CVS MODULE
The heart consists of four chambers, two atria (upper chambers) and two ventricles
(lower chambers). There is a valve through which blood passes before leaving each
chamber of the heart. The valves prevent the backward flow of blood. These valves
are actual flaps that are located on each end of the two ventricles (lower chambers
of the heart). They act as one-way inlets of blood on one side of a ventricle and
one-way outlets of blood on the other side of a ventricle. Normal valves have three
flaps, except the mitral valve, which has two flaps. The four heart valves include
the following:
•
•
•
•
tricuspid valve: located
between the right atrium
and the right ventricle.
pulmonary valve: located
between the right ventricle
and the pulmonary trunk.
mitral valve: located
between the left atrium and
the left ventricle.
aortic valve: located
between the left ventricle
and the aorta.
As the heart muscle
contracts and relaxes,
the valves open and
shut, letting blood flow
into the ventricles and
atria at alternate times.
1) Tricuspid valve which has 3 cups:
Each cup consists of 2 layers of endocardium and thin fibrous tissue layer in
between,
The cup attached by its base to the fibrous ring surrounds the orifice while its apex
hangs into ventricular cavity which gives insertion to the Chordae tendineae.
The atrial surface is smooth, and the ventricular surface is rough.
Between the right atrium and right ventricle.
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2)pulmonary valve:
It guards the pulmonary trunk, exists between the right ventricle and the pulmonary
trunk.
Consists of 3 semilunar cusps, its base attached to the wall of wall the pulmonary
trunk while its free edges directed upwards into the lumen of the trunk.
3) Mitral valve (bicuspid):
Opens into the left ventricle, has only 2 cusps.
4) Aortic valve:
A 3 semilunar valve
between the left
ventricle and the aorta.
They are all part of the
endocardium.
The most common
organism of Rheumatic
fever is Streptococcus.
Especially streptococcus
pyogenes.
It’s a major humanspecific bacterial
pathogen that causes a
wide array of
manifestations ranging
from mild localized
infections to lifethreatening invasive
infections.
gram-positive, catalase-negative, oxidase negative, non-sporulated, non-motile,
has a hyaluronic acid capsule which is chemically similar to that of host
connective tissue. β-hemolytic streptococci. It is a facultative anaerobe, grows
best in 5 to 10% carbon dioxide, and forms pinpoint colonies on blood agar
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plates. Lancefield serological grouping system is used to differentiate group A
streptococci (GAS) from other streptococci. The type A antigen of S. pyogenes is
a polysaccharide which is comprised of N-acetylglucosamine attached to a
rhamnose polymer backbone.
M protein is the major surface protein presents on S. pyogenes cell wall, S.
pyogenes usually colonizes, pharynx, anus, and genital mucosa. Infections
caused by S. pyogenes are highly contagious. Transmission can occur through
airborne droplets, hand contact with nasal discharge or with objects or
surfaces contaminated with bacteria, skin contact with contaminated lesions,
or contaminated food sources.
Multiple virulence factors are responsible for clinical manifestations of the S.
pyogenes. The bacterial capsule consisting of hyaluronic acid provides protection
against phagocytosis. M protein, lipoteichoic acid, and protein F are responsible for
the attachment of the bacteria to host cells. M protein is also responsible for
inhibiting opsonization by binding to complement regulators and to fibrinogen. M
protein is the most important virulence factor for S. pyogenes since experiments
have shown that M mutants cannot survive in phagocyte-containing human blood.
S. pyogenes also produce exotoxins, like a pyrogenic (erythrogenic) toxin, which is
responsible for the rash of scarlet fever and toxic shock syndrome. Other virulent
factors include streptokinase, streptodornase, hyaluronidase, and streptolysins,
which help in the invasion of tissues.
What is rheumatic?
Its an acute immunologically mediated, multisystem inflammatory diseases that
occurs after group A β-hemolytic streptococcal infections usually pharyngitis or
skin infections.
Rheumatic valvular disease is the cardiac manifestation of rheumatic fever, its
associated with inflammation of all parts of the heart, valvular inflammation and
scarring produce the most important clinical features.
The valvular disease takes the form of deforming fibrotic mitral stenosis.
Rheumatic heart disease is essentially the only cause of acquired mitral stenosis.
