BIL TABLE OF CONTENT PAGE

1 Acknowledgement

2 Introduction of topic

3 Rational of topic

4 General objective

5 Specific objective

6 Defination

7 Pathophysiology

8 Etiology

9 Clinical manifestation

10 Laboratory investigation

11 Assessment / Diagnosis treatment

Rheumatic (roo-MAT-ik) heart disease was formerly
one of the most serious forms of heart disease of
childhood and adolescence. Rheumatic heart disease
involves damage to the entire heart and its
membranes.

Rheumatic heart disease is a complication of

rheumatic fever and usually occurs after attacks of
rheumatic fever. The incidence of rheumatic heart
disease has been greatly reduced by widespread use
of antibiotics effective against the streptococcal
bacterium that causes rheumatic fever.
Rheumatic fever is a systemic disease affecting the peri-arteriolar connective tissue
and can occur after an untreated Group A Beta hemolytic streptococcal pharyngeal
infection. It is believed to be caused by antibody cross-reactivity. This cross-
reactivity is a Type II hypersensitivity reaction and is termed molecular mimicry.
Usually, self reactive B cells remain anergic in the periphery without T cell co-
stimulation. During a Strep. infection, mature antigen presenting cells such as B
cells present the bacterial antigen to CD4-T cells which differentiate into helper T2
cells. Helper T2 cells subsequently activate the B cells to become plasma cells and
induce the production of antibodies against the cell wall of Streptococcus. However
the antibodies may also react against the myocardium and joints, producing the
symptoms of rheumatic fever.Group A streptococcus pyogenes has a cell wall
composed of branched polymers which sometimes contain M protein that are highly
antigenic. The antibodies which the immune system generates against the M protein
may cross react with cardiac myofiber protein myosin[10],heart muscle glycogen and
smooth muscle cells of arteries, inducing cytokine release and tissue destruction.
However, the only proven cross reaction is with perivascular connective tissue.[citation
needed]
This inflammation occurs through direct attachment of complement and Fc
receptor-mediated recruitment of neutrophils and macrophages. Characteristic
Aschoff bodies, composed of swollen eosinophilic collagen surrounded by
lymphocytes and macrophages can be seen on light microscopy. The larger
macrophages may become Aschoff giant cells. Acute rheumatic valvular lesions may
also involve a cell-mediated immunity reaction as these lesions predominantly
contain T-helper cells and macrophages.]In acute RF, these lesions can be found in
any layer of the heart and is hence called pancarditis. The inflammation may cause
a serofibrinous pericardial exudates described as “bread-and-butter” pericarditis,
which usually resolves without sequelae. Involvement of the endocardium typically
results in fibrinoid necrosis and verrucae formation along the lines of closure of the
left-sided heart valves. Warty projections arise from the deposition, while
subendothelial lesions may induce irregular thickenings called MacCallum
plaques.Chronic rheumatic heart disease is characterized by repeated inflammation
with fibrinous resolution. The cardinal anatomic changes of the valve include leaflet
thickening, commissural fusion and shortening and thickening of the tendinous
cords.
Rheumatic fever causes rheumatic heart disease. Rheumatic

fever results from an untreated strep throat. Rheumatic fever

can damage the heart valves. If the heart valves are damaged,

they will fail to open and close properly. When this damage is

permanent, the condition is called rheumatic heart disease.

Acute rheumatic fever occurs most frequently in children from 5 to 15 years

of age and is less frequent among children in the first three years of life and

among adults. The onset of the disease usually is characterized by an acute

febrile illness that may manifest itself in one of several ways

What are the investigation procedures rheumatic heart
disease
Laboratory Findings

