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Cardiology Presentation. Myocarditis - A Review of Management in Paediatrics. Case 1. Three month old female, HIV IC2 but not yet on HAART, admitted on the 1/7/07 with a 4 day history of - cough - shortness of breath - diarrhoea

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cardiology presentation

Cardiology Presentation

Myocarditis - A Review of Management in Paediatrics

case 1
Case 1
  • Three month old female, HIV IC2 but not yet on HAART, admitted on the 1/7/07 with a 4 day history of

- cough

- shortness of breath

- diarrhoea

  • Birth history: Born at term at a clinic - 3200g
  • Past medical history: previous cough treated at a peripheral hospital
On Examination
  • Anthropometry: wt 4.9kg ( =10th);

Length 57cm ( =10th)

  • Afebrile; RR 80/min; PR 140bpm; oxygen saturation 58% on nasal oxygen
  • Dusky in colour, 5% dehydration,

generalised significant lymphadenopathy

Examination continued:
  • Chest: Severe distress with subcostal and intercostal recession; harsh breath sounds bilaterally with soft crackles at bases; bronchial breathing RUL, anterior
  • CVS: All pulses palpable; Apex beat not displaced; Normal S1 and S2; no gallop but


  • Abdomen: Soft not distended; 2cm hepar and

tip of spleen

  • CNS: Irritable
CXR: enlarged CTR of 69%

RUL and LUL consolidation

“globular” heart

  • Blood investigations:
  • FBC 47.7/9.1/408
  • CRP 4.3
  • U+E 135/6.6/94/7/7.5/50
  • CK 704
  • CKMB 16.9%
  • Troponin T 0.05
  • Blood culture grew Strep pneumoniae
  • LP clear
  • Patient commenced on ampicillin and gentamicin and PCP treatment (was later changed to cefotaxime)
Serial cardiac enzymes done:

2/7/2007: CK 606; CKMB 44%; Trop T <0.03

3/7/2007: CK 514; CKMB 100%; Trop T <0.03

5/7/2007: CK 680; CKMB 59%; Trop T <0.03

  • Cardiologists consulted on 2/7/2007 and an echo was done : LV function decreased

Normal coronaries

Normal intracardiac anatomy

  • Digoxin was added
  • Patient demised on 6/7/07
case 2
Case 2
  • 2 month old female, ex-prem at 32/40, admitted to hospital on 2/7/07 with history of:

- cough and blocked nose

- fever

- vomited once

  • Birth history: Born in hospital at 32/40

Birthweight of 2750g

Normal delivery

  • Past medical history: Admitted to hospital one week previously with bronchopneumonia
  • Anthropometry: wt 4.3kg; length 58 cm = 50th
  • Vital signs: Temp 38.5; PR 230bpm; RR 100/min
  • General: No lymphadenopathy, 10% dehydrated, pallor
  • CVS: Tachycardic

Apex beat 4th interspace, mid-clavicular line; normal heart sounds; no gallop

  • Chest: Acidotic breathing with harsh breath sounds
  • Abdomen: Soft; no organomegaly
  • CNS: Increased tone globally
Initial Investigations:

FBC 17.7/10.1/429

CRP 29.1

U+E 151/5/109/11/10.9/94

HIV negative

CK 352

CKMB 46.9%

Trop T 0.21

  • Pt was commenced on Tazocin and Amikacin
  • Slow rehydration
Cardiologists consulted on 2/7/07 and an echo was done:

- Poor LV function

- Normal intracardiac anatomy

Assessment of probable myocarditis was made on basis of poor LV function, and Polygam was ordered as well as digoxin

  • Repeat echo done 3 days later showed significant improvement in LV function
  • Discharged home on 8/7/07 on digoxin
  • Despite three decades of study, the diagnosis and management remain controversial.
  • The exact incidence and prevalence remain unknown.
  • Clinical presentation varies
  • Most patients are asymptomatic and recover without treatment
So why then should physicians concern themselves with a disease that is clinically uncommon, diagnostically challenging and that has an excellent recovery?!
Myocarditis represents a clinically and pathogenetically highly variable disease entity.
  • Fulminant disease  acute heart failure and arrhythmias
  • Some patients are asymptomatic
  • However, asymptomatic myocarditis may be a cause of unexplained deaths in 1% of cases
causes of myocarditis
Causes of myocarditis

