Chapter 11

Rheumatic Valvular Disease

Page 405 – 407

Pathogrnesis
Rheumatic Valvular Disease
• Acute Rheumatic fever - is a hypersensitivity
reaction induced by host antibodies elicited
by group A streptococci.

• Since 3 % of the patient experience RF,

genetic susceptibility is likely to influence the
development of the pathogenic antibodies.

• The chronic sequelae result from progressive

fibrosis due to healing of the acute
inflammatory lesions.
 Clinical Features
Acute RF appears :
a. children aged 5 to 15 years,
b. but about 20% of first attacks occur in adults.
• 2 to 3 weeks – the symptom occur an episode of streptococcal
pharyngitis.

The predominant clinical manifestations are:

a. arthritis – is far more common in adults.
- begins with polyarthritis accompanied by fever in which one large
joint after another becomes painful and swollen for a period of days
b. carditis - include pericardial friction rubs and arrhythmias.
- Myocarditis can be so severe that resulting cardiac dilation causes
functional mitral insufficiency and even CHF.
• After an initial attack there is increased vulnerability to disease
reactivation with subsequent pharyngeal infections.

• Chronic rheumatic carditis - usually does not cause clinical

manifestations for years or even decades after the initial episode of
RF.
• The signs and symptoms of valvular disease depend on which valve(s)
are involved:
• mitral valve is the one most commonly involved and its stenosis is
the most common manifestation.
• Surgical repair or replacement of diseased valves - has greatly
improved the outlook for patients with RHD.

• Diagnosis of acute RHD is made by serologic evidence of a

previous streptococcal infection, in conjunction with two or
more of the following Jones criteria:
1. Carditis
2. migratory polyarthritis of the large joints
3. subcutaneous nodules
4. erythema marginatum of the skin
5. Sydenham chorea
Infective Endocarditis
• is a serious infection requiring
prompt diagnosis and intervention.

• It is characterized by microbial
invasion of heart valves or mural
endocardium.

• Classified into:

a. Acute endocarditis
b. Subacute endocarditis
 Acute endocarditis

• usually suggests a tumultuous,

destructive infection,
frequently involving a highly
virulent organism attacking a
previously normal valve.

• - causing death within days to

weeks in more than 50% of
patients despite antibiotics and
surgery.
A, Endocarditis of mitral valve
(subacute, caused by Streptococcus viridans)
 Subacute endocarditis

• - refers to infections by
organisms of low virulence
colonizing a previously abnormal
heart, especially when there are
deformed valves.

• - appears insidiously and

B, Acute endocarditis of congenitally
bicuspid aortic valve
(caused by Staphylococcus aureus)
follows a protracted course of
weeks to months with most
patients recovering after
appropriate antibiotic therapy.
 Morphology

• In both acute and subacute forms of the disease, friable, bulky, and
potentially destructive vegetations containing fibrin, inflammatory cells, and
microorganisms are present on the heart valves .
Most common site of infection:
a. Aortic valve
b. mitral valve

• Vegetations may be single or multiple and may involve more than one valve;
• They can erode into the underlying myocardium to produce an abscess
cavity (ring abscess).
• The appearance of vegetations is influenced by the infecting organism, the
degree of host response, and antibiotic therapy.
• Systemic emboli
- may occur at any time because of the friable nature of
the vegetations.
• Because the embolic fragments contain large numbers of
virulent organisms, abscesses often develop at the sites of such
infarcts (septic infarcts).

• Subacute endocarditis is typically associated with less valvular

destruction than is acute endocarditis.
 Pathogenesis
• Infective Endocarditis - can develop on previously normal valves,
but the presence of cardiac abnormalities predisposes to such
infections.
• RHD - was previously a major antecedent disorder, but it has
been displaced by:
• mitral valve prolapsed
• bicuspid aortic valves
• calcific valvular stenosis.
•  Increase the risk of IE:
a. Neutropenia
b. Immunodeficiency
c. Malignancy
d. therapeutic immunosuppression
e. diabetes mellitus
f. alcohol or intravenous drug abuse

• The causative organisms differ depending on the underlying risk

factors.

• viridans Streptococci
- a relatively banal group of normal oral flora.
• In contrast, the more virulent S. aureus (common to skin) can
attack deformed and healthy valves and is responsible for 10% to
20% of cases overall
• it is also the major offender in intravenous drug abusers.
• Additional bacterial agents include enterococci and the so-called
HACEK group
a. Haemophilus,
b. Actinobacillus
c. Cardiobacterium
d. Eikenella
e. Kingellaity
 Clinical Features

• Fever - is the most consistent

sign of IE.
• subacute disease (particularly
in the elderly)
• - fever may be absent, and the
only manifestations may be
nonspecific fatigue, weight loss,
and a flulike syndrome.
• Acute endocarditis
- has a stormy onset with • Splenomegaly
rapidly developing fever, chills, - is common in subacute IE.
weakness, and lassitude.
• Murmurs are present in 90% of patients with left-sided lesions
- but these may merely relate to the pre-existing cardiac
abnormality predisposing to IE.

• Diagnosis is largely made on the basis of positive blood cultures,

echocardiographic findings, and other clinical and laboratory findings.

• 1st weeks of the onset of IE - Complications begin.

• These include glomerulonephritis due to glomerular trapping of antigen-

antibody complexes.
 Questions

1. It is a hypersensitivity reaction induced by host antibodies elicited

by group A streptococci.
a. Acute Rheumatic fever
b. Chronic rheumatic fever
c. Acute rheumatic carditis
d. Chronic rheumatic carditis
2. Acute rheumatic fever appears in children aged __ to __ years.
a. 8 to 15 years
b. 5 to 15 years
c. 7 to 15 years
d. None of the above
3. It is a serious infection requiring prompt diagnosis and intervention.
a. Infective endocarditis
b. Acute Rheumatic fever
c. Chronic rheumatic fever
d. Acute rheumatic carditis
4. Infective endocarditis classified into __________ and ___________.
e. Acute endocarditis and chroninc endocarditis
f. Acute endocarditis and subacute endocarditis
g. Chroninc endocarditis and subacute endocarditis
h. None of the above
5. True or False: After an initial attack there is increased vulnerability to
disease reactivation with subsequent pharyngeal infections. TRUE.