndrome, inflammatory bowel disease, scleroderma, polymyositis, myasthenia gravis, sarcoidosis, Wegener granulomatosis, graft rejection

The Central Honesty: No Echo Finding Is Pathognomonic

This is worth stating as plainly as the sources do: echocardiographic findings in myocarditis are frequently indistinguishable from dilated cardiomyopathy, and no single finding confirms the diagnosis. Equally important — the echocardiogram can be entirely normal in confirmed myocarditis. Neither a DCM-like appearance nor a normal study should be read as settling the question in either direction.

Formal Diagnostic Criteria (2025 ESC)

Rather than relying on imaging alone, the current framework classifies myocarditis as definite, possible, or unlikely/rejected based on clinical presentation plus a structured set of additional criteria:

Category	Additional criterion
Clinical	Non-specific findings
ECG	ST-T changes
Biomarkers	Troponin elevation
Imaging	Abnormal strain, wall motion, or reduced EF; myocardial edema and/or LGE on CMR

• Definite: clinical presentation (chest pain or infarct-like symptoms, arrhythmia, heart failure, or aborted sudden cardiac death) plus CMR- or endomyocardial biopsy-proven findings.
• Possible: clinical presentation plus at least one additional criterion, with CMR or biopsy uncertain or unavailable.
• Unlikely/rejected: clinical presentation alone, without additional criteria.

A genuinely strong, actionable rule worth internalizing: if ECG changes are present, myocarditis should always be actively considered or excluded — not treated as a routine, nonspecific finding.

Echocardiographic Findings

Core Assessment

Evaluation centers on four components: LV ejection fraction, valvular function, segmental wall thickening, and RV function. In the acute phase, expect some combination of:

• Global or regional transient wall thickening, from myocardial edema
• Regional wall motion abnormality in a patchy distribution that doesn’t follow a coronary artery territory, or global LV systolic dysfunction
• Pericardial effusion, when pericardial involvement accompanies the myocardial process (myopericarditis)
• Or — genuinely possible — a completely normal echocardiogram

A Genuine, Temporary HCM Mimic: Edema-Related Wall Thickening

Myocardial edema can produce a real, if transient, increase in wall thickness during the acute phase — worth recognizing specifically as a mimic of true hypertrophy, since it resolves as inflammation subsides rather than representing fixed structural disease. The same inflammatory cell infiltration can also increase myocardial echogenicity and brightness by altering the tissue’s acoustic properties — though, consistent with the “granular sparkling” caution established elsewhere in this section (see Cardiac Amyloidosis), this finding is nonspecific and shouldn’t be relied upon for diagnosis on its own.

Excluding the Key Mimic: Ischemic Disease

Because abnormal wall motion can result from either myocarditis or coronary disease, and the two can look similar on a single study, coronary CT angiography — with high sensitivity, specificity, and negative predictive value for obstructive CAD — is an excellent noninvasive way to exclude ischemic disease as the cause of troponin elevation when myocarditis is clinically suspected, rather than assuming the diagnosis from wall motion pattern alone. Invasive coronary angiography remains an option when CTA is inconclusive or unavailable.

Functional Mitral Regurgitation

Regional or global LV dysfunction frequently produces functional mitral regurgitation — see Mitral Regurgitation for the general secondary-MR mechanism this follows. A genuinely distinctive finding worth knowing from an illustrative case of acute fulminant presentation: a posteriorly-directed, wall-hugging MR jet with a diastolic component on continuous-wave Doppler, reflecting acute elevation in LV filling pressure — a specific marker of the acute hemodynamic stress this disease can produce, distinct from the holosystolic pattern MR usually shows.

Diastolic Function

Diastolic dysfunction is common and genuinely variable in severity — ranging from mild impairment to a fully restrictive filling pattern. See LV Diastolic Function for the general grading framework. A specific, important prognostic point: persistence of diastolic dysfunction after LV systolic function has recovered or normalized is independently associated with worse long-term outcome — making diastolic reassessment a genuine part of follow-up, not something to stop tracking once the ejection fraction looks reassuring.

Strain Imaging

Global longitudinal strain, global circumferential strain, and strain rate are all reduced in acute myocarditis — even with a preserved ejection fraction — making strain a genuinely useful tool for detecting subclinical disease that conventional measures miss.

• Regional GLS impairment correlates with the extent of myocardial injury seen on CMR, and can predict ventricular arrhythmia and outcomes.
• Abnormal RV strain and left atrial strain have both been detected in acute myocarditis with preserved EF — genuine subclinical markers worth incorporating when myocarditis is suspected, even when the standard structural and functional assessment looks unremarkable.
• A practical caveat worth stating honestly: routine clinical use of strain imaging for myocarditis diagnosis remains guided primarily by clinical presentation and confirmed by complementary CMR — strain adds genuine diagnostic and prognostic value, but isn’t yet a standalone diagnostic tool here.

Eosinophilic Myocarditis: A Distinctive Pattern Worth Recognizing Separately

Eosinophilic myocarditis is a rare, potentially life-threatening form presenting with peripheral eosinophilia, and it has its own recognizable echo pattern distinct from the general findings above: LV hypokinesis with thrombus, most commonly located at the apex. With disease progression, endomyocardial fibrosis and restrictive cardiomyopathy can develop — the same disease spectrum covered in depth on the Endomyocardial Fibrosis page, where this pattern, its staged necrosis-to-fibrosis progression, and its distinctive diagnostic criteria are discussed fully. Endocardial fibrosis and thrombus can also extend to involve the valve leaflets and subvalvular apparatus, producing restricted leaflet motion and mitral or tricuspid regurgitation.

