RHEUMATIC HEART DISEASE

A LECTURE BY
DR Shogade Tolulope Taiwo
 OUTLINE
• PREAMBLE
• EPIDEMIOLOGY
• PATHOGENESIS
• PATHOPYSIOLOGY
• TYPES
• CLINICAL FEATURES
• DIAGNOSIS
• MANAGEMENT
• PROGNOSIS
• CONCLUSION
 PREAMBLE
• RHD remain significant cause of cardiovascular
diseases in the world today.
• It is a non-suppurative cardiovascular sequel
of group A streptococcal pharyngitis
• RHD an important sequel of acute rheumatic
fever remains one of the most common
acquire heart disease worldwide
• It is a major cause of CV morbidity and death
during first five decades of life in developing
countries
• It remain medical and public health problems
especially in industrializing countries.
• The most devastating effects are on children
and young adults in their most productive
years.
 EPIDEMIOLOGY
• Group A beta hemolytic streptococci are the most
common bacterial cause of pharyngitis, with a
peak incidence in children 5–15 years of age.
• The incidence of this infections can vary between
countries and within the same country.
• Depending upon season, age group,
socioeconomic conditions, environmental factors
and the quality of health care.
 What is Rheumatic Heart Disease
(RHD)?

• An acquired heart disease (AHD) of

poverty
• Common & highly preventable
• Cripples and kills young people in the
most productive years of life
• The major cause of:
– Acquired Heart Disease in children in
Low and Middle Income Country(LMIC).
– Heart disease in young adults worldwide
(most of these have RHD and live in
LMIC)
 Rheumatic Heart Disease
How many are affected?
 >33 million have RHD (2015 estimates)
 ~319,400 died of it in 2015
 ~350,000 new cases every year
 Half of all school children with RHD live in
SSA

Most clinicians in Nigeria are familiar with RHD and

its complications
• 0.3-3% of cases of group A beta-hemolytic
streptococcal pharyngitis in children later dev. Acute
rheumatic fever.
• At least 3 million had congestive heart failure(CHF)
that required repeated hospitalisation .
• A large proportion of which required cardiac valve
surgery within 5–10 years.
• The mortality rate for RHD varied from 0.5 per 100
000 population in Denmark, to 8.2 per 100 000
population in China.
• The estimated annual number of deaths from RHD for
2000 was 332000 worldwide.
• The mortality rate per 100 000 population varied
from 1.8 (Americas) to 7.6(South-East Asia) Region.
• Disability adjusted life years (DALYs) per 100000
population ranges from 27.4- 173.4.
• An estimated 6.6 million DALYs are lost per year
worldwide.
• Data from developing countries suggest that
mortality due to RF and RHD remains a problem in
children and young adults
• A local study (I Essien et al) showed that :
• Mitral valve disease 98.2%
• MR 64.8% mixed mitral valve 25.9% MS 9.3%
• MV+AV 33.3% MV+ TV 24.1% MV + PV 9.3%
• Isolated aortic valve disease 1.8%
• Jayesimi and Antia MV 95%
• Danbauchi et al MV 97% and isolated aortic valve 3%
• Saudi Arabia juvenile MS 43% (1981) has declined to
14% by 2000
 REMEDY HIGHLIGHTS
• 3343 patients enrolled (25 hospitals in 12 African
countries + India and Yemen)
• 66% Female
– 522 are women of reproductive age 15 – 49 years
• Contraception in only 3.4%; pregnancy can be lethal in these women
• Implications for integration into maternal, child and adolescent
health programmes
• Very few (18%) with indication for valve surgery could
have it
– Mainly in the upper-middle income countries
– Exhorbitant cost
– Still require life-long medication and follow-up
• There is a definite burden of RHD in Africa and
middle/low-income countries
www.rhdafrica.org REMEDY
 Rheumatic Heart Disease
Mortality in Africa

Estimated number of deaths due to

RHD

Region 1990 2005 2010

Sub-Saharan Africa, 8,323 7,684 7,786
West
Sub-Saharan Africa, 1,661 3,704 2,853
Southern
Sub-Saharan Africa, 11,71 11,783 11,812
East 1

Sub-Saharan Africa, 2,839 3,423 3,819

Central
North Africa / Middle 33,74 30,346 31,634
East 4
 RHD Mortality in Africa

