• An inflammatory process of
myocardium that result into the injury
to cardiac myocytes.
Major Causes of Myocarditis
• Transplant rejections
Giant cell myocarditis
• Active phase – heart may be normal or dilated
• Advanced stages: the ventricular myocardium is
flabby and often mottled.
• Mural thrombi may be present in any chamber.
• Mononuclear interstitial inflammatory infiltrate
associated with focal myocyte necrosis.
• Later-inflammatory lesions either resolve,
leaving no residual changes, or heal by
Hypersensitivity myocarditis- perivascular
interstitial infiltrates, composed of lymphocytes,
macrophages, and a high proportion of
Giant-cell myocarditis (uncertain cause)• inflammatory cellular infiltrate containing
multinucleate giant cells interspersed with
lymphocytes, eosinophils, plasma cells, and
• Chagas disease: trypanosoma cruzi, mixed
inflammatory cell infiltrate.
Chagas disease - scattered trypanosomes accompanied by
an inflammatory infiltrate of neutrophils, lymphocytes,
macrophages, and occasional eosinophils
• May be asymptomatic- recover completely
• Features of heart failure or arrhythmias,
occasionally with sudden death.
• fatigue, dyspnea, palpitations, precordial
discomfort, and fever.
• Occasionally, patients develop DCM - late
complication of myocarditis.
OTHER CAUSES OF MYOCARDIAL
Adriamycin, doxorubicin and daunorubicin
• caused by deposition of an insoluble extracellular fibrillar
deposits of protein fragments that are prone to forming
• Cardiac amyloidosis may appear along with systemic
• restricted to the heart, senile cardiac amyloidosis.
• amyloid deposits generally occur in the ventricles and
• caused by the deposition of transthyretin
normal to firm and rubbery.
Usually the chambers are of normal size
Can be dilated and have thickened walls.
Numerous small, semi-translucent nodules
resembling drips of wax
• Eosinophilic deposits of amyloid may be found in
the interstitium, conduction tissue, valves,
endocardium, pericardium, and small intramural
• special stains - Congo red- classic apple-green
birefringence when viewed under polarized light
• Amyloid deposits often form rings around
cardiac myocytes and capillaries.
• Intramural arteries and arterioles may
have sufficient amyloid in their walls to
compress and occlude their lumens,
inducing myocardial ischemia (“smallvessel disease”).
• Diseases of the pericardium include
inflammatory conditions and effusions.
• Isolated pericardial disease is unusual,
and pericardial lesions are almost always
associated with disease in other portions
of the heart or surrounding structures, or
are secondary to a systemic disorder.
• Primary pericarditis is uncommon.
• In most cases it is caused by infection.
– Viruses, bacteria and fungi
– Secondary to acute MI, cardiac surgery, irradiation to
the mediastinum, or processes involving other
thoracic structures (e.g., pneumonia or pleuritis).
– Uremia is the most common systemic disorder
associated with pericarditis.
– Rheumatic fever, SLE, and metastatic malignancies.
Fibrinous pericarditis (uremia): an irregular
appearance to the pericardial surface (so-called
Fibrinopurulent (in acute bacterial pericarditis):Areas
of frank pus;
Tuberculous pericarditis: areas of caseation.
Chronic pericarditis: The appearance of chronic
pericarditis ranges from delicate adhesions to dense,
fibrotic scars that obliterate the pericardial space. In
extreme cases the heart is so completely encased by
dense fibrosis that it cannot expand normally during
diastole, so-called constrictive pericarditis.
• Atypical chest pain, not related to exertion and
often worse on reclining, and a prominent friction
• When associated with significant fluid
accumulation, acute pericarditis can cause
cardiac tamponade, with declining cardiac output
• Chronic constrictive pericarditis produces a
combination of right-sided venous distention and
• The cardiomyopathies are a group of diseases
that primarily affect the heart muscle and are not
the result of congenital, acquired valvular,
hypertensive, coronary arterial, or pericardial
• Primary cardiomyopathies -confined to the heart
• Secondary cardiomyopathies -myocardial
involvement as a component of a systemic or
Clinical Classification of
• Dilated: Left and/or right ventricular enlargement,
impaired systolic function, congestive heart failure,
• Restrictive: Endomyocardial scarring or myocardial
infiltration resulting in restriction to left and/or right
• Hypertrophic: Disproportionate left ventricular
hypertrophy, typically involving septum more than free
wall, with or without an intraventricular systolic pressure
gradient; usually of a nondilated left ventricular cavity
Diagnosed as an isolated finding or associated
with other congenital heart anomalies
DILATED CARDIOMYOPATHY (DCM)
• Progressive four chamber hypertrophy
• Contractile (systolic) dysfunction
• Can occur at any age
• Slow progressive to CHF.
• It is sometimes called congestive
Various acquired myocardial insults
Alcohol or other toxicity
• 20%- 50% - is familial and caused by inherited
• Autosomal-dominant inheritance is the
• Most commonly affect genes that encode
cytoskeletal proteins (dystrophin). Duchene and
• Mutation in enzyme involved in beta-oxidation of
• Myocarditis (postviral).
– DCM is a consequence of myocarditis.
• Alcohol and other toxins
– No morphologic features serve to distinguish
alcoholic cardiomyopathy from DCM of other
– Chronic alcoholism may be associated with
• The histologic abnormalities in DCM are
nonspecific and usually do not point to a
specific etiologic agent.
• Heart is usually enlarged, heavy (>2-3X), and
• Mural thrombi are common
• No primary valvular alterations
• Most muscle - are hypertrophied with enlarged
• Some are attenuated, stretched, and irregular.
• Interstitial and endocardial fibrosis –present
May occur at any age ( common 20 –50yrs).
MR & Arrhythmias
Ejection fractions < 25%
50%- die within 2 years
25% survive > 5 years
Death - cardiac failure or arrhythmia
Embolism from dislodgment of an intracardiac thrombus
• Cardiac transplantation is frequently done,
• Characterized by myocardial hypertrophy,
abnormal diastolic filling and in 1/3 casesintermittent ventricular outflow obstruction.
• The heart is thick-walled, heavy, and
• Causes primarily diastolic dysfunction;
systolic function is usually preserved.
• Mutations of genes encoding sarcomeric
• Mutations - gene encoding β-myosin
heavy chain (β-MHC, cardiac TnT, αtropomyosin, and myosin-binding protein
• Massive myocardial hypertrophy, without
• Classic pattern is disproportionate
thickening of the ventricular septum as
compared with the free wall of the left
• On cross-section- “banana-like” left
• Histologic Features –
– Extensive myocyte hypertrophy to a degree unusual
in other conditions, with transverse myocyte
diameters frequently greater than 40 μm (15 μm);
– Haphazard disarray of bundles of myocytes, individual
myocytes, and contractile elements in sarcomeres
within cells (termed myofiber disarray)
– Interstitial and replacement fibrosis
• Characterized by primary decrease in
ventricular compliance, resulting in
impaired ventricular filling during diastole.
• May be idiopathic or associated with
distinct diseases - principally radiation
fibrosis, amyloidosis, sarcoidosis,
metastatic tumors, inborn errors of
• Ventricles are of normal size or slightly
• Cavities are not dilated
• Myocardium is firm and noncompliant
• May be only patchy or diffuse interstitial
• Endomyocardial fibrosis - disease of
children and young adults
• Fibrous tissue markedly diminishes the
volume and compliance of affected
chambers - induces a restrictive functional
• Ventricular mural thrombi sometimes