Myocarditis vs infarction

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myocarditis versus myocardial infarction differentiation

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Myocarditis vs. Myocardial Infarction

1. Core Definition

	Myocarditis	Myocardial Infarction (MI)
Essence	Inflammation of the myocardium - infectious, immune, or toxic	Ischemic necrosis of myocardium from arterial occlusion
Primary mechanism	Immune/inflammatory injury to myocytes	Oxygen supply-demand mismatch due to plaque rupture + thrombosis
Vessels	Normal coronary arteries (usually)	Atherosclerotic coronary artery occlusion

2. Pathogenesis

Myocarditis

The most common cause in the US is viral infection - coxsackie B viruses and enteroviruses predominate historically; more recently parvovirus B19, HHV-6, SARS-CoV-2, and HIV are increasingly implicated. Injury occurs via two mechanisms:

Direct viral cytotoxicity - viral proteins disrupt sarcolemmal integrity
Immune-mediated injury - virus-specific T cells attack infected myocytes; molecular mimicry can trigger cross-reactive immune response against myosin heavy chain

Three disease stages have been proposed:

Acute - cytotoxicity, focal necrosis
Subacute - humoral autoimmune injury
Chronic - diffuse fibrosis, dilated cardiomyopathy (DCM) in up to 16% of adults, 46% of children

Non-viral causes include Trypanosoma cruzi (Chagas disease - endemic in Latin America, ~300,000 infected in the US), Toxoplasma, Lyme disease (Borrelia - presents mainly as AV block), drug hypersensitivity, SLE, polymyositis, and post-mRNA COVID-19 vaccination (rare, mainly young males after the second dose, usually self-limited).

Myocardial Infarction

The vast majority are caused by acute coronary thrombosis overlying a disrupted or eroded atherosclerotic plaque. The sequence:

Plaque erosion/rupture exposes subendothelial collagen and necrotic plaque contents
Platelets adhere and release TXA2, ADP, serotonin - further aggregation and vasospasm
Coagulation activation via tissue factor
Complete luminal occlusion within minutes

In ~10% of MIs, occlusive atherosclerosis is absent - causes include coronary vasospasm, emboli from mural thrombi (e.g. AF), valve vegetations, small vessel vasculitis, amyloid deposition, or sickle cell disease. Within 4 hours, angiography shows thrombosis in ~90% of STEMI cases.

Progression of myocardial necrosis after coronary artery occlusion - wavefront from subendocardium outward

Necrosis begins subendocardially (most distal from epicardial vessels) and expands outward as a wavefront - Robbins & Kumar Basic Pathology

3. Who Gets It? (Epidemiology)

	Myocarditis	MI
Age	Young (teens-40s); no strong age predilection	Risk rises progressively with age; 45% occur before age 65
Sex	Males more common (especially post-vaccine myocarditis)	Men > women; gap narrows after menopause
Risk factors	Viral illness, autoimmune disease, immunosuppression, drug exposure	Atherosclerosis risk factors (HTN, DM, dyslipidemia, smoking, family history)
Prodrome	Flu-like symptoms (fever, myalgias, fatigue) 1-2 weeks prior	Usually none; or unstable angina prodrome

4. Clinical Presentation

Feature	Myocarditis	MI
Chest pain	Variable; pleuritic or positional component possible	Severe, crushing, pressure-like; radiates to arm/jaw
Fever	Common	Absent (mild inflammatory fever may occur 24-48h post-MI)
Dyspnea	Common (especially in children)	Present if significant LV dysfunction
Palpitations/arrhythmias	Prominent - PVCs, NSVT, AV block	Present - VF most feared early complication
Hemodynamic instability	Can be fulminant, especially in infants	Cardiogenic shock in large STEMI
Prodrome	Flu-like illness precedes by days-weeks	Typically absent or pre-existing angina

Key clinical clue from Rosen's Emergency Medicine: "Patients with myocarditis are usually young and have few risk factors for coronary artery disease. In myocarditis, chest pain continues without evolving ischemic ECG changes."

5. ECG Findings

	Myocarditis	MI
Pattern	Non-specific; sinus tachycardia, low voltages, prolonged QT, widened QRS	Evolving pattern: hyperacute T waves → ST elevation → Q waves → T inversion
ST changes	Diffuse or multifocal ST changes (not following one coronary territory)	ST changes in specific coronary territory (e.g. II/III/aVF for inferior MI)
AV block	Can occur (especially in Lyme, Chagas)	Can occur in inferior MI (RCA occlusion)
Key distinction	ECG abnormalities may extend beyond the distribution of a single coronary artery	Changes localized to one vascular territory
Q waves	Absent	Develop in STEMI (transmural necrosis)

6. Biomarkers

Both conditions elevate troponin - this is a common pitfall.