Viruses: Enteroviruses

Influenza A and B




Bacteria: Beta-hemolytic Streptococcus

Corynebacterium diphtheria

Borrelia burgdorferi

Enterococcus spp

Chlamydia psittaci

Neisseria meningitidis

Mycoplasma pneumonia

Staphylococcus aureus

Protozoa: Trypanosoma cruzii

Toxoplasma gondi

Helminths: Trichinella spiralis


Autoimmunity: Infection associated

Auto-immune disease associated

Primary autoimmunity

Hypersensitivity: Penicillins



Toxicity: Catecholamines



  • Three phases:

Viral Replication

Autoimmune injury

Dilated cardiomyopathy

Phase 1

Viral replication

  • Cardiotropic RNA viruses are taken into myocytes by receptor-mediated endocytosis.
  • Directly translated intracellularly to produce viral protein.
  • Virus infection directly contributes to cardiac tissue destruction by cleaving the cytoskeleton protein dystrophin, leading to a disruption of the dystrophin-glycoprotein complex.
Phase 2


  • Phase 1 concludes with activation of the host system.
  • Ideally, the immune system should down-regulate to a resting state once viral proliferation is controlled.
  • If host immune activation continues unabated  autoimmune disease.
  • T cells target the host’s own tissue through molecular mimicry.
Phase 3

Dilated Cardiomyopathy

  • Re-modelling mechanisms lead to dilated cardiomyopathy (DCM).
  • The persistent myocyte viral gene expression  progressive DCM.
  • Cytokines: activate matrix metalloproteinases (gelatinase, collagenase, elastases).
clinical presentation
Clinical Presentation
  • Asymptomatic to cardiogenic shock.
  • May include a viral prodrome of fevers, myalgias, respiratory symptoms or gastroenteritis.
  • May present with rapidly deteriorating LV function or arrhythmias and heart block.
  • Acute myocarditis is defined histologically as inflammation of the myocardium with associated myocellular necrosis.
  • Gold Standard is endomyocardial biopsy.
  • Previously Dallas criteria were used, now WHO/ International Society and Federation of Cardiology Task Force define:

- Active myocarditis: > 14 leucocytes/mm with necrosis and degeneration

- Chronic myocarditis >14 leucocytes/mm but no necrosis or degeneration

  • Further classified according to inflammatory infiltrate i.e. neutrophils, monocytes and macrophages in the acute stage, with lymphocytes and fibroblasts in the later stages.
Diagnosis continued:
  • Cardiac biomarkers i.e. creatine kinase and troponin T and I are routinely measured
  • CKMB is not useful due to low predictive value.
  • Lauer et al reported 28 of 80 patients (35%) with suspected myocarditis had elevated troponin levels.
  • Trop T > 0.1ng/mL had a sensitivity of 53% and a specificity of 94%
  • ESR found to have low sensitivity and specificity.
  • Echo changes i.e. LV dysfunction (in 69%), and segmental wall motion abnormalities (64%), do not differentiate myocarditis from other cardiomyopathies.
management of myocarditis
Management of myocarditis
  • Management is dictated by clinical signs and symptoms.
  • MANY proposed therapies, most have only a theoretical basis. Some have been tested in animal models
  • Conventional heart failure therapy is currently the only accepted therapy for myocarditis including ACE inhibitors, angiotensin receptor blocking agents, diuretics, β-blockers or amiodarone.
diet and lifestyle
Diet and Lifestyle
  • Restrict salt intake to 2-3g of sodium per day
  • Exercise especially during the acute phase of Coxsackie virus B3 murine myocarditis enhances viral replication rate, enhances immune mechanisms and increases inflammatory lesions and necrosis.Resumption of physical activity can take place within 2 months of the acute disease.
controversial therapy immunosuppresive is therapy
Controversial Therapy: Immunosuppresive (IS) Therapy
  • The idea that autoimmune mechanisms play an important role in the pathogenesis of myocarditis and post-viral cardiomyopathy suggests the potential benefits of immunosuppressives.
  • The Myocarditis Treatment Trial studied the effect of IS on ventricular function in 111 pts with myocarditis (Dallas criteria) and LVEF <45%
  • Patients were randomised with some on prednisone and cyclosporine, or prednisone and azathioprine , or to conventional therapy for 6 months.
  • Both IS and control groups showed an increase in LVEF from 25% to 34% at 28 weeks
  • No survival difference
  • Conclusion: selected pts might benefit from appropriately timed IS
However the study included patients with symptom duration as long as 2 years! Can they extrapolate the results for a paediatric population with a much shorter symptom duration?
  • Latham et al studied the effect of prednisone on survival in 52 pts with new onset DCM.
  • Patients were randomised to prednisone or no prednisone for 3 months.
  • Myocardial inflammation resolved in all patients and there was no survival difference at 2 years.
  • One matched-cohort trial showed a benefit of prednisone with azathioprine or cyclosporine in children
The role of immunosuppressive therapy in lymphocytic myocarditis remains controversial due to limitations in research field:
  • Low incidence of symptomatic myocarditis
  • Myocarditis varies in presentation – wide spectrum of disease
  • Immunosuppressive agents influence inflammatory mediators differently i.e. effect of prednisone vs intravenous immune globulin
  • Numerous viruses implicated with different treatment response i.e. adenovirus-positive myocarditis may benefit from Ig treatment.
5. Myocarditis affects persons of all ages, and disease and treatment response vary between children and adults.

