Myocarditis, nicvd
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Transcript of Myocarditis, nicvd
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MYOCARDITIS
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DR GOURANGA KUMAR SAHA
MBBS,MD,FESC,FACCAssociate Professor Cardiology
NICVD, DHAKA
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Definition of Myocarditis
Myocarditis is clinically and pathologically defined asinflammation of the myocardium in the absence of
the predominant acute or chronic ischaemiacharacteristic of CAD.
It is a clinical syndrome of non-ischaemic myocardialinflammation resulting from a heterogeneous group
of infectious, immune and nonimmune diseases . Histopathologically, it is characterised by an
inflammatory cellular infiltrate with or withoutevidence of myocyte injury
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clinicopathologic classification :
Fulminant myocarditis - Follows a viral prodrome; distinct onsetof illness comprising severe cardiovascular compromise withventricular dysfunction and multiple foci of active myocarditis;
either resolves spontaneously or results in death. Acute myocarditis - Less distinct onset of illness, with established
ventricular dysfunction; may progress to dilated cardiomyopathy
Chronic active myocarditis - Less distinct onset of illness, withclinical and histologic relapses; development of ventriculardysfunction associated with chronic inflammatory changes(including giant cells) .
Chronic persistent myocarditis - Less distinct onset of illness;persistent histologic infiltrate with foci of myocyte necrosiswithout ventricular dysfunction despite symptoms (eg, chestpain, palpitations)
http://emedicine.medscape.com/article/152696-overviewhttp://emedicine.medscape.com/article/152696-overview -
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Aetiology of Myocarditis
Infectious causes:Viral:
*Influenza A
*Adenovirus
*Coxsackie B virus
*Hepatitis C virus
*HIV
*Echovirus
*EBV*CMV
*Parvovirus
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Aetiology of Myocarditis(continued)
Bacterial:
Mycobacterial
Streptococcal species
Mycoplasma pneumoniae
Treponema pallidum
TB
Staphylococcal species
Clostridium species
Neisseria gonorrhea
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Aetiology of Myocarditis(continued)
Mycotic:
Aspergillus species Candida species
Coccidiomycosis
Cryptococcus species Histoplasma species
Sporotrichosis species
Blastomycosis
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Aetiology of Myocarditis(continued)
Protozoal:
Trypanosoma cruzi (Chagas disease) African trypanosomiasis (sleeping sickness)
Toxoplasmosis
Malaria
Parasitic
Schistosomiasis
Larva migrans
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Aetiology of Myocarditis(continued)
Helminthic :*Trichinosis
*Echinococcosis
*schistosomiasis
*heterophyiasis
*cysticercosis*visceral larva migrans
*filariasis
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Aetiology of Myocarditis(continued)
Drugs (usually causing hypersensitivity myocarditis)
Chemotherapeutic drugs - Doxorubicin and
anthracyclines, streptomycin, cyclophosphamide,interleukin-2, anti-HER-2 receptorantibody/Herceptin
Antibiotics - Penicillin, chloramphenicol,sulfonamides
Antihypertensive drugs - Methyldopa, spironolactone Antiseizure drugs - Phenytoin, carbamazepine
Amphetamines, cocaine, catecholamines
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Aetiology of Myocarditis(continued)
Chemicals - Hydrocarbons, carbon monoxide, arsenic, lead,phosphorus, mercury, cobalt
Physical agents (radiation, heatstroke, hypothermia) Acute rheumatic fever
Systemic inflammatory disease - Giant cell myocarditis,sarcoidosis, Kawasaki disease, Crohn disease, systemiclupus erythematosus, ulcerative colitis, Wegenergranulomatosis, thyrotoxicosis, scleroderma, rheumatoidarthritis
Peripartum cardiomyopathy
Posttransplant cellular rejection
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Pathophysiology
Damage occurs through the following mechanisms:
Direct cytotoxic effect of the causative agent
Secondary immune response, which can be
triggered by the causative agent
Cytokine expression in the myocardium (eg,
tumor necrosis factor-alpha, nitric oxide
synthase)
Aberrant induction of apoptosis 3
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Pathophysiology
Acute phase (first 2 wk): Myocyte destruction is adirect consequence of the offending agent,
which causes cell-mediated cytotoxicity andcytokine release, contributing to myocardialdamage and dysfunction. Detection of the causalagent is uncommon during this stage.
Chronic phase (>2 wk): Continuing myocytedestruction is autoimmune in nature, withassociated abnormal expression of humanleukocyte antigen (HLA) in myocytes (and in thecase ofviral myocarditis, persistence of viralgenome in myocardium).
http://emedicine.medscape.com/article/890740-overviewhttp://emedicine.medscape.com/article/890740-overview -
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History
Patients may present with mild symptoms of chest pain (inconcurrent pericarditis), fever, sweats, chills, and dyspnea .
Population studies suggest that adults may present withfew symptoms, rather than the acute toxic state ofcardiogenic shock or frank heart failure (fulminantmyocarditis) that is often associated with myocarditis.
