RHEUMATIC

FEVER &
RHEUMATIC
HEART DISEASE
 ACUTE RHEUMATIC FEVER

 Autoimmune consequence of infection (pharyngeal

infection not the skin infection) with Group A beta
haemolytic streptococcal infection

 Generalized inflammatory response affecting brains,

joints, skin, subcutaneous tissues & the heart

 Modified Duckett-Jones criteria form the basis of

the diagnosis of the condition
 ACUTE RHEUMATIC FEVER
Supporting evidences:

 About 66% of the patients with an acute episode of

rheumatic fever have a history of an upper
respiratory tract infection several weeks before

 The peak age (6-15 yrs) & seasonal incidence of acute

rheumatic fever closely parallel those of GABHS
infections
 ACUTE RHEUMATIC FEVER

Features suggestive of GABHS infection

 Patient 5 to 15 years of age

 Presentation in winter or early spring

 Fever, Headache

 Sudden onset of sore throat

 Nausea, vomiting & abdominal pain; Pain with

swallowing
 Beefy, swollen, red uvula

 Soft palate petechiae (“doughnut lesions”)

 Tender, enlarged anterior cervical nodes

 Tonsillopharyngeal erythema & exudates

 ACUTE RHEUMATIC FEVER
Redness & swelling
of throat & tonsils;

Beefy, swollen, red

uvula; Soft palate
petechiae
(“doughnut
lesions”)

Tonsillopharyngeal
erythema &
Sore throat: fever, exudates
white draining
patches on the
throat & swollen or
tender lymph glands
in the neck
 ACUTE RHEUMATIC FEVER
Supporting evidences:
 Patients with acute rheumatic fever almost always

have serologic evidence of a recent GABHS infection

 Their antibody titers are usually considerably higher

than those in patients with GABHS infections without

acute rheumatic fever
 Antimicrobial therapy against GABHS: prevents initial

episodes of acute rheumatic fever &

 Long-term, continuous prophylaxis: prevents

recurrences of acute rheumatic fever

 ACUTE RHEUMATIC FEVER
Predisposing factors:

 Family history of rheumatic fever

 Low socioeconomic status (poverty, poor hygiene,
medical deprivation)
 Age: 6-15 years
 EPIDEMIOLOGY

 Prevalence of Acute rheumatic fever & RHD:

0.67/1000 to 11/1000 children

 The INCIDENCE of rheumatic fever varies from

0.2 to 0.75/1000/ year in schoolchildren 5–15 years
of age (2001 Govt. Census)
certain M proteins
(M1, M5, M6, and
M19) share
epitopes with
human
tropomyosin &
myosin
strong correlation between progression
Common antigenic determinants are
shared between components of GAS
to RHD & HLA-DR class II alleles &
(M protein, protoplast membrane, the inflammatory protein-encoding genes
cell wall group A carbohydrate, MBL2 and TNFA
capsular hyaluronate) & specific
mammalian tissues (e.g., heart, brain, Pathogenetic pathway for ARF & RHD
joint)
CLINICAL MANIFESTATIONS

 No pathognomonic clinical or laboratory finding for

acute rheumatic fever
 Duckett Jones in 1944 proposed guidelines to aid in
diagnosis & to limit overdiagnosis
 Jones criteria for the diagnosis of acute rheumatic
fever 2 major criteria or 1 major & 2 minor
criteria along with the absolute requirement
 There are 5 major and 4 minor criteria & an
absolute requirement for evidence (microbiologic or
serologic) of recent GABHS infection
 DIAGNOSIS
SUPPORTING EVIDENCE OF
MAJOR MINOR ANTECEDENT GROUP A
MANIFESTATIONS MANIFESTATIONS STREPTOCOCCAL
INFECTION******
Carditis Clinical features: -Elevated or increasing
Arthralgia streptococcal antibody titer
Fever
Polyarthritis
Erythema
marginatum
Laboratory features: History of (<45 days)
Subcutaneous Elevated acute phase -Positive throat culture or rapid
nodules reactants: ESR, C-reactive streptococcal antigen test or
Chorea protein streptococcal sore throat or
Prolonged PR interval scarlet fever)
 First episode
or Recurrence
ARF & RHD without
established
heart
disease: 2
major
criteria or 1
major & 2
minor criteria
& the
absolute
requirement
Recurrence
with
established
heart
disease: 2
minor criteria
and the
absolute
requirement
MAJOR
MANIFESTATIONS
 Migratory Polyarthritis