6. Previous trials show an improvement in myocarditis with conservative treatment. Therefore difficult to interpret the effectiveness of IS in studies without a control group.

7. The validity of the historical gold standard of endomyocardial biopsy as the basis of diagnosis if conservative therapies are the standard treatment?

Randomised Treatment Trial on Myocarditis (ESETCID)
  • The ESETCID is the 1st trial of immune therapy for myocarditis that uses different treatment regimens based on the causes of myocardial inflammation
  • The ESETCID is an ongoing prospective, randomised, placebo-controlled trial studying the effects of immune therapy on ventricular function and exercise capacity in pts with biopsy-proven myocarditis and LVEF <45%
  • Three treatment arms:

- acute viral infection no IS is given

Enterovirus-positive patients treated with interferon-alpha
  • CMV and adenovirus+ patients are treated with immunoglobulins
  • Autoreactive myocarditis is treated with azathioprine and prednisone for 6 months
human immunoglobulin for iv use igiv
Human immunoglobulin for IV use (IGIV)
  • Appropriate use can be life-saving
  • IGIV is produced from human plasma using a number of preparatory steps  supply is finite
  • Can lead to numerous side effects and potential adverse consequences
  • Currently only 6 clinical indications for which IGIV has been licensed by the United States Food and Drug Administration (FDA):
Primary immunodeficiency or primary humoral immunodeficiency
  • Idiopathic thrombocytopenic purpura  when a rapid increase in platelet count is needed
  • Kawasaki disease  prevention of coronary artery aneurysms
  • B-cell chronic lymphocytic leukemia  prevention of bacterial infections in patients with hypogammaglobulinemia or recurrent bacterial infections
  • HIV infection - indicated for HIV positive paediatric patients to decrease the frequency of serious and minor bacterial infections
  • Bone marrow transplantation  patients older than 20 years of age to decrease septicemia and acute GVHD in the 1st 100 days post transplant.
  • Products are produced from plasma from whole blood donations or from a pool of plasmapheresis donors.
  • Tests for Hep B s-Ag, HIV p24 antigen and antibodies to HIV, Hep C and syphilis are done.
  • IGIV is supplied in lyophilized powder or as a premixed solution with final concentration of IgG of 3%, 5%, 6%, 10% or 12%
  • The IgA content varies from <0.4ug/mL to 720ug/mL
  • Dose for antibody replacement is 0.3 – 0.6g/kg per month given every 2 – 4 weeks IVI.
  • For other uses a dose of 0.4g/kg per day for 5 days
  • For a rapid course  1 to 2 g/kg over 1 or 2 days
adverse reactions
Adverse Reactions
  • Most are mild i.e. back or abdominal pain, nausea, rhinitis, asthma, chills, low grade fever, myalgias or headache.
  • Slowing or stopping the infusion for several minutes will reverse the symptoms.
  • Adverse reactions are more likely in 1st infusion of IGIV or if there has been a recent bacterial infection
  • More serious reactions include anaphylaxis, Stevens-Johnson syndrome, hypotension, MI, thrombosis, hemolysis, stroke, ARDS, seizures, pulmonary oedema and acute bronchospasm.