‫بسم اهلل الرمحن الرحيم‬

Cardiac pathology
 Valvular diseases
• Mitral valve (between left atrium and left ventricle).
• Tricaspid valve (between R. atrium and R.ventricle).
• Aortic & pulmonary valves.
 Valvular heart disease
• Valvular involvement by disease causes stenosis,
insufficiency (regurgitation), or both.

• Stenosis is the failure of a valve to open completely.

• Insufficiency, regurgitation, in contrast, results from

failure of a valve to close completely, allowing
reversed flow.

• Abnormalities of flow often produce abnormal heart

sounds known as murmurs.
 Rheumatic disease
• Rheumatic fever is an acute, immunologically
mediated, multisystem inflammatory disease that
occurs a few weeks after an episode of group A
(beta -hemolytic) streptococcal pharyngitis .

Cardiac involvement :
1- myocarditis
2- pericarditis.
3- endocarditis (valve involvement) .
 Morphological features:
• focal inflammatory lesions are found in various
sites.
• In heart where they called Aschoff bodies, “Foci of
fibrinoid degeneration surrounded by lymphocytes,
occasional plasma cells, and plump macrophages”
• These distinctive cells have abundant amphophilic
cytoplasm and central round-to-ovoid nuclei.
Some of the larger altered histiocytes become
multinucleated to form Aschoff giant cells
• Acute rheumatic carditis, microscopic is marked by a
peculiar form of granulomatous inflammation with so-
called "Aschoff nodules" seen best in myocardium
• These are centered in interstitium around vessels as
shown here
• The myocarditis may be severe enough to cause
congestive heart failure
• Here is an Aschoff nodule at high magnification
• The Aschoff giant cell
• Several appear here as large cells with two or more
nuclei that have prominent nucleoli
• Scattered inflammatory cells accompany them and
can be mononuclears or occasionally neutrophils
• involvement of the endocardium and the left-sided
valves by inflammatory foci typically comprises
fibrinoid necrosis within the cusps in which sit small
(1 to 2 mm) vegetations-- verrucae--along the lines
of closure.

• These irregular, warty projections probably

result from the precipitation of fibrin at sites of
erosion related to underlying inflammation and
fibrinoid degeneration.
 pathogenesis
• It is proposed that antibodies directed against
the M proteins of certain strains of
streptococci.
• cross-react with tissue glycoproteins in
the heart, joints, and other tissues.
• Occur in 2 to 3 weeks after infection and
the absence of streptococci from the lesions
support the concept that rheumatic fever
results from an immune response against
the offending bacteria
Clinical Manifestations:
Onset of symptoms 2-3 weeks after streptococcal
pharyngitis; (jones Major criteria) include
(1) migratory polyarthritis of the large joints.
(2) carditis.
(3) subcutaneous nodules.
(4) erythema marginatum of the skin.
(5) Sydenham chorea-- a neurologic disorder with
involuntary purposeless, rapid movements
Jones minor criteria “fever, arthralgia, or evidence of
previous streptococcal infection.
• Lab (positive anti–streptolysin O [ASO] titer) ,high ESR.
Rheumatic Heart Disease:

• Presents with valvular heart disease (usually

mitral stenosis, but aortic stenosis as well);
valvular disease may lead to hypertrophy of heart,
arrhythmias, and HF

• Treatment: Penicillin for streptococcal infection;

salicylates for fever and arthritis; endocarditis
prophylaxis if indicated
• Infective endocarditis:
• Pericarditis:
• Myocarditis:
 Infective endocarditis
• Serious infections.
• colonization or invasion of the heart valves,
the mural endocardium, by a microbial agents.

• formation of bulky, friable vegetation

composed of thrombotic debris and organisms,
often associated with destruction .
• Acute endocarditis:
destructive, infection, frequently of a previously
normal heart valve with a highly virulent
organism, that leads to death within days to
weeks of more than 50% of patients despite
antibiotics and surgery.
• Subacute endocarditis:
organisms of low virulence can cause infection
in a previously abnormal heart, particularly on
deformed valves.

Most patients with subacute infective

endocarditis recover after appropriate therapy.
 Causes :
• Virulent Staphylococcus aureus (acute).

• alpha-hemolytic (viridans) streptococci (subacute).

• Prosthetic valve endocarditis is caused most

commonly by coagulase-negative staphylococci
(e.g., Staphylococcus epidermidis).

• Other agents causing endocarditis include gram-

negative bacilli and fungi.
 Risk factors
• In years past, rheumatic heart disease.
• more common is mitral valve prolapse.
• degenerative calcific valvular stenosis.
• bicuspid aortic valve.
• artificial (prosthetic) valves.
• intravascular devices such as pacing leads and
vascular grafts.
• poor dental hygiene, immunodeficiency, therapeutic
immunosuppression, diabetes mellitus, and alcohol
or intravenous drug abuse.
 Gross appearance
• friable, bulky, and potentially destructive
vegetation containing fibrin, inflammatory cells,
and bacteria.

• The appearance of the vegetation is influenced by:

1- the type of organism responsible.

2- the degree of host reaction to the infection.

3- previous antibiotic therapy.

 Microscopical changes:
• Vegetations of typical subacute infective
endocarditis often have granulation tissue at their
bases.
• With the passage of time, fibrosis, calcification,
and a chronic inflammatory infiltrate may
develop.
 Clinical Features:
1-Fever :
subacute fever may be slight or absent, nonspecific fatigue,
loss of weight, and a flu like syndrome.

2-Murmurs are present in 90% of patients with left-sided

lesions but may merely relate to the preexisting cardiac
abnormality predisposing to endocarditis.

3- Petechiae, subungual hemorrhages, and Roth spots in the

eyes (secondary to retinal microemboli) have now become
uncommon owing to the shortened clinical course of the
disease as a result of antibiotic therapy.
 Complications:
• Cardiac complications:
• Valvular insufficiency or stenosis with cardiac failure.
• Myocardial ring abscess
• Suppurative pericarditis.
• artificial valves, partial dehiscence with paravalvular leak
• Embolic complications:
• left-sided lesions lead to embolization to the brain (cerebral
infarct or abscess, meningitis), heart (MI), spleen (abscess),
kidneys (abscess), other sites
• right-sided lesions lead to embolization to the lungs (infarct,
abscess, pneumonia).
• Other complications:
1-Splenomegaly.
2-Anemia.
3-Hematuria.
4-clubbing of fingers with splinter hemorrhage.
5- glomerulonephritis
 Pericarditis:
• It is an inflammatory reaction involving the visceral
and / or parietal pericardial layer.
Clinical features:
• Chest pain, a pericardial friction rub is a
characteristic feature of acute fibrinous pericarditis.
• Large pericardial effusion leads to dullness
percussion, and heart sound may be diminished
 Causes:

• viral pericarditis (coxsackie virus, herpis

simplx, and influenza).
• Myocardial infarction.
• Uremia.
• Bacterial pericarditis.
• Post-cardiac surgery.
• Malignancy and T.B.
 Morphological types:
• Fibrinous and Serofibrinous Pericarditis.
• Purulent or Suppurative Pericarditis.
• Hemorrhagic Pericarditis.
• Caseous Pericarditis.
• Healed Pericarditis
 Myocarditis:

• Causes:
viral (coxsackie, influenza, and H.I.V), Bacterial
infection, (diphtheria, meningococuss), Parasites,
trypanoasomiasis, Radiation, and Drugs.

• Clinicpathological Features:
In most patients, the myocarditis is a self limiting
condition with only mild chest pain. The biopsy
shows lymphocytic infiltrate, with myocyte necrosis.
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