 Most common (75%)

 Involves larger joints: the knees, ankles, wrists &
elbows
 Rheumatic joints: hot, red, swollen & exquisitely
tender (friction of bedclothes is uncomfortable)
 The pain can precede & can appear to be
disproportionate to the other findings
 Migratory Polyarthritis

 The joint involvement is characteristically migratory

in nature
 Monoarticular arthritis is unusual unless anti
inflammatory therapy is initiated prematurely,
aborting the progression of the migratory
polyarthritis
 Migratory Polyarthritis

 If a child with fever and arthritis is suspected of

having acute rheumatic fever: withhold salicylates &
observe for migratory progression
 A dramatic response to even small doses of
salicylates is another characteristic feature of the
arthritis
 Rheumatic arthritis is typically not deforming
 Migratory Polyarthritis

 Arthritis; earliest manifestation of acute rheumatic

fever
 Correlate temporally with peak antistreptococcal
antibody titers
 An inverse relationship between the severity of
arthritis & the severity of cardiac involvement
 Carditis

 Carditis & chronic rheumatic heart disease: most

serious manifestations of acute rheumatic fever
 Account for essentially all of the associated
morbidity and mortality
 Occurs in 50% of patients
 Rheumatic carditis: pancarditis with active
inflammation of myocardium, pericardium &
endocardium
 Acute rheumatic carditis: tachycardia out of
proportion to fever & cardiac murmurs, with or
without evidence of myocardial or pericardial
involvement
 Carditis

 Consists of either isolated mitral valvular disease or

combined aortic & mitral valvular disease
 Valvular insufficiency: characteristic of both acute &
convalescent stages of acute rheumatic fever
 Mitral regurgitation: a high-pitched apical
holosystolic murmur radiating to the axilla
 In patients with significant mitral regurgitation-
associated with an apical mid-diastolic murmur of
relative mitral stenosis
 Aortic insufficiency: a high-pitched decrescendo
diastolic murmur at the upper left sternal border
 Carditis

 Valvular stenosis: appears several years or even

decades after the acute illness
 However, in developing countries where acute
rheumatic fever often occurs at a earlier age, mitral
stenosis & aortic stenosis may develop in young
children
 Moderate to severe rheumatic carditis:
cardiomegaly & congestive heart failure with
hepatomegaly & peripheral & pulmonary edema
 Myocarditis &/or pericarditis without evidence of
endocarditis: rarely due to rheumatic heart disease
 Carditis

 Echocardiographic findings: pericardial effusion,

decreased ventricular contractility & aortic &/or
mitral regurgitation

 The major consequence of acute rheumatic carditis

is chronic, progressive valvular disease
 During an episode of
ARF, valve changes can
be minor and are still
able to regress

After recurrent
episodes of ARF,
thickening of subvalvar
apparatus, chordal
thickening and
shortening and
progression to
permanent valve damage
is evident
 Chorea

 St. Vitus’dance
 Sydenham chorea: 10-15% of patients with acute
rheumatic fever
 Often in prepubertal girls (8-12 yrs)
 A long latency period (1-6 mo) between
streptococcal pharyngitis & the onset of chorea
 Neuropsychiatric disorder
 Neurologic signs: choreic movement & hypotonia
 Psychiatric signs: emotional lability, hyperactivity,
separation anxiety, obsessions & compulsions
 Chorea

 Begins with emotional lability & personality changes

(poor school performance)
 Replace in 1-4 weeks by characteristic spontaneous,
purposeless movement of chorea (lasts 4-8 months)
followed by motor weakness
 Exacerbation by stress & disappearing with sleep
are characteristic
 Elevated titers of “antineuronal antibodies” against
basal ganglion tissues have been found in over 90%
of patients
 Chorea