How rheumatic valvular disease happens?
Acute rheumatic fever is a hypersensitivity reaction, the antibodies of
Astreptococcal molecules cross react with the host myocardial antigen because of
antigenic similarity between the streptococcal and human connective tissue.
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Antibodies against M protein bind to proteins in myocardium and cardiac valves,
this binding causes injury through activation of complement and Fc
receptorsbearing cells, CD4+T cells that recognize streptococcal peptides can
cross-react with host antigens and elicit cytokine-mediated inflammatory
responses.
Deforming fibrotic lesions develop after healing its associated with resolution of
acute inflammation.
The pathological changes in the
valves:
Fibrinoid necrosis and fibrin
deposition along lines of closure
forming 1-2 mm vegetations
(verrucae) which cause
disturbance in cardiac function.
In chronic rheumatic fever the
most important functional
consequence of RHD is:
Valvular stenosis and
regurgitation, stenosis tends to
predominate.
Mitral valve alone involved in
70% of cases, combined with
aortic is 25%.
With the pressure overload the
atrium progressively dilates
leading to atrial fibrillation and thrombosis
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With left sided heart failure because of the long standing passive venous
congestion leads to right ventricular hypertrophy and failure.
Prevention measures and role of long acting penicillin:
Treatment of acute rheumatic fever consists of antibiotic therapy, antiinflammatory
therapy, heart failure management, and commencement of ongoing care (secondary
prevention and provision of education), Hospitalization is advisable for optimal
management of ARF, especially for an initial episode, so that all tests can be
completed, response to therapy can be observed, and long-term preventative
measures can be started with appropriate education for the patient and their
caregivers.
Prevention of initial development of rheumatic fever (primary prevention) is
accomplished by prompt diagnosis and antibiotic treatment of group
A Streptococcus (GAS) tonsillopharyngitis and, in some settings, GAS pyoderma.
Appropriate antibiotic treatment of pharyngitis prevents ARF in most cases,
However, at least one-third of ARF episodes occur in the setting of subclinical
streptococcal infection, In addition, ARF is not preventable in symptomatic
patients who are not able to access medical care.
Patients who have had an attack of ARF and develop subsequent group
A Streptococcus (GAS) pharyngitis are at high risk for a recurrent attack of ARF.
Rheumatic heart disease (RHD) becomes more severe with each recurrent episode.
Thus, the most effective method to limit progression of RHD severity is prevention
of recurrent GAS pharyngitis.
long-term antimicrobial prophylaxis better than recognition and treatment of acute
GAS pharyngitis episodes, because GAS infection does not need to be
symptomatic to trigger a recurrent attack of ARF.
Long-term prophylaxis is warranted for patients with a well-documented history of
ARF (including cases with Sydenham chorea [SC] as the sole manifestation), as
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well as those with definite evidence of RHD. Antibiotic prophylaxis is usually
provided in the primary care.
Antibiotic selection — For most patients, long-acting penicillin G benzathine
administered intramuscularly (IM) every 28 days rather than other regimens,
However, there is regional variation in use of penicillin G benzathine depending
upon availability and cost. In regions where ARF is endemic, penicillin G
benzathine continues to be the preferred agent since it is highly effective, low
cost, and readily available.
By contrast, in nonendemic regions (eg, the United States and Europe), penicillin G
benzathine is more costly, and recurrent shortages are a substantial and recurring
problem, Thus, oral agents (eg, penicillin V) are more commonly used in
nonendemic compared with endemic regions.
Oral agents are also appropriate for patients with the following features:
●Proven penicillin allergy (where a macrolide such as azithromycin is used)
●Severe valvular disease from RHD due to increased risk for sudden death
following IM injections
●Bleeding problems following injections that cannot be addressed
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References
https://www.columbiadoctors.org/treatments-conditions/heart-valves-anatomyandfunction#:~:text=tricuspid%20valve%3A%20located%20between%20the,left%
20v entricle%20and%20the%20aorta
https://www.ncbi.nlm.nih.gov/books/NBK554528/
https://www.uptodate.com/contents/acute-rheumatic-fever-treatmentandprevention?sectionName=PRIMARY%20PREVENTION&topicRef=114019&
anc hor=H7&source=see_link#H7
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