• REMEDY: 16.9% case fatality over 2 years (500

deaths)
• ~11X greater than the 1.5% used until recently
to determine global estimates of RHD deaths.
• Determinants of the disease burden of rheumatic
fever and rheumatic heart disease
• Poverty
• Undernutrition,
• Overcrowding
• Poor housing.
• Shortage of resources for providing quality health care
• Inadequate expertise of health-care providers.
• low level of awareness of the disease in the
community
 PATHOGENESIS
• Delayed autoimmune response to Group A
streptococcal pharyngitis (URT).
• The severity of the clinical manifestation of
the response in an individual is determined
by:
• Host genetic susceptibility,
• Virulence of the infecting organism,
• Conducive environment .
• Major histocompatibiltiy antigens, potential tissue-specific
antigens, and antibodies developed during and immediately
after a streptococcal infection.
• T-cell lymphocytes play an important role in the pathogenesis of
rheumatic carditis.
• Particular M types of group A streptococci have rheumatogenic
potential.
• Heavily encapsulated, and form large, mucoid colonies that are
rich in M-protein.
• These characteristics enhance the ability of the bacteria to
adhere to tissue, as well as their ability to resist phagocytosis in
the human host:SELECTIVE RHEUMATOLOGY
 STREPTOCOCCAL M_PROTEIN
• The streptococcal M-protein extends from the
surface of the streptococcal cell as an alpha–
helical coiled dimer.
• It shares structural homology with cardiac
myosin, tropomyosin, keratin and laminin etc.
• It is also a target for a polyreactive antibody
that recognizes M-protein, myosin and
laminin.
Acute Rheumatic Fever (ARF) is the cause
of RHD Rheumatogenic Group A Streptococcus
(GAS)
Rheumatog Throat infection
enic GAS
Acute Rheumatic Fever

Recurrent ARF

Rheumatic heart disease

Cardiac Stroke, Dea

surgery endocarditis, th
• The M-protein molecule has a hypervariable N-
terminal region, a conserved C-terminal region.
• It is divided into A, B and C repeat regions on the
basis of peptide sequence periodicity
• M types such as 1, 3, 5, 6, 14, 18, 19 and 24 have
been associated with RF.
• Serotypes 2, 49, 57, 59, 60 and 61 have been
associated with pyoderma and acute
glomerulonephritis
 STREPTOCCOCAL SUPERANTIGEN
• Superantigens are a unique group of glycoproteins
synthesized by bacteria and viruses
• They can bridge Class II major histocompatibility complex
molecules to nonpolymorphic V b-chains of the T-cell
receptors, simulating antigen binding.
• The T-cells bearing the appropriate V b-chain are activated
to release cytokines or become cytotoxic, regardless of
their antigenic specificity.
• Streptococcal erythrogenic toxin streptolysin S and O may
behave like a superantigen for the B-cell, leading to the
production of autoreactive antibodies
• Others are:GRAB (an alpha-2 macroglobulin-
binding protein expressed by Streptococcus
pyogenes),
• streptococcal fibronectin-binding protein 1
(sfb1), which mediates streptococcal adherence
and invasion into human epithelial cells,
• streptococcal C5a peptidase (SCPA), which
inactivates complement chemotaxin C5a and
allows streptococci to adhere to tissues
• Activation of T-cell and B-cell lymphocytes by
streptococcal antigens and superantigens
• Lead to the production of cytokines and
antibodies directed against streptococcal
carbohydrate and myosin.
• Injury to the valvular endothelium by the anti-
carbohydrate antibodies leads to an up-
regulation of VCAM1
• VCAM1 interacts with VLA4 on activated lymphocytes
and leads to an influx of activated CD4+ and CD8+ T-
cells.
• A break in the endothelial continuity of a heart valve
would expose subendothelial structures (vimentin,
laminin and valvular interstitial cells) and lead to a “chain
reaction” of valvular destruction.
• Once valve leaflets are inflamed through the valvular
surface endothelium.
• New vascularization occurs which allows T-cells to
infiltrate and perpetuate the cycle of valvular damage.
 The role of the human host in the development of rheumatic fever
and rheumatic heart disease

• Only 0.3–3% of individuals with acute streptococcal

pharyngitis go on to develop RF .
• This immune response is genetically controlled.
• High responsiveness being expressed through a single
recessive gene
• Low responsiveness through a single dominant gene.
• Gene controlling the low-level response to streptococcal
antigen is closely linked to the Class II HLA.
• The link between susceptibility to RF and Class II HLA was
highly diverse and link to a susceptibility gene present at,
or nearby, the HLA-DR locus.
• Eg DR4 in Caucasian RF patients;
• DR2 in African-American .
• DR1 and DRw6 in South African.
• HLA-DR3 in India.
• DQW2 in Asian RF patients
 HOST PATHOGEN INTERACTION
• Infection by streptococci involves specific processes
of
• Adherence: The binding of bacterial surface ligands
to host surface receptors is crucial in the colonization
of the host
• Colonization is initiated by fibronectin and by
streptococcal fibronectin-binding proteins (17).
• Invasion
• The host responses include type-specific antibody
production, opsonization and phagocytosis
 RHEUMATIC HEART DISEASE
• Acute rheumatic heart disease often produces a pancarditis
characterized by
• endocarditis, myocarditis, and pericarditis
• PROPORTION OF AFFECTATION
• Mitral valve 65-70%
• Aortic valve 25%.
• Tricuspid valve 10%.
• Pulmonary valve is rarely affected.
• Endocarditis results in valvulitis which only leads to
permanent damage, its presence determine prophylatic
strategy.
• MYOCARDITIS :cardiomegaly with congestive
cardiac failure
• PERICARDITIS:present with pericardial
effusion rarely affects cardiac function or
results in constrictive pericarditis.
• Carditis is the single most important
prognostic factor in RF.
• It is important to differentiate between
• The recurrence of carditis as the cause of CHF, and
the decompensation of chronic progressive valvular
disease.
• Because the use of steroids may be lifesaving in
active carditis, but of no benefit in valvular disease.
• The recurrent carditis is likely to remain subclinical in
the absence of CHF.
• Its diagnosis becomes even more difficult when
previous cardiac findings are not known.
• 2002–2003 WHO criteria for the diagnosis of rheumatic fever and rheumatic heart
• disease (based on the revised Jones criteria3,4)
• Diagnostic categories Criteria
• Primary episode of RF. Two major or one major and two minor
• manifestations plus evidence of a
• preceding group A streptococcal infection.