Systemic lupus erythematosus-induced myocarditis has its own associated pattern worth knowing specifically: pericardial effusion alongside valvular abnormalities — leaflet thickening, vegetations, and valve distortion or dysfunction — reflecting the broader autoimmune valvulopathy that can accompany lupus-related cardiac involvement.

ECG and Biomarkers

ECG is frequently abnormal, though the findings are nonspecific: diffuse ST-T changes, ST-segment elevation that can mimic acute myocardial infarction, conduction abnormalities, and low voltage from either myocardial edema or an accompanying pericardial effusion. Cardiac troponin is often elevated but is similarly nonspecific — and a genuinely important caveat — normal troponin values do not exclude myocarditis.

Cardiac MRI: The Current Diagnostic Backbone

CMR is recommended (Class I, Level B) in suspected myocarditis to reach a clinical diagnosis and determine the cause of acute myocardial injury — assessing edema, ischemia, and necrosis, fibrosis, or scarring directly. The updated Lake Louise Criteria require at least one T2-based criterion (detecting myocardial edema) plus, ideally, one T1-based criterion (detecting necrosis or fibrosis) — having both increases diagnostic specificity, though a diagnosis of possible myocarditis can still be made with only one criterion, with correspondingly lower specificity. Supportive findings include pericardial abnormalities (suggesting concomitant pericarditis) and global or regional LV systolic dysfunction on cine imaging.

• The resulting LGE pattern in myocarditis is non-ischemic — mid-wall, subepicardial, or patchy — and does not follow a coronary artery distribution, the same principle underlying the echo wall-motion pattern above.
• Timing matters: diagnostic accuracy is higher when CMR is performed early in the disease course, ideally within the first two weeks.
• CMR is also recommended for follow-up, at least within the first six months (Class I, Level C), to distinguish a healed from an ongoing process, support risk stratification and personalized therapy, and inform the decision to return to exercise.
• A genuine limitation worth stating: imaging evidence of myocardial inflammation confirms that inflammation is present, but does not reveal the underlying histotype — lymphocytic, eosinophilic, and giant cell myocarditis can look similar on CMR despite being genuinely different diseases with different treatments.

Endomyocardial Biopsy

Remains the definitive method for histologic diagnosis, distinguishing active, persistent, and resolved lymphocytic myocarditis, eosinophilic myocarditis, giant cell myocarditis, and sarcoidosis from one another by their specific inflammatory cell populations and necrosis pattern. Biopsy carries genuine procedural risk, including cardiac perforation and tamponade, and is generally not recommended for routine initial assessment — reserved instead for situations (fulminant presentations, suspected giant cell myocarditis, or cases where the result would change management) where its added specificity is worth the risk.

Follow-Up

LV systolic function should be reassessed over time, since myocarditis can evolve into dilated cardiomyopathy in a meaningful subset of patients — the same evolution discussed from the DCM side on that page’s differential diagnosis section. Serial imaging tracks this trajectory, distinguishes genuine recovery from a healed-but-altered substrate, and — paired with CMR follow-up — supports decisions about resuming exercise and athletic activity.

How to Diagnose It: A Practical Sequence

1. Approach the study without expecting a single confirmatory finding — myocarditis frequently resembles DCM, and a normal echocardiogram never excludes the diagnosis.
2. Assess the four core components systematically: LVEF, valvular function, segmental wall thickening, and RV function.
3. Look specifically for a patchy, non-coronary pattern of regional wall motion abnormality, and pursue coronary CTA (or invasive angiography) when the clinical picture doesn’t clearly exclude ischemic disease.
4. Note any transient wall thickening and consider myocardial edema as the explanation, particularly in the acute phase — without over-interpreting it as fixed hypertrophy.
5. Add strain imaging — GLS, and RV and LA strain where feasible — since these can detect subclinical disease even with a preserved ejection fraction.
6. Assess diastolic function fully, and continue tracking it even after systolic function appears to recover, given its independent prognostic weight when persistently abnormal.
7. Consider eosinophilic myocarditis specifically when LV hypokinesis accompanies apical thrombus and peripheral eosinophilia, and watch for its potential evolution toward endomyocardial fibrosis.
8. Correlate with ECG and troponin, remembering that a normal troponin doesn’t rule out the diagnosis and that ST-T changes should always prompt active consideration of myocarditis.
9. Recommend CMR, ideally within two weeks of presentation, as the test that actually confirms the diagnosis in most cases — and plan follow-up CMR within six months to assess resolution.
10. Reserve endomyocardial biopsy for fulminant presentations, suspected giant cell myocarditis, or cases where histologic confirmation would directly change management.

Clinical Importance

Myocarditis is the condition in this section that most directly tests whether a diagnostic approach actually understands echocardiography’s limits rather than just its findings — because here, the honest answer to “what does the echo show” is often “something that looks like DCM, or nothing at all,” and the real diagnostic work happens in the combination of ECG, biomarkers, strain, and CMR that echo alone was never meant to replace. Recognizing that limitation isn’t a weakness in the echocardiographic assessment — it’s precisely what the 2025 ESC framework was built to formalize.