	Myocarditis	MI
Troponin	May be elevated (timing uncertain; negative serial troponin does NOT rule out)	Rises 2-4h, peaks 48h, remains elevated 7-10 days
CK-MB	May be elevated	Rises 2-4h, peaks 24-48h, normalizes ~72h
Pattern	Scattered, unpredictable	Predictable rise-and-fall kinetics
Inflammatory markers	ESR/CRP/WBC often elevated, but of no specific diagnostic value	Mild elevation post-MI (inflammatory response)

Cardiac biomarker kinetics after MI - Troponin I peaks at 24h and stays elevated; CK-MB peaks at 24h, normalizes by 72h

Biomarker kinetics in MI - Robbins & Kumar Basic Pathology

7. Echocardiography

	Myocarditis	MI
Wall motion	Global hypokinesis (diffuse, not matching a coronary territory)	Regional wall motion abnormality (territory-specific)
EF	Often reduced	Reduced in proportion to infarct size
Distinguishing feature	Wall motion abnormalities do NOT follow coronary artery anatomy	Wall motion abnormalities ARE in a coronary artery distribution
Pericardial effusion	Can be present (myopericarditis)	Rare (Dressler syndrome, days-weeks post-MI)

8. Advanced Imaging: Cardiac MRI (CMR)

CMR is the most powerful non-invasive tool for differentiation:

CMR Finding	Myocarditis	MI
Late gadolinium enhancement (LGE) pattern	Patchy, mid-wall or epicardial, non-coronary distribution; often septal	Subendocardial or transmural, following a coronary territory
T2 signal (edema)	Diffuse or patchy myocardial edema	Edema in area at risk (territory-specific)
Microvascular obstruction	Absent	Present in large STEMIs ("no-reflow")
Prognostic role	Septal/mid-wall LGE predicts SCD and VT risk	Infarct size predicts HF and mortality

9. Coronary Angiography

Myocarditis: Normal coronary arteries (key diagnostic finding when coronary disease is suspected)
MI: Culprit lesion with plaque rupture and thrombus; angiography demonstrates thrombotic occlusion in ~90% of STEMIs within 4 hours

10. Histopathology

Myocarditis (Dallas Criteria)

Formal diagnosis requires endomyocardial biopsy showing:

Interstitial mononuclear (lymphocytic) infiltrate
Myocyte injury/necrosis adjacent to the infiltrate
Edema and hemorrhage in active disease
No ischemic pattern - not subendocardial-predominant

Myocarditis histology - dense interstitial lymphocytic infiltrate with myocyte injury between viable cardiac muscle fibers

Viral myocarditis: diffuse lymphocytic infiltrate with myocyte necrosis - Rosen's Emergency Medicine

Myocardial Infarction

Follows a predictable temporal sequence of morphological changes:

Time	Gross	Microscopy
0-4h	None	Waviness of fibers at border
4-12h	Occasional dark mottling	Coagulative necrosis, edema, hemorrhage begins
12-24h	Dark mottling	Ongoing coagulation necrosis; pyknosis; early neutrophils
1-3 days	Mottling with yellow center	Neutrophilic infiltrate; loss of nuclei and striations
3-7 days	Hyperemic border, yellow-tan center	Dead myofibers; macrophage infiltration begins
7-10 days	Maximally yellow-tan, soft	Granulation tissue at margins
Weeks	White scar forming	Progressive fibrosis

Key: coagulative necrosis (not liquefactive), subendocardial predilection, neutrophil-then-macrophage-then-fibrosis sequence. Myocardial necrosis proceeds to scar without significant regeneration.

11. Complications

	Myocarditis	MI
Acute	Arrhythmias, AV block, fulminant heart failure, cardiogenic shock, SCD	VF/VT (80-90% of cardiac deaths in acute phase), pump failure, mechanical complications (free wall rupture, papillary muscle rupture, VSD)
Chronic	Dilated cardiomyopathy (16% adults, 46% children), persistent VT circuits from scar, SCD	LV aneurysm, Dressler syndrome, chronic HF, recurrent ischemia
SCD in young	Myocarditis is among the top causes of SCD in patients <21 years	CAD is top cause in patients >30 years

12. Management

	Myocarditis	MI
Specific therapy	Supportive; treat underlying cause (antivirals if applicable, immunosuppression in autoimmune forms)	Urgent reperfusion - thrombolysis or PCI (STEMI); antithrombotic therapy
HF management	ACEi, diuretics, beta-blockers	ACEi, beta-blockers, aldosterone antagonists, diuretics
Activity	Restrict exercise (risk of SCD during myocarditis)	Graduated cardiac rehabilitation
Arrhythmia	Beta-blockers, amiodarone; consider ICD after recovery if EF remains low	ICD if EF <35% at 40 days post-MI
Transplant	In refractory fulminant myocarditis	In end-stage ischemic cardiomyopathy

13. Quick Differentiation Summary

Clue	Points to Myocarditis	Points to MI
Age	Young (teens-40s)	Older; cardiovascular risk factors
Prodrome	Flu-like illness	None (or angina)
Chest pain character	Pleuritic, variable	Crushing, pressure, radiating
ECG ST changes	Multi-territory, non-focal	Single coronary territory
Echo wall motion	Global, non-territorial	Regional, territorial
CMR LGE	Mid-wall/epicardial, patchy	Subendocardial/transmural
Coronary angiography	Normal	Culprit lesion/thrombus
Biopsy	Lymphocytic infiltrate + myocyte necrosis	Coagulative necrosis, no inflammation initially

Sources:

Robbins & Kumar Basic Pathology, Myocardial Infarction (p. 353-359) and Myocarditis (p. 375-376)
Rosen's Emergency Medicine: Concepts and Clinical Practice, Myocarditis (p. 1119-1120)
Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine, Myocarditis and Arrhythmias
Goldman-Cecil Medicine, Myocarditis and Myocardial Infarction chapters

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