Symptoms of palpitations, syncope, or even suddencardiac death may develop, due to underlying ventriculararrhythmias or atrioventricular block (especially in giant
cell myocarditis). Adults may present with heart failure years after initial
index event of myocarditis (as many as 12.8% of patientswith idiopathic dilated cardiomyopathy had presumed priormyocarditis in one case series).
http://emedicine.medscape.com/article/151907-overviewhttp://emedicine.medscape.com/article/151907-overviewhttp://emedicine.medscape.com/article/348284-overviewhttp://emedicine.medscape.com/article/348284-overviewhttp://emedicine.medscape.com/article/151907-overviewhttp://emedicine.medscape.com/article/151907-overview -
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Physical
Patients with myocarditis usually present with
signs and symptoms of acutedecompensation of heart failure (eg,
tachycardia, gallop, mitral regurgitation,
edema) and pericardial friction rub in those
with concomitant pericarditis
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Physical
Sarcoid myocarditis - Lymphadenopathy, also witharrhythmias, sarcoid involvement in other organs (up to70%)
Acute rheumatic fever (usually affects heart in 50-90%) -Associated signs such as erythema marginatum,polyarthralgia, chorea, subcutaneous nodules (Jonescriteria)
Hypersensitive/eosinophilic myocarditis - Pruriticmaculopapular rash and history of using offending drug
Giant cell myocarditis - Sustained ventricular tachycardiain rapidly progressive heart failure15
Peripartum cardiomyopathy - Heart failure developing inthe last month of pregnancy or within 5 months followingdelivery
http://emedicine.medscape.com/article/153153-overviewhttp://emedicine.medscape.com/article/153153-overview -
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Laboratory Studies
CBC - Leukocytosis (may be eosinophilia)
ESR (and other acute phase reactants eg. CRP.)
Elevated cardiac enzymes (CK or cardiac troponins):
These are an indicator for cardiac myonecrosis help
identify those with resolution of viral myocarditis. The
test has 89% specificity and 34% sensitivity
Serum viral antibody titers for viral myocarditis
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Imaging Studies
*Echocardiography:to exclude other causes of heartfailure & to evaluate the degree of cardiac
dysfunction .*Cardiac angiography:
*(MRI): This imaging technique is used for assessmentof the extent of inflammation and cellular edema,although it is still nonspecific.
*Nuclear imaging: Antimyosin scintigraphy(sensitivity(91-100%) and specificity (31-44%)
* Electrocardiogram - Often nonspecific (eg, sinustachycardia, nonspecific ST or T-wave changes)
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Endomyocardial biopsy (EMB): Standard for
diagnosis of myocarditis. Routine EMB in
establishing diagnosis of myocarditis rarely is helpfulclinically, however, since histologic diagnosis seldom
has an impact on therapeutic strategies, unless giant
cell myocarditis is suspected.
Histologic Findings:Biopsy specimens from EMBshould reveal the simultaneous findings of
lymphocyte infiltration and myocyte necrosis.
Procedures
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Treatment:Medical Care
controlling or treating the underlying cause of
the inflammation reducing the workload of the heart
treating heart abnormalities that result from
the inflammation
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Medications
ACE inhibitors and beta-blockers
Steroids and other medications Diuretics
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Treatment:Medical Care
Withdrawal of the offending agent
Anticoagulation may be advisable as a preventive measure
Antiarrhythmics can be used cautiously:*Supraventricular arrhythmias should be convertedelectrically.
*High-grade ventricular ectopy and ventriculartachyarrhythmia should be treated cautiously with betablockers and antiarrhythmics
*Patients are usually very sensitive to digoxin and should use itwith caution and in low doses.
*Complete heart block is an indication for temporarytransvenous pacing.
* Implantable defibrillators rarely are indicated in lymphocyticmyocarditis
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Surgical Care
Left ventricular assistive devices (LVADs)and extracorporeal membrane oxygenationmay be indicated for short-term circulatorysupport if needed for cardiogenic shock.
Cardiac transplantation :beneficial to thosewith biopsy-proven giant cell myocarditis; the5-year survival rate after transplantation was71%, despite a 25% incidence ofposttransplantation recurrence,
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Complications
Cardiogenic shock may occur in fulminant
cases of myocarditis Severe heart block requiring permanent
pacemaker placement occurred in 1% of
patients in the Myocarditis Treatment trial.
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Prognosis
The prognosis for long-term damage is not
predictable.
After the initial phase of myocarditis, some
patients can experience complete recovery,
others may develop chronic heart failure.
some patients develop fulminant heart
failure,
http://www.medicinenet.com/script/main/art.asp?articlekey=42321http://www.medicinenet.com/script/main/art.asp?articlekey=42321 -
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Prognosis
Patients who have survived fulminant myocarditishave a good prognosis :In a study of 147 cases of
myocarditis monitored for an average of 5.6 years,93% of the 15 patients with fulminant disease werealive without transplant 11 years after biopsy,compared with 45% of the 132 patients with lesssevere disease.
Predictors of death or need for heart transplantationafter acute myocarditis in multivariate analysesinclude syncope, low ejection fraction, and leftbundle-branch block, all indicators of advancedcardiomyopathy
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Thank you