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{{Adult patient  | pediatric page=Myocarditis (peds)}}
==Background==
==Background==
*Inflammatory (dilated) cardiomyopathy caused by necrosis of myocytes  
[[File:Triggers of myocarditis.png|thumb|Triggers of myocarditis. Myocarditis can be induced by both infectious and non-infectious pathogens, with viral infection being the most common cause (red background).]]
*Inflammatory [[cardiomyopathy]] caused by damage and necrosis of myocytes
*Viral-induced is the most common etiology<ref>Cooper LT Jr. Myocarditis. ''N Engl J Med''. 2009;360(15):1526-38. PMID 19357408</ref>
*Clinical presentation ranges from smoldering [[heart failure]] to fulminant [[cardiogenic shock]] or sudden death
*Maintain high index of suspicion in younger patients without traditional CAD risk factors
*Incidence: estimated 1.5 million cases worldwide annually
*'''Giant cell myocarditis''' is a rapidly fatal variant requiring early recognition


===Causes===
===Causes===
*Infectious agents
*Viral (most common):
**[[Enterovirus]] (Coxsackie B) and [[adenovirus]] most common
**Enterovirus (Coxsackie B) and adenovirus (historically most common)
**[[Influenza]] A and B
**Parvovirus B19 and HHV-6 (currently most detected on biopsy)
**[[Hepatitis B]]
**Influenza A and B, [[HIV]], [[hepatitis]] B/C, COVID-19
**[[Beta-hemolytic streptococcus]]
*Bacterial: [[Lyme disease]], beta-hemolytic strep, [[Mycoplasma]], diphtheria
**[[Mycoplasma]]
*Parasitic: Chagas disease (most common cause worldwide), toxoplasma, trichinosis
**[[Mumps]]
*Autoimmune: [[sarcoidosis]], [[SLE]], giant cell myocarditis
**[[CMV]]
*Drugs/toxins: cocaine, doxorubicin, immune checkpoint inhibitors, [[amphetamines]]
**[[Toxoplasma]]
**[[Chagas]] (most common cause worldwide
**[[Trichinosis]]
**[[Diphtheria]]
**[[Lyme disease]]
*Drugs
**[[Doxorubicin]]
**[[Cocaine]]


===Phases===
===Phases===
*Acute
*Acute: direct cytotoxicity and focal necrosis from viral, autoimmune, or toxins
**Viral cytotoxicity and focal necrosis  
*Subacute: host immune response (viral molecular mimicry, anti-myocyte antibody production)
*Subacute
*Chronic: diffuse myocardial fibrosis and cardiac dysfunction
**Host's humoral/immune response leading to further cell injury
*Chronic
**Diffuse myocardial fibrosis and cardiac dysfunction


==Clinical Features==
==Clinical Features==
*Typically young patients (20 - 50 years) with few risk factors for CAD  
*Typically young patients (20-50 years) with few risk factors for CAD
*[[Chest pain]]  
*Preceding viral illness in 50-80% of cases (1-2 weeks prior)
*Pericardial friction rub
*Chest pain or chest pressure/tightness (mimics [[ACS]])
*Flu like syndrome
*Flu-like symptoms: [[fever]], fatigue, [[myalgia]]s, nausea/vomiting
**Fever, fatigue, myalgia, nausea and vomiting
*Tachycardia out of proportion to fever
**Tachycardia (out of proportion to fever)
*New-onset [[heart failure]]: fatigue, [[orthopnea]], [[dyspnea]] on exertion
**Tachypnea
*Consider this diagnosis in the septic-appearing patient who worsens after IV fluids
*New onset [[congestive heart failure]]
*May present with [[sudden cardiac arrest]] (especially in young athletes)
*Pediatric patients:
*Pediatric patients: see [[myocarditis (peds)]]
**Grunting
**Retractions
**Ronchi
*Infants may have fulminant syndrome
**Fever
**Cyanosis
**Respiratory distress
**Tachycardia
**Heart failure
**Ventricular dysrhythmias


*Consider this diagnosis in the septic-appearing patient who gets WORSE after receiving IV fluids
==Differential Diagnosis==
*[[Acute coronary syndrome]] (most important to rule out)
*[[Pericarditis]] / [[myopericarditis]]
*[[Takotsubo cardiomyopathy]] (stress cardiomyopathy)
*[[Pulmonary embolism]]
*[[Pneumonia]]
*[[Sepsis]] from other cause


