Myocarditis, nicvd

7/27/2019 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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Mycotic:

Aspergillus species Candida species

Coccidiomycosis

Cryptococcus species Histoplasma species

Sporotrichosis species

Blastomycosis


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Protozoal:

Trypanosoma cruzi (Chagas disease) African trypanosomiasis (sleeping sickness)

Toxoplasmosis

Malaria

Parasitic

Schistosomiasis

Larva migrans


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Helminthic :*Trichinosis

*Echinococcosis

*schistosomiasis

*heterophyiasis

*cysticercosis*visceral larva migrans

*filariasis


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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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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).


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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


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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

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Myocarditis, nicvd