 Clinical maneuvers to elicit features of chorea

include
(1) demonstration of milkmaid's grip (irregular
contractions of the muscles of the hands while
squeezing the examiner's fingers)
(2) spooning and pronation of the hands when the
patient's arms are extended
(3) wormian darting movements of the tongue upon
protrusion
(4) examination of handwriting to evaluate fine motor
movements
 Chorea
 Diagnosis: based on clinical findings with supportive
evidence of GABHS antibodies
 In patients with a long latent period: antibody levels
may have declined to normal
 SUBCLINICAL CARDITIS-30%
 Although the acute illness is distressing, chorea
rarely, if ever, leads to permanent neurologic
sequelae
 Erythema Marginatum

 A rare (<3% of patients with acute rheumatic fever)

but characteristic rash of acute rheumatic fever
 It consists of erythematous,
serpiginous, macular lesions with
pale centers that are not pruritic
 It occurs primarily on the trunk
& extremities, not on the face &
it can be accentuated by warming
the skin
 Subcutaneous Nodules
 A rare (≤1% of patients with acute rheumatic fever)
finding
 Consist of firm nodules approximately 1 cm in
diameter along the extensor surfaces of tendons
near bony prominences
 A correlation between the presence of these
nodules & significant
rheumatic heart disease
MINOR
MANIFESTATIONS
 MINOR MANIFESTATIONS

Clinical:
 1. Arthralgia (in the absence of polyarthritis as a

major criterion)
 2. Fever (typically temperature ≥102°F & occurring
early in the course of illness)
Laboratory minor manifestations:
 1.Elevated acute-phase reactants (C-reactive protein,
erythrocyte sedimentation rate, polymorphonuclear
leukocytosis)
 2. Prolonged PR interval on electrocardiogram (1st

degree heart block)

ESSENTIAL CRITERIA
An absolute requirement for the
diagnosis of acute rheumatic fever is
supporting evidence of a recent GABHS
infection
Recent Group A Streptococcus infection

 Hallmarks of GAS sore throat:

 High fever, tender anterior cervical lymph nodes

 Close contact with infected person

 Strawberry tongue, petechiae on palate

 Excoriated nares( crusted lesions) in infants

 Tonsillar exudates in older children

 Abdominal pain

GOLD STANDARD: POSITIVE THROAT CULTURE

Recent Group A Streptococcus infection

 Acute rheumatic fever typically develops 2-4 wk

after an acute episode of GABHS pharyngitis at a
time when clinical findings of pharyngitis are no
longer present & only 10-20% of the throat culture
or rapid streptococcal antigen test results are
positive

 Therefore, evidence of an antecedent GABHS

infection is usually based on elevated or increasing
serum antistreptococcal antibody titers
Recent Group A Streptococcus infection

1. ASO titre:
 well standardized

 elevated in 80% of patients with ARF

 ASO titre of 333 Todd unit in children & 250 Todd

unit in adults are considered elevated

2. Antideoxyribonuclease B titre:
 ≥240 Todd unit in children & ≥120 Todd unit in adults
Recent Group A Streptococcus infection

3. Slide agglutination test (Streptozyme):

 Detect antibodies against 5 different GABHS

antigens
 Rapidly, relatively simple to perform & widely

available
 Less standardized & less reproducible than other
tests and should not be used as a diagnostic test for
evidence of an antecedent GAS infection
Recent Group A Streptococcus infection

 Single antibody measured: 80-85% of patients have

an elevated titer
 If 3 different antibodies (antistreptolysin O, anti-
DNase B, antihyaluronidase) measured: 95-100% have
an elevation
 Therefore in suspectedARF clinically: perform
multiple antibody tests
 Diagnosis of ARF should not be made in patients with
elevated or increasing streptococcal antibody titers
who do not fulfill the Jones criteria
 True for younger, school-aged children having
GABHS pyoderma or GABHS pharyngitis
DIFFERENTIAL DIAGNOSIS

ARTHRITIS
Rheumatoid arthritis

Reactive arthritis (Shigella, Salmonella, Yersinia)

Serum sickness
Sickle cell disease
Malignancy
Systemic lupus erythematosus
Lyme disease (Borrelia burgdorferi)
Gonococcal infection (N.gnorrhoeae)
DIFFERENTIAL DIAGNOSIS

