Cardiology presentation
Download
1 / 36

Cardiology Presentation - PowerPoint PPT Presentation


  • 244 Views
  • Uploaded on

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

loader
I am the owner, or an agent authorized to act on behalf of the owner, of the copyrighted work described.
capcha
Download Presentation

PowerPoint Slideshow about 'Cardiology Presentation' - milton


An Image/Link below is provided (as is) to download presentation

Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author.While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server.


- - - - - - - - - - - - - - - - - - - - - - - - - - E N D - - - - - - - - - - - - - - - - - - - - - - - - - -
Presentation Transcript
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

    tachycardic

  • 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


Examination
Examination

  • 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



Myocarditis
Myocarditis

  • 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?!



Causes of myocarditis
Causes of myocarditis highly variable disease entity.

Viruses: Enteroviruses

Influenza A and B

Adenovirus

Herpes

HIV

Bacteria: Beta-hemolytic Streptococcus

Corynebacterium diphtheria

Borrelia burgdorferi

Enterococcus spp

Chlamydia psittaci

Neisseria meningitidis

Mycoplasma pneumonia

Staphylococcus aureus


Protozoa highly variable disease entity.: Trypanosoma cruzii

Toxoplasma gondi

Helminths: Trichinella spiralis

Echinococcus

Autoimmunity: Infection associated

Auto-immune disease associated

Primary autoimmunity

Hypersensitivity: Penicillins

Methyldopa

Sulfamethoxazole

Toxicity: Catecholamines

Cocaine

Ethanol


Pathogenesis
Pathogenesis highly variable disease entity.

  • Three phases:

    Viral Replication

    Autoimmune injury

    Dilated cardiomyopathy


Phase 1 highly variable disease entity.

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 highly variable disease entity.

Autoimmunity

  • 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 highly variable disease entity.

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 highly variable disease entity.

  • 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.


Diagnosis
Diagnosis highly variable disease entity.

  • 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: highly variable disease entity.

  • 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 highly variable disease entity.

  • 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 highly variable disease entity.

  • 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: highly variable disease entity. 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) treatment response vary between children and adults.

  • 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



Human immunoglobulin for iv use igiv
Human immunoglobulin for IV use (IGIV) treatment response vary between children and adults.

  • 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 treatment response vary between children and adults.

  • 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
Products treatment response vary between children and adults.

  • 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 treatment response vary between children and adults.

  • 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 treatment response vary between children and adults.

  • 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.


ad