Diferencia entre revisiones de «Myocarditis»

Sin resumen de edición
(Comprehensive update: expanded causes (checkpoint inhibitors, giant cell), added EM-focused management (avoid NSAIDs, fluid caution, MCS), activity restriction, updated references with PMIDs)
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{{AdultPage|myocarditis (peds)}}
{{Adult patient  | pediatric page=Myocarditis (peds)}}
==Background==
==Background==
[[File:KVIR A 2180951 F0001 OC.jpg|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).]]
[[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
*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 Apr 9;360(15):1526-38. doi: 10.1056/NEJMra0800028. PMID: 19357408; PMCID: PMC5814110.</ref>
*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
*Clinical presentation ranges from smoldering [[heart failure]] to fulminant [[cardiogenic shock]] or sudden death
*Maintain a high index of suspicion in younger patients without traditional CAD risk factors
*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]]
**[[Sarcoidosis]]
**[[Systemic lupus erythematosus]]
**[[Diphtheria]]
**[[Lyme disease]]
**[[COVID-19]]<ref>[https://link.springer.com/article/10.1007/s11739-021-02635-w Mele D, Flamigni F, Rapezzi C, Ferrari R. Myocarditis in COVID-19 patients: current problems. Internal and Emergency Medicine. 2021. doi:10.1007/s11739-021-02635-w]</ref>
*Drugs
**[[Doxorubicin]]
**[[Cocaine]]


===Phases===
===Phases===
*Acute
*'''Acute''': direct cytotoxicity and focal necrosis from viral, autoimmune, or toxins
**Direct cytotoxicity and focal necrosis from viral, autoimmune, or toxins
*'''Subacute''': host immune response (viral molecular mimicry, anti-myocyte antibody production)
*Subacute
*'''Chronic''': diffuse myocardial fibrosis and cardiac dysfunction
**Host's humoral/immune response (viral molecular mimicry and anti-myocyte antibody production) 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]] or chest pressure/tightness
*'''Preceding viral illness''' in 50-80% of cases (1-2 weeks prior)
*[[Flu-like symptoms]]
*Chest pain or chest pressure/tightness (mimics [[ACS]])
**[[Fever]], [[fatigue]], [[myalgia]], [[nausea and vomiting]]
*Flu-like symptoms: [[fever]], fatigue, [[myalgia]]s, nausea/vomiting
**[[Tachycardia]] (out of proportion to fever)
*'''Tachycardia out of proportion to fever'''
**[[Tachypnea]]
*New-onset [[heart failure]]: fatigue, [[orthopnea]], [[dyspnea]] on exertion
*New onset [[congestive heart failure]], which may include fatigue, orthopnea, or dyspnea on exertion
*'''Consider this diagnosis in the septic-appearing patient who worsens after IV fluids'''
*Consider this diagnosis in the septic-appearing patient who gets WORSE after receiving IV fluids
*May present with [[sudden cardiac arrest]] (especially in young athletes)
*Pediatric patients: See [[myocarditis (peds)]]
*Pediatric patients: see [[myocarditis (peds)]]
 


==Differential Diagnosis==
==Differential Diagnosis==
''Consider other causes of [[CHF]]''
*[[Acute coronary syndrome]] (most important to rule out)
{{Chest Pain DDX}}
*[[Pericarditis]] / [[myopericarditis]]
*[[Takotsubo cardiomyopathy]] (stress cardiomyopathy)
*[[Pulmonary embolism]]
*[[Pneumonia]]
*[[Sepsis]] from other cause