CARDITIS
Viral myocarditis

Viral pericarditis

Infective endocarditis
Kawasaki disease
Congenital heart disease
Mitral valve prolapse
Innocent murmurs
DIFFERENTIAL DIAGNOSIS

CHOREA
Huntington chorea

Wilson disease

Systemic lupus erythematosus

Cerebral palsy
Tics
Hyperactivity
 DIFFERENTIAL DIAGNOSIS

Patients with infective endocarditis: present with

both joint and cardiac manifestations

These patients can usually be distinguished from

patients with acute rheumatic fever by blood
cultures & the presence of associated findings
(hematuria, splenomegaly, splinter hemorrhages)
 TREATMENT

 Bed rest

 Antibiotic Therapy:
 10 days of orally administered penicillin or
erythromycin or a single intramuscular injection of
benzathine penicillin to eradicate GABHS from the
upper respiratory tract
 Afterwards, the patient should be started on long-
term antibiotic prophylaxis
 TREATMENT

 Anti-inflammatory Therapy:
 Anti-inflammatory agents (salicylates,
corticosteroids) should be withheld if arthralgia or
atypical arthritis is the only clinical manifestation of
presumed acute rheumatic fever
 Acetaminophen can be used
 Patients with typical migratory polyarthritis & with
carditis without cardiomegaly or congestive heart
failure:
treatment with oral salicylates, 100 mg/kg/day in 4
divided doses PO for 3-5 days, followed by
75 mg/kg/day in 4 divided doses PO for 4-8 wk
 TREATMENT

 Patients with carditis & cardiomegaly or congestive

heart failure:
 treatment with corticosteroids
 Prednisone 2 mg/kg/day in 4 divided doses for 2-6 wk
followed by a tapering of the dose that reduces the
dose by 5 mg/24 hr every 2-3 days. At the beginning
of the tapering of the prednisone dose, aspirin should
be started at 75 mg/kg/day in 4 divided doses to
complete 12 wk of therapy
 TREATMENT

 Supportive therapies for patients with moderate to

severe carditis include digoxin, fluid & salt
restriction, diuretics & oxygen
 The cardiac toxicity of digoxin is enhanced with
myocarditis
 TREATMENT

Sydenham Chorea
 Occurs after the resolution of the acute phase of

the disease
 Anti-inflammatory agents are usually not indicated

 Sedatives: phenobarbital (16-32 mg every 6-8 hr PO)

is the drug of choice
 If phenobarbital is ineffective, then haloperidol
(0.01-0.03 mg/kg/24 hr divided bid PO) or
chlorpromazine (0.5 mg/kg every 4-6 hr PO) should
be initiated
 Long-term antibiotic prophylaxis
 PREVENTION

PREVENTION

SECONDARY-Secondary
PRIMARY-10 days course prevention is directed at
of penicillin therapy; preventing acute GABHS
about 30% of patients with pharyngitis in patients at
acute rheumatic fever do substantial risk of
not recall a preceding recurrent acute rheumatic
episode of pharyngitis fever
 SECONDARY PREVENTION

 Who should receive prophylaxis?

Patients with documented history of rheumatic fever,
including those with isolated chorea & those without
evidence of rheumatic heart disease MUST receive
prophylaxis
 SECONDARY PREVENTION

 For how long?

CATEGORY DURATION
Rheumatic fever without carditis At least for 5 yr or until
age 21 year, whichever is
longer
Rheumatic fever with carditis but At least for 10 yr or well
without residual heart disease (no into adulthood, whichever is
valvular disease) longer
Rheumatic fever with carditis & At least 10 yr since last
residual heart disease (persistent episode & at least until age
valvular disease) 40 yr; sometime lifelong
 SECONDARY PREVENTION

 What method of prophylaxis should be used?