==Differential Diagnosis==
{{Chest pain DDX}}
''Consider other causes of [[CHF]]''
{{Chest Pain DDX}}


==Evaluation==
==Evaluation==
*[[ECG]]
[[File:12 lead EKG ST elevation with myocarditis.jpg|thumb|Diffuse ST elevation in a patient with combined myocarditis and pericarditis.]]
**Sinus tachycardia
===ECG===
**Low voltages
*'''Must be obtained to rule out STEMI'''
**[[Prolonged QTc]]
*Sinus tachycardia (most common finding)
**AV block
*Diffuse ST changes, nonspecific ST-T wave abnormalities
**ST elevations (Usually >1 vessel distribution)  
*Low voltages
*Elevated troponin
*Prolonged QTc
*Echocardiogram
*AV block (especially with [[Lyme disease]] or [[sarcoidosis]])
**Decreased LVEF
*Wide QRS / new [[LBBB]]
**Global hypokinesis
*Normal ECG does NOT rule out myocarditis
**Regional wall motion abnormalities  
 
*Contrast MR
===Labs===
*Nuclear Study
*Troponin: elevated in ~50% of cases; sensitivity limited
**Widespread uptake indicating myocyte necrosis
*BNP/NT-proBNP: reflects degree of heart failure
*Viral titres
*CBC, BMP, LFTs
*Endocardial biopsy: Gold standard, but rarely used
*[[ESR]], [[CRP]] (usually elevated but nonspecific)
*Consider viral serologies, Lyme titer, ANA (if autoimmune suspected)
*Blood cultures (if infectious etiology suspected)
 
===Imaging===
*CXR: cardiomegaly, pulmonary edema, or pleural effusion
*Echocardiography (essential in ED):
**Decreased LVEF, global hypokinesis or regional wall motion abnormalities
**Can detect pericardial effusion (myopericarditis)
**Fulminant myocarditis may show normal LV dimensions with increased wall thickness
*Cardiac MRI (noninvasive gold standard): myocardial edema and late gadolinium enhancement
*Endomyocardial biopsy: invasive gold standard, reserved for unexplained cardiomyopathy or suspected giant cell myocarditis


==Management==
==Management==
*Acute phase
===ED Management===
**Antiviral agents (Pleconaril/[[Ribavirin]]) may be effective
*IV access, continuous monitoring, 12-lead ECG
*Subacute phase
*Rule out ACS: may require coronary angiography if ST elevation or high clinical suspicion
**Studies have not shown efficacy of immunosupressants
*Avoid NSAIDs and aspirin in acute phase (animal studies suggest increased inflammation)
**Pediatric patients may receive high-dose [[IVIG]]
*'''Volume status''': use caution with IV fluids — may worsen [[heart failure]]
*Chronic phase
**If [[cardiogenic shock]]: consider vasopressors/inotropes (dobutamine, milrinone)
**Treatment for CHF symptoms
*Dysrhythmia management:
**Ventricular Assist Devices (VAD)
**Avoid class IC antiarrhythmics
**Cardiac transplant
**Amiodarone for sustained [[VT]]
**Temporary pacing for complete heart block
*Anticoagulation consideration if severely reduced LVEF with LV thrombus risk
 
===Definitive Treatment===
*Supportive care is mainstay; most viral myocarditis self-resolves
*GDMT for heart failure: ACE-I/ARB, beta-blockers, diuretics (as tolerated by hemodynamics)
*Mechanical circulatory support (ECMO, VAD) for refractory cardiogenic shock
*Giant cell myocarditis: requires immunosuppression (cyclosporine + corticosteroids)
*Cardiac transplant for end-stage disease
*'''Activity restriction''': no competitive sports for 3-6 months per AHA guidelines<ref>Caforio ALP, et al. Current state of knowledge on aetiology, diagnosis, management, and therapy of myocarditis: a position statement of the ESC. ''Eur Heart J''. 2013;34(33):2636-2648. PMID 23824828</ref>