There is no specific laboratory test to indicate the presence of rheumatic fever. The
appraisal of rheumatic activity by laboratory finding is, however, of value.Since
various tests may indicate continued rheumatic inflammation when clinical features
are not apparent. Streptococcal anti body test to disclose preceding streptococcal
infection.Streptococcal from other acute respiratory infections and are increased
following asymptomatic as well as symptomatic streptococcal infection. These
antibody levels are increased in the early stages of acute rheumatic fever.They may
be declining or low if the interval between the acute streptococcal infection and the
detection of rheumatic fever has been longer than 2 months, a situation which occurs
most often in patients whose presenting rheumatic manifestation is chorea.
However, patients whose only major manifestation is rheumatic carditis also may
have low antibody titers when first seen. Their rheumatic attack may have been in
progress several months before becoming symptolymatic and recognized. Except in
these two instances, one should be reluctant to make the diagnosis of acute
rheumatic fever in the absence of serologic evidence of a recent streptococcal
infection.The antistreptolysin O (ASO) test is the most widely used and best-
standardized streptococcal antibody test. In general, single titers of at least 250
Toadd units in adults and at least 333 units in children over 5 years of age are
considered to be increased. Depending on the general prevalence of streptococcal
infections, a varying percentage of the normal population may shows titers of this
magnitude.About 20 percent of patients in the early stages of acute rheumatic fever,
and most patients who present with chorea. Have a low or borderline ASO titer. In
these instances, it is advisable to obtain a different streptococcal antibody test such
as anti-DNase B or antihyaluronidase (AH). The antistreptozyme (ASTZ) test is a
hemagglutination reaction to a concentrate of extracellular streptococcal antigens
absorbed to red blood cells.It is a very sensitive indicator of recent streptococcal
infection; virtually all patients with acute rheumatic fever have titers greater than
200 units per milliliter. A rise in titer of two dilution tubes or more can be
demonstrated for at least one of the specific streptococcal antibodies in almost all
recurrent as well as primary attacks of rheumatic fever. Increased streptococcal
antibodies.However, do not reflect rheumatic activity per se, and their rate of decline
is independent of the course of the rheumatic attacks. Because it almost always
occurs within the first 4 to 5 weeks of the antecedent streptococcal
pharyngitis.Polyarthritis is the clinical manifestation most promptly recognized and
therefore most reliably associated with rising streptococcal antibody titers. The
absences of increased or increasing streptococcal antibody titers in patients with
acute polyarthritis therefore makes rheumatic fever a very unlikely cause.Isolation of
group A streptococci: Some patients continue to harbor group A streptococci at the
onset of acute rheumatic fever, but these organisms are usually present in small
numbers and may be difficult to isolate by a single throat culture. The administration
of penicillin or other antibiotics also may result in failure to isolate the infecting
organism. In addition, a significant number of normal individuals, particularly
children, may harbor group. A streptococci in the upper respiratory tract. For these
reasons, throat culture are less satisfactory than antibody test as supporting
evidence of recent streptococcal infection, Acute phase reactants: These tests offer
objective but nonspecific confirmation of the presence of an inflammatory process.
The erythrocyte sedimentation rate and the test for C- Reactive protein in serum are
used most commonly. Unless the patient has received glucocorticoids or salicylates,
these reaction are almost always abnormal in patients presenting with polyarthritis
or acute carditis, where as they are often normal in patients with “pure” chorea.
Other laboratory finding which reflect inflammation include reactions such as
leukocytosis and increase in serum complement, mucoproteins, and alpha2 and
gamma globulins. Prolongation of the PR Interval of he electrocardiogram, although
neither specific for rheumatic fever nor diagnostic of serious cardiac involvement, is
frequent in acute rheumatic fever and other nonspecific electrocardiograpic changes
are also common. Anemia, due to the suppression of erythropoiesis characteristic of
chronic inflammatory diseases, is another feature of rheumatic activity.

Table:

Investigation in Acute rheumatic fever indicated by three manifestations

Major Manifestations Percent

• Carditis 14%

• Polyarthritis 14%

• Chorea 4%

• Carditis and polyarthritis 44%

• Carditis and Chorea 14%

• Carditis, Chorea, polyarthritis 6%

• Chorea and polyarthritis 4%

Rheumatic heart disease: Self Assessment Tools

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 Heart Attack -- Self Assessment Tools

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 Smoking -- Self Assessment Tools

 Weight Management -- Self Assessment Tools

 Heart Disease -- Self Assessment Tools