DRUG DOSE ROUTE
600,000 U for children, ≤27 kg
Penicillin G benzathine 1.2 million U for children >27 kg, Intramuscular
every 3 wk
OR
Penicillin V 250 mg, twice a day Oral
OR
0.5 g, once a day for patients
Sulfadiazine or
≤60 lb; 1.0 g, once a day for Oral
sulfisoxazole
patients >60 lb
For people who are allergic to penicillin and sulfonamide drugs
Macrolide or azalide Variable Oral
 RHEUMATIC HEART DISEASE
Rheumatic involvement of the valves & endocardium
The valvular lesions begin as small verrucae composed of fibrin and
blood cells along the borders of one or more of the heart valves
The mitral valve is affected most often, followed in frequency by
the aortic valve; right-sided heart manifestations are rare
At the end of inflammation: verrucae disappear & leave scar tissue
Repeated attacks of rheumatic fever: new verrucae form near the
previous ones & the mural endocardium & chordae tendineae become
involved
 MITRAL INSUFFICIENCY
Backflow of blood from the LV to the LA during
systole
 MITRAL INSUFFICIENCY

Pathophysiology:
 Loss of valvular substance & shortening &

thickening of the chordae tendineae

 Because of the high volume load & inflammatory
process, the left ventricle becomes enlarged
 The left atrium dilates as blood regurgitates into
this chamber
 Increased left atrial pressure results in pulmonary

congestion & symptoms of left-sided heart failure

 MITRAL INSUFFICIENCY

Clinical manifestations:
 Exertion Dyspnea ( exercise intolerance), fatigue

 Mild disease : NO signs of heart failure

 Severe mitral insufficiency: signs of left sided heart

failure
 The heart is enlarged, with a forcible & hyperkinetic

apical left ventricular impulse & often an apical

systolic thrill
 Soft S1
 MITRAL INSUFFICIENCY

Clinical manifestations:
 The 2nd heart sound may be accentuated if

pulmonary hypertension is present

 A 3rd heart sound is generally prominent

 A holosystolic murmur is heard at the apex with

radiation to the axilla
 A short mid-diastolic rumbling murmur is caused by
increased blood flow across the mitral valve as a
result of the insufficiency
 MITRAL INSUFFICIENCY

Imaging studies:
 ECG: prominent bifid P waves, signs of left

ventricular hypertrophy & associated right

ventricular hypertrophy if pulmonary hypertension is
present
 X-rays: prominence of the left atrium & ventricle;

congestion of perihilar vessels, a sign of pulmonary

venous hypertension
 2 D ECHO: enlargement of the left atrium & ventricle

& Doppler studies demonstrate the severity of the

mitral regurgitation
 MITRAL INSUFFICIENCY

Complications:
 cardiac failure

 chronic mitral insufficiency -right ventricular failure

 atrial and ventricular arrhythmias

 MITRAL INSUFFICIENCY

Management:
 Medical:

 Prophylaxis against recurrences of rheumatic fever

 Treatment of heart failure, arrhythmias and

infective endocarditis
 Afterload-reducing agents (ACE inhibitors or

angiotensin receptor blockers):

reduce the regurgitant volume & preserve left
ventricular function
 MITRAL INSUFFICIENCY

Management:
 Surgical:

 For patients who despite adequate medical therapy

have persistent heart failure, dyspnea with moderate

activity & progressive cardiomegaly, often with
pulmonary hypertension
 Valve repair surgery preferred over valve replacement
 MITRAL STENOSIS
Obstruction of LV inflow that prevents proper
filling during diastole
Normal MV Area: 4-6 cm
2

Transmitral gradients & symptoms begin at

areas less than 2 cm2

 MITRAL STENOSIS

Pathophysiology:
 From fibrosis of the mitral ring, commissural

adhesions & contracture of the valve leaflets, chordae

& papillary muscles
 It takes 10 years or more for the lesion to become
fully established
 MITRAL STENOSIS

Pathophysiology:
 Significant mitral stenosis results in increased

pressure, enlargement & hypertrophy of the left

atrium, pulmonary venous hypertension, increased
pulmonary vascular resistance & pulmonary
hypertension
 Right ventricular hypertrophy & right atrial

dilatation ensue & are followed by right ventricular

dilation, tricuspid regurgitation & clinical signs of
right-sided heart failure
 MITRAL STENOSIS
Clinical manifestations:
 Correlation between symptoms & the severity of
obstruction
 Patients with mild lesions: asymptomatic