==Disposition==
==Disposition==
*If [[CHF]] is present, admit to monitored bed
*Admit all patients with suspected myocarditis to a monitored bed
*If hemodynamically unstable, admit to ICU
*ICU admission for hemodynamic instability, arrhythmias, or reduced LVEF
*Early cardiology consultation
*Consider transfer to center with mechanical circulatory support capability


==Prognosis==
==Prognosis==
*Fulminant myocarditis has best prognosis  
*Fulminant myocarditis paradoxically has the best long-term prognosis if patient survives the acute phase
*Mortality: 20% 1 yr/ 50% 5 yr
*Overall mortality: ~20% at 1 year, ~50% at 5 years for non-fulminant forms
*Children with 70% survival rate at 5 yrs<br>
*Children: ~70% survival rate at 5 years
*Most patients with mild disease recover completely


==Complications==
==Complications==
*Ventricular dysrhythmias  
*[[Ventricular dysrhythmias]] / [[sudden cardiac arrest]]
*LV anneurysm
*[[Dilated cardiomyopathy]]
*[[CHF]]
*Chronic [[heart failure]]
*LV aneurysm / thrombus formation


==See Also==
==See Also==
*[[Cardiomyopathy]]  
*[[Cardiomyopathy]]
*[[Pericarditis]]  
*[[Pericarditis]]
*[[Heart failure]]
*[[Cardiogenic shock]]
*[[Myocarditis (peds)]]
 
==External Links==
*[https://www.jacc.org/doi/10.1016/j.jacc.2024.10.080 2024 ACC Expert Consensus on Myocarditis]


==References==
==References==
<references/>
<references/>
*Ammirati E, et al. Clinical presentation and outcome in a contemporary cohort of patients with acute myocarditis. ''Circulation''. 2018;138(11):1088-1099. PMID 29764898
*Tschöpe C, et al. Myocarditis and inflammatory cardiomyopathy: current evidence and future directions. ''Nat Rev Cardiol''. 2021;18(3):169-193. PMID 33046850
*Writing Committee; Drazner MH, et al. 2024 ACC Expert Consensus Decision Pathway on Myocarditis. ''J Am Coll Cardiol''. 2025;85(4):391-431. PMID 39665703
[[Category:Cardiology]]
[[Category:Cardiology]]

Revisión actual - 09:24 22 mar 2026

Template:Adult patient

Background

File:Triggers of myocarditis.png
Triggers of myocarditis. Myocarditis can be induced by both infectious and non-infectious pathogens, with viral infection being the most common cause (red background).
  • Inflammatory cardiomyopathy caused by damage and necrosis of myocytes
  • Viral-induced is the most common etiology[1]
  • Clinical presentation ranges from smoldering heart failure to fulminant cardiogenic shock or sudden death
  • Maintain high index of suspicion in younger patients without traditional CAD risk factors
  • Incidence: estimated 1.5 million cases worldwide annually
  • Giant cell myocarditis is a rapidly fatal variant requiring early recognition

Causes

  • Viral (most common):
    • Enterovirus (Coxsackie B) and adenovirus (historically most common)
    • Parvovirus B19 and HHV-6 (currently most detected on biopsy)
    • Influenza A and B, HIV, hepatitis B/C, COVID-19
  • Bacterial: Lyme disease, beta-hemolytic strep, Mycoplasma, diphtheria
  • Parasitic: Chagas disease (most common cause worldwide), toxoplasma, trichinosis
  • Autoimmune: sarcoidosis, SLE, giant cell myocarditis
  • Drugs/toxins: cocaine, doxorubicin, immune checkpoint inhibitors, amphetamines

Phases

  • Acute: direct cytotoxicity and focal necrosis from viral, autoimmune, or toxins
  • Subacute: host immune response (viral molecular mimicry, anti-myocyte antibody production)
  • Chronic: diffuse myocardial fibrosis and cardiac dysfunction

Clinical Features

  • Typically young patients (20-50 years) with few risk factors for CAD
  • Preceding viral illness in 50-80% of cases (1-2 weeks prior)
  • Chest pain or chest pressure/tightness (mimics ACS)
  • Flu-like symptoms: fever, fatigue, myalgias, nausea/vomiting
  • Tachycardia out of proportion to fever
  • New-onset heart failure: fatigue, orthopnea, dyspnea on exertion
  • Consider this diagnosis in the septic-appearing patient who worsens after IV fluids
  • May present with sudden cardiac arrest (especially in young athletes)
  • Pediatric patients: see myocarditis (peds)

Differential Diagnosis

Template:Chest pain DDX

Evaluation

File:12 lead EKG ST elevation with myocarditis.jpg
Diffuse ST elevation in a patient with combined myocarditis and pericarditis.

