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Myocarditis
is characterized by myocardial inflammation (inflammation of the
muscular layer) that result in injury to the cardiac myocytes.
An inflammatory
infiltrate is present in the myocardium together with necrosis and
degeneration of the myocytes.
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Clinical presentation:
Patients
may remain asymptomatic or there may be abrupt onset of
arrhythmia, congestive cardiac failure or sudden death. Most patients
recover quickly and without sequelae.
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Causes of
Myocarditis:
- Microbial infection:
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Bacteria-Image
Link:
Stapylococci,beta-hemolytic streptococci, diphtheria, tuberculosis,
brucellosis, clostridia,
meningococci.
Chlamydia- C. psittaci
Fungi-
Candidiasis,
cryptococcosis,
histoplasmosis,
actinomycosis ,
blastomycosis,
coccidioidomycosis, aspergillosis.
Viruses (viral myocarditis is most common amongst the infectious
causes)- Coxsackievirus
types A and B (specially TypeB ,
Adenovirus, Echovirus, Epstein Barr virus, Hepatitis C virus, Herpes
virus,
Measles,
Influenza, Rubella, Poliomyelitis virus, Human immunodeficiency virus
, Mumps, Parvovirus
B19.
Cytomegalovirus
; Image
Link1
;
Image Link2
;
Image Link3.
Protozoa- Trypanosoma cruzi (Chaga's
disease), toxoplasmosis,
malaria,
leishmaniasis.
Helminth- Trichinosis,
schistosomiasis, echinococcosis, cysticercosis.
Rickettsia-
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. Scrub typhus, Q-fever, Rocky Mountain spotted fever.
Spirochetal- Syphilis, Lyme
disease, Weil disease, Borrelia.
-
Immune mediated reaction:
Postviral ;
Poststreptococcal ; Systemic lupus erythematosus ; Drug
hypersensitivity ; Transplant rejection.
- Unknown:
Sarcoidosis ;
Giant cell myocarditis .
- In
connective tissue disease:
Rheumatic fever ;
Rheumatoid arthritis ; Polyarteritis nodosa ; Dermatomyositis
- Caused by
physical agents ,chemical poisons, drugs, metabolic disorders:
Trauma ; Irradiation ;
Chemical poisons (arsenic, lead, hydrocarbons, mercury) ; Radiation ;
Heatstroke ; Bites and stings ; Drugs (
Adriamycin
,
streptomycin ,
catecholamines, acetaminophen, methyldopa, penicillin, sulphonamide,
phenytoin) ; Uremia ; Hypokalemia.
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Gross features:
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;
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Flabby ventricular myocardium, often with four chamber dilatation
and patchy or diffuse hemorrhagic mottling. There may be mural thrombi in
dilated chambers.
The endocardium and valves
are unaffected.
Microscopic features:
Image Link1
;
Image Link2
;
Image Link3.
Myocardial inflammatory infiltrate associated with myocyte
necrosis or degeneration.
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;
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. In
late stage, delicate interstitial fibrosis and focal scarring may
occur.
Dallas Classification
(1987)
Myocarditis:
Myocardial necrosis,
degeneration, or both, in the absence of significant coronary
artery disease with adjacent inflammatory infiltrate with or
without fibrosis.
Borderline myocarditis:
Inflammatory
infiltrate too sparse or myocyte damage not apparent.
No
myocarditis:
WHO Marburg Criteria
(1996)
Acute (active) myocarditis:
A clear-cut infiltrate (diffuse,
focal or confluent) of >14 leukocytes/mm˛ (preferably activated
T-cells). The amount of the infiltrate should be quantitated by
immunohistochemistry. Necrosis or degeneration are compulsory,
fibrosis may be absent or present and should be graded.
Chronic myocarditis: An
infiltrate of >14 leukocytes/mm˛ (diffuse, focal or confluent,
preferably activated T-cells). Quantification should be made by
immunohistochemistry. Necrosis or degeneration are usually not
evident, fibrosis may be absent or present and should be graded.