 More severe degrees of obstruction: exercise

intolerance & dyspnea

 Critical lesions: orthopnea, paroxysmal nocturnal
dyspnea, & overt pulmonary edema, as well as atrial
arrhythmias
 MITRAL STENOSIS
Clinical manifestations:
 Pulmonary hypertension: right ventricular dilatation-
functional tricuspid insufficiency, hepatomegaly,
ascites & edema
 Hemoptysis: rupture of bronchial or pleurohilar veins
or by pulmonary infarction
 MITRAL STENOSIS

Clinical manifestations:
 Jugular venous pressure is increased in severe

disease with heart failure

 prominent "a" wave in jugular venous pulsations: Due

to pulmonary hypertension & right ventricular

hypertrophy
 Mild disease: heart size is normal, tapping apex

 Severe mitral stenosis: moderate cardiomegaly

 Cardiac enlargement massive: atrial fibrillation &

heart failure
 A parasternal right ventricular lift is palpable when

pulmonary pressure is high

 MITRAL STENOSIS

Clinical manifestations:
 Auscultatory findings:

 Loud 1st heart sound,

 An opening snap of the mitral valve, and

 A long, low-pitched, rumbling mitral diastolic murmur

with presystolic accentuation at the apex
 Murmur absent in patients with significant heart

failure
 MITRAL STENOSIS

Clinical manifestations:
 A holosystolic murmur secondary to tricuspid

insufficiency
 Pulmonary hypertension: pulmonic component of the

2nd heart sound is accentuated

 An early diastolic murmur: associated AR or pulmonary
valvular insufficiency secondary to pulmonary
hypertension
 MITRAL STENOSIS

Imaging studies:
 ECG: prominent & notched P waves & varying degrees

of right ventricular hypertrophy, Atrial fibrillation

 X-rays: Left atrial enlargement & prominence of the

pulmonary artery & right-sided heart chambers;

calcifications may be noted in the region of the
mitral valve
 Severe obstruction is associated with a

redistribution of pulmonary blood flow so that the

apices of the lung have greater perfusion (the
reverse of normal)
 MITRAL STENOSIS

Imaging studies:
 2 D ECHO: thickening of the mitral valve, distinct

narrowing of the mitral orifice during diastole and

left atrial enlargement
 Doppler can estimate the transmitral pressure

gradient
 Cardiac catheterization quantitates

 Diastolic gradient across the mitral valve

 Allows for the calculation of valve area

 Assesses the degree of elevation of pulmonary

arterial pressure
 MITRAL STENOSIS

Management:
 Medical:

 Mild & moderate MS: anticongestive measures

(digoxin & diuretics)

 Atrial fibrillation: digoxin; procainamide for
conversion to sinus rhythm in hemodynamiclly stable
patients
 chronic AF warfarin

 IE prophylaxis

 percutaneous mitral balloon valvotomy: failure to

thrive with repeated respiratory infections
 MITRAL STENOSIS

Management:
 Surgical: indicated in

 patients with clinical signs & hemodynamic evidence of

severe obstruction
 or ANY SYMPTOMATIC Patient with NYHA Class III
or IV Symptoms
 or Asymptomatic moderate or severe MS with a
pliable valve
 MITRAL STENOSIS

Management:
 Surgical valvotomy or balloon catheter mitral

valvuloplasty
 Balloon valvuloplasty is indicated for symptomatic,

stenotic, pliable, noncalcified valves of patients

without atrial arrhythmias or thrombi
 AORTIC INSUFFICIENCY
Leakage of blood into LV during diastole due to
ineffective coaptation of the aortic cusps
Regurgitation of blood leads to volume overload

with dilatation & hypertrophy of the left

ventricle
 AORTIC INSUFFICIENCY

Pathophysiology:
 Combined pressure AND volume overload

 Compensatory Mechanisms: LV dilation & LV

hypertrophy

 Progressive dilation leads to heart failure

 AORTIC INSUFFICIENCY
Clinical manifestations:
 Symptoms are unusual except in severe aortic
insufficiency
 The large stroke volume & forceful left ventricular

contractions result in palpitations

 Sweating and heat intolerance are related to
excessive vasodilation
 Dyspnea on exertion can progress to orthopnea and

pulmonary edema
 Nocturnal attacks with sweating, tachycardia, chest
pain, & hypertension
 AORTIC INSUFFICIENCY