ECG

  • Must be obtained to rule out STEMI
  • Sinus tachycardia (most common finding)
  • Diffuse ST changes, nonspecific ST-T wave abnormalities
  • Low voltages
  • Prolonged QTc
  • AV block (especially with Lyme disease or sarcoidosis)
  • Wide QRS / new LBBB
  • Normal ECG does NOT rule out myocarditis

Labs

  • Troponin: elevated in ~50% of cases; sensitivity limited
  • BNP/NT-proBNP: reflects degree of heart failure
  • CBC, BMP, LFTs
  • ESR, CRP (usually elevated but nonspecific)
  • Consider viral serologies, Lyme titer, ANA (if autoimmune suspected)
  • Blood cultures (if infectious etiology suspected)

Imaging

  • CXR: cardiomegaly, pulmonary edema, or pleural effusion
  • Echocardiography (essential in ED):
    • Decreased LVEF, global hypokinesis or regional wall motion abnormalities
    • Can detect pericardial effusion (myopericarditis)
    • Fulminant myocarditis may show normal LV dimensions with increased wall thickness
  • Cardiac MRI (noninvasive gold standard): myocardial edema and late gadolinium enhancement
  • Endomyocardial biopsy: invasive gold standard, reserved for unexplained cardiomyopathy or suspected giant cell myocarditis

Management

ED Management

  • IV access, continuous monitoring, 12-lead ECG
  • Rule out ACS: may require coronary angiography if ST elevation or high clinical suspicion
  • Avoid NSAIDs and aspirin in acute phase (animal studies suggest increased inflammation)
  • Volume status: use caution with IV fluids — may worsen heart failure
  • Dysrhythmia management:
    • Avoid class IC antiarrhythmics
    • Amiodarone for sustained VT
    • Temporary pacing for complete heart block
  • Anticoagulation consideration if severely reduced LVEF with LV thrombus risk

Definitive Treatment

  • Supportive care is mainstay; most viral myocarditis self-resolves
  • GDMT for heart failure: ACE-I/ARB, beta-blockers, diuretics (as tolerated by hemodynamics)
  • Mechanical circulatory support (ECMO, VAD) for refractory cardiogenic shock
  • Giant cell myocarditis: requires immunosuppression (cyclosporine + corticosteroids)
  • Cardiac transplant for end-stage disease
  • Activity restriction: no competitive sports for 3-6 months per AHA guidelines[2]

Disposition

  • Admit all patients with suspected myocarditis to a monitored bed
  • ICU admission for hemodynamic instability, arrhythmias, or reduced LVEF
  • Early cardiology consultation
  • Consider transfer to center with mechanical circulatory support capability

Prognosis

  • Fulminant myocarditis paradoxically has the best long-term prognosis if patient survives the acute phase
  • Overall mortality: ~20% at 1 year, ~50% at 5 years for non-fulminant forms
  • Children: ~70% survival rate at 5 years
  • Most patients with mild disease recover completely

Complications

See Also

External Links

References

  1. ↑ Cooper LT Jr. Myocarditis. N Engl J Med. 2009;360(15):1526-38. PMID 19357408
  2. ↑ Caforio ALP, et al. Current state of knowledge on aetiology, diagnosis, management, and therapy of myocarditis: a position statement of the ESC. Eur Heart J. 2013;34(33):2636-2648. PMID 23824828
  • Ammirati E, et al. Clinical presentation and outcome in a contemporary cohort of patients with acute myocarditis. Circulation. 2018;138(11):1088-1099. PMID 29764898
  • Tschöpe C, et al. Myocarditis and inflammatory cardiomyopathy: current evidence and future directions. Nat Rev Cardiol. 2021;18(3):169-193. PMID 33046850
  • Writing Committee; Drazner MH, et al. 2024 ACC Expert Consensus Decision Pathway on Myocarditis. J Am Coll Cardiol. 2025;85(4):391-431. PMID 39665703
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