{{Chest pain DDX}}


==Evaluation==
==Evaluation==
[[File:PericarditisMyocarditis.jpg|thumb|Diffuse ST elevation in a patient with combined myocarditis and [[pericarditis]].]]
[[File:12 lead EKG ST elevation with myocarditis.jpg|thumb|Diffuse ST elevation in a patient with combined myocarditis and pericarditis.]]
*[[ECG]] needs to be obtained to rule out ischemia. Myocarditis may exhibit the following findings:
===ECG===
**Sinus [[tachycardia]]
*'''Must be obtained to rule out STEMI'''
**Nonspecific ST-T changes
*Sinus tachycardia (most common finding)
**[[low voltage ECG|Low voltages]]
*Diffuse ST changes, nonspecific ST-T wave abnormalities
**[[Prolonged QTc]]
*Low voltages
**[[AV block]] may be present in [[Lyme disease]] or [[Sarcoidosis]] as the infiltrative process involves the AV node
*Prolonged QTc
**Wide QRS, including [[Left bundle branch block]], may be seen
*AV block (especially with '''[[Lyme disease]]''' or '''[[sarcoidosis]]''')
**Note that a normal EKG does not rule out myocarditis
*Wide QRS / new [[LBBB]]
*Elevated [[troponin]] or [[Brain natriuretic peptide]]
*'''Normal ECG does NOT rule out myocarditis'''
*CXR
 
**May demonstrate indirect signs such as cardiomegaly, pulmonary edema, or pleural effusion
===Labs===
*[[Echocardiography]]
*'''Troponin''': elevated in ~50% of cases; sensitivity limited
**Decreased LVEF
*'''BNP/NT-proBNP''': reflects degree of heart failure
**Global hypokinesis or regional wall motion abnormalities
*CBC, BMP, LFTs
**Changes to LV geometry
*[[ESR]], [[CRP]] (usually elevated but nonspecific)
**Detection of concomitant pericarditis (if present, would then be named myopericarditis)
*Consider viral serologies, Lyme titer, ANA (if autoimmune suspected)
*Cardiac MRI with contrast
*Blood cultures (if infectious etiology suspected)
**Noninvasive gold standard for structural-functional changes
*Nuclear Study
**Widespread uptake indicating myocyte necrosis
*Viral titres
*Endomyocardial biopsy (EMB): Invasive gold standard, but rarely used
*Coronary angiography is indicated in selected patients where [[acute coronary syndrome]] is 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===
**Discontinue offending agent, if possible/known
*'''IV access, continuous monitoring, 12-lead ECG'''
**Antiviral agents (Pleconaril/[[Ribavirin]]) may be effective for specific viruses
*'''Rule out ACS''': may require coronary angiography if ST elevation or high clinical suspicion
**COVID-related: limited/conflicting evidence regarding efficacy of high-dose [[steroids]] and/or [[IVIG]] <ref>[https://link.springer.com/article/10.1007/s11739-021-02635-w Mele D, Flamigni F, Rapezzi C, Ferrari R. Myocarditis in COVID-19 patients: current problems. Internal and Emergency Medicine. 2021. doi:10.1007/s11739-021-02635-w]</ref>
*'''Avoid NSAIDs and aspirin''' in acute phase (animal studies suggest increased inflammation)
*Subacute phase
*'''Volume status''': use caution with IV fluids — may worsen [[heart failure]]
**Studies have not shown efficacy of immunosuppressants for acute myocarditis, unless in specific EMB-proven cases
**If [[cardiogenic shock]]: consider vasopressors/inotropes (dobutamine, milrinone)
**Pediatric patients may receive high-dose [[IVIG]]
*'''Dysrhythmia management''':
*Chronic phase
**Avoid class IC antiarrhythmics
**Treatment for CHF symptoms, which may include GDMT meds or diuresis
**Amiodarone for sustained [[VT]]
**Ventricular Assist Devices ([[LVAD|VAD]])
**Temporary pacing for complete heart block
**Cardiac transplant
*'''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 a 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 aneurysm]]  
*[[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==
==External Links==
2024 ACC Expert Consensus on Myocarditis<ref>Writing Committee; Drazner MH, Bozkurt B, Cooper LT, Aggarwal NR, Basso C, Bhave NM, Caforio ALP, Ferreira VM, Heidecker B, Kontorovich AR, Martín P, Roth GA, Van Eyk JE. 2024 ACC Expert Consensus Decision Pathway on Strategies and Criteria for the Diagnosis and Management of Myocarditis: A Report of the American College of Cardiology Solution Set Oversight Committee. J Am Coll Cardiol. 2025 Feb 4;85(4):391-431. doi: 10.1016/j.jacc.2024.10.080. Epub 2024 Dec 10. PMID: 39665703.</ref>
*[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 del 19:35 21 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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