RHEUMATIC

FEVER &
RHEUMATIC
HEART DISEASE
5TH YEAR LECTURE

Dr. Luke
 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”)

Tonsillopharynge
Sore throat: fever, al erythema &
white draining exudates
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
certain M
proteins (M1, M5,
M6, and M19)
share epitopes
with human
tropomyosin &
myosin
strong correlation between
Common antigenic determinants
are shared between components
progression to RHD & HLA-DR class
of GAS (M protein, protoplast II alleles & the inflammatory protein-
membrane, cell wall group A encoding genes MBL2 and TNFA
carbohydrate, capsular
hyaluronate) & specific Pathogenetic pathway for ARF & RHD
mammalian tissues (e.g., heart,
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 (ASOT)
Migratory
Polyarthritis
Erythema
Laboratory features:
marginatum
Elevated acute phase History of (<45 days)
Subcutaneous reactants: ESR, C- -Positive throat culture or
nodules reactive protein rapid streptococcal antigen
Sydenham’s Prolonged PR interval on test or streptococcal sore
Chorea ECG throat or scarlet fever)
 First
episode or
ARF & RHD Recurrence
without
established
heart
disease: 2
major
criteria or 1
major & 2
minor
criteria &
the
absolute
requiremen
t
Recurrence
with
established
heart
disease: 2
minor
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:
 [Link] 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 ([Link])
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
 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 At least for 5 yr or until
carditis age 21 year, whichever is
longer
Rheumatic fever with carditis At least for 10 yr or well
but without residual heart into adulthood, whichever
disease (no valvular disease) is longer
Rheumatic fever with carditis & At least 10 yr since last
residual heart disease episode & at least until
(persistent valvular disease) age 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 Intramuscular
kg, every 3 wk
OR
Penicillin V 250 mg, twice a day Oral
OR
For people who are allergic to penicillin and sulfonamide drugs
Macrolide 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(P2) 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
 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 cm2

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