No
myocarditis: No
infiltrating cells or <14 leukocytes/mm˛. |
Characteristic microscopic
features in each condition:
Microbial infection :
VIRAL MYOCARDITIS:
Initially,
interstitial tissue is infiltrated by lymphocytes, and neutrophils and
there is necrosis of individual muscle fibres ; Later lymphocytes and
histiocytes predominate and some degree of connective tissue
proliferation occurs.
RICKETTSIA:
Interstitial edema ;
Focal or patchy infiltration by inflammatory cells ; Anitschkow
cells, mast cells and eosinophils are noted in close association with
small vessels ; Neutrophils are few unless necrosis is present ;
Vascular changes - capillary and arteriolar endothelial swelling and
phlebitis with thrombosis. ; Necrotizing arteritis of the
myocardium (epidemic typhus).
BACTERIA AND FUNGUS:
Abscess may develop in the myocardium as a result of infection
by pyogenic (staphylococci and beta-hemolytic streptococci) and fungal organisms.
Pyogenic organisms may produce a more diffuse suppurative myocarditis.
Fibrosis is seen in the later phase of certain myocardial lesions.
Granulomatous inflammation of the
myocardium caused by certain bacterial infections (tuberculosis ,
tularemia and brucellosis). Visit
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Giant cell myocarditis.
PROTOZOA:
Trypanosoma cruzi (Chaga's
disease): Dense inflammatory
infiltrate in the myocardium ; Cellular infiltration consisting
of histiocytes, plasma cells, lymphocytes, and some polymorphonuclear
leukocytes ; Degeneration and necrosis of muscle fibres may be
prominent.
Toxoplasma gondii:
Focal necrosis,
edema and inflammatory infiltrate in the myocardium ; Infiltrate
composed of plasma cells, macrophages, and lymphocytes ; Pseudocysts
containing organisms are seen in the myocardium within or outside
muscle fibres often separated from the foci of inflammation.
HELMINTH:
Trichinella
spiralis:
Inflammatory reaction is a response to the larvae ; Larvae are rarely
identified in the lesions ; Focal necrosis of the muscle fibres ;
inflammatory infiltrate composed of lymphocytes and eosinophils.
Echinococcus
disease: Hydatid
cysts occasionally occur in the myocardium ; Hydatid cyst of the heart
tends to rupture into the lumen of the cardiac chamber or into the
pericardial sac.
Polyarteritis nodosa
:
Necrotizing
vasculitis with extension of the inflammatory reaction to the adjacent
perivascular tissue ; Formation of thrombi in the vessels ;
Secondary ischemic changes including infarction may occur in the
myocardium.
Dermatomyositis :
Degeneration
; Loss of striation ; Vacuolization and necrosis of muscle
fibres may be seen ; Interstitial edema may be present ;
Inflammatory infiltrate composed of mainly lymphocytes and
histiocytes is present interstitially or perivascularly ;
Hyalinized thickening of the intramyocardial arterioles with narrowing
of the lumens .
Certain chemical poisons or drugs :
Myofiber swelling, fatty change
and individual cell lysis ; Edema and small hemorrhage may be
present ; A nonspecific inflammatory reaction consisting of
lymphocytes and histiocytes occur in response to necrotic tissue ; Myocarditis characterized by an interstitial exudate with many
eosinophils has been noted as a complication of therapy with a variety
of drugs.
Cardiac trauma :
Nonspecific myocarditis may be seen in association with with
contusions of the myocardium ; Lesion consisting of an
infiltrate of neutrophils and a few eosinophils and mononuclear cells
together with focal necrosis of muscle fibers and hemorrhage.
Uremia :
Fatty degeneration and edema of the myocardium due to uremic
intoxication.
Cardiac transplant rejection :
Characterized by the presence of
interstitial lymphocytes and myocyte degeneration.
GIANT CELL MYOCARDITIS:
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