Clinical manifestations:
 Wide pulse pressure with bounding peripheral pulses

 Systolic blood pressure elevated & diastolic pressure

is lowered
 Severe aortic insufficiency: enlarged heart with a
left ventricular apical heave
 Diastolic thrill unusual

 Murmur begins immediately with the 2nd heart sound

& continues until late in diastole over the upper &
midleft sternal border with radiation to the apex and
upper right sternal border
 AORTIC INSUFFICIENCY

Clinical manifestations:
 It has a high-pitched blowing quality & is easily

audible in full expiration with the diaphragm of the

stethoscope placed firmly on the chest & the patient
leaning forward
 An aortic systolic ejection murmur is frequent

because of the increased stroke volume

 An apical presystolic murmur (Austin Flint

murmur) resembling MS is sometimes heard (due to

the large regurgitant aortic flow in diastole
preventing the mitral valve from opening fully)
Auscultatory and peripheral findings
in severe AR
 AORTIC INSUFFICIENCY

Imaging studies:
 ECG: signs of left ventricular hypertrophy & strain

with prominent P waves in severe cases

 X-rays: Enlargement of the left ventricle & aorta
 AORTIC INSUFFICIENCY

Imaging studies:
 2 D ECHO:

 A large left ventricle & diastolic mitral valve flutter

or oscillation caused by regurgitant flow hitting the

valve leaflets
 Doppler studies demonstrate the degree of aortic
runoff into the left ventricle
 Magnetic resonance angiography can be useful in

quantitating regurgitant volume

 Cardiac catheterization is necessary only when the

echocardiographic data are equivocal

 AORTIC INSUFFICIENCY

Management:
 Mild and moderate lesions are well tolerated. Unlike

mitral insufficiency, aortic insufficiency does not

regress
 Medical:

 Afterload reducers (ACE inhibitors or angiotensin

receptor blockers)
 Prophylaxis against recurrence of acute rheumatic

fever
 IE prophylaxis
 AORTIC INSUFFICIENCY

Management:
 Surgical: Definitive Treatment

 Surgical intervention (valve replacement) should be

carried out well in advance of the onset of heart

failure, pulmonary edema, or angina, when signs of
decreasing myocardial performance become evident
as manifested by increasing left ventricular
dimensions on the echocardiogram
 AORTIC INSUFFICIENCY

Management:
 Surgery is considered when early symptoms are

present, ST-T wave changes are seen on the

electrocardiogram, or evidence of decreasing left
ventricular ejection fraction is noted
 ANY Symptoms at rest

 Asymptomatic treatment if: EF drops below 50% or

LV becomes dilated
 TRICUSPID VALVE DISEASE

 Primary tricuspid involvement : rare

 Tricuspid insufficiency: secondary to right
ventricular dilatation resulting from unrepaired left-
sided lesions
 Signs: prominent pulsations of the jugular veins,
systolic pulsations of the liver & a blowing
holosystolic murmur at the lower left sternal border
that increases in intensity during inspiration
 Signs of tricuspid insufficiency decrease or
disappear when heart failure produced by the left-
sided lesions is successfully treated
 Tricuspid valvuloplasty may be required in rare cases
PULMONARY VALVE DISEASE

 Pulmonary insufficiency usually occurs on a functional

basis secondary to pulmonary hypertension & is a late
finding with severe mitral stenosis
 The murmur (Graham Steell murmur) is similar to
that of aortic insufficiency, but peripheral arterial
signs (bounding pulses) are absent
 The correct diagnosis is confirmed by two-
dimensional echocardiography and Doppler studies
 SUMMARY

 Rheumatic heart disease is the

only truly preventable chronic
heart condition
 Primary prevention:
Penicillin for suspected strep sore
throat
 Secondary prevention
Penicillin prophylaxis