• Recurrent attack of RF in a patient without Two major or one major and two minor
• established rheumatic heart disease. manifestations plus evidence of a
• preceding group A streptococcal infection
• .
• Recurrent attack of RF in a patient with T wo minor manifestations plus evidence of
• established rheumatic heart disease. a preceding group A streptococcal infection.

• Rheumatic chorea. Other major manifestations or evidence of

• Insidious onset rheumatic carditis. group A streptococcal infection not required.

• Chronic valve lesions of RHD (patients Do not require any other criteria to be
• presenting for the first time with pure diagnosed as having rheumatic heart disease
• mitral stenosis or mixed mitral valve disease.
• disease and/or aortic valve
•
• Major manifestations — carditis
• — polyarthritis
• — chorea
• — erythema marginatum
• — subcutaneous nodules

• Minor manifestations — clinical: fever, polyarthralgia

• — laboratory: elevated acute phase reactants (erythrocyte
• sedimentation rate)
• -ECG: prolong PR interval
•

• Supporting evidence of a preceding

• streptococcal infection within the last — elevated or rising antistreptolysin-O or
• 45 days other streptococcal antibody, or
• — a positive throat culture, or
• — rapid antigen test for group A streptococci, or
• — recent scarlet fever.
 CLINICAL FEATURES
• Pancarditis is the most serious and second most
common complication of rheumatic fever (50%).
• dyspnea,orthopnea, orthopnea
• mild-to-moderate chest discomfort,
• pleuritic chest pain, incr cardiac dullness,
• muffled heart sounds and pulsus paradoxical
• edema,
• cough.
• tachycardia out of proportion to fever.
• New or changing murmurs
• MR :apical pansystolic murmur is a high-pitched,
blowing-quality murmur that radiates to the left axilla.
• Apical soft early diastolic murmur (also known as a
Carey-Coombs murmur) accompany severe MR,
higher pitch than MS rumbling murmur
• AR :Basal early diastolic murmur, is high-pitched,
blowing, decrescendo.
• Heard best along the right upper sternal border after
deep expiration while patient is leaning forward
 DIAGNOSIS
• Radionuclide imaging
• Gallium-67 , radiolabelled leukocytes and radiolabelled
antimyosin antibody
• have all been used to image myocardial inflammation.
• Although radionuclide imaging has been used
successfully to identify rheumatic carditis.
• Studies have revealed that gallium-67 imaging has better
diagnostic characteristics than antimyosin scintigraphy
• Rheumatic carditis is predominantly infiltrative, rather
than degenerative, in nature.
 ECHOCARDIOGRAPHY
• M-mode echocardiography provides parameters for
assessing valve leaflet for:
• Thickening, focal nodules, reduced motility, commisural
fusion, calcification, anterior movement of posterior mitral
valve
• 2D echocardiography provides a realistic real-time image
of anatomical structure for:
• Calcification, diastolic doming, restricted movement of
anterior mitral valve leaflet, ventricular function, LA
thrombus
• .
• Pulse wave, continous wave and colour flow
Doppler echocardiography are most sensitive
for detecting abnormal blood flow and
valvular regurgitation.
• Diagnosis of recurrent rheumatic carditis
• In patients with preexisting RHD, recurrence of
RF is almost invariably manifested as:
• Pericarditis
• New valvular regurgitation
• Aggravation of the existing valve lesions;
• Increased cardiac enlargement; and
congestive heart failure.
 CHRONIC RHEUMATIC HEART DISEASE
• Chronic manifestations due to residual and
progressive valve deformity occur in 9-39% of
adults with previous RHD.
• Valve stenosis and/or insufficiency develops 2-
10 years after acute rheumatic fever, and
recurrent episodes may aggravate progression.
• Fusion occurs at the level of the valve
commissures, cusps, chordal attachments, or
any combination of these.
• MITRAL STENOSIS
• In North America, MS is most commonly an indolent and slowly
progressive disease, with a latency period as long as 20–40 years
• In developing countries, progresses much more rapidly, may lead to
symptoms in the late teens and early twenties
• Mitral stenosis occurs in 25% of patients with chronic RHD
• In association with mitral insufficiency in another 40%.
• It result from progressive fibrosis, ie, thickening and calcification of
the valve.
• Which leads to enlargement of the left atrium and LA mural thrombi.
• The stenotic valve is funnel-shaped,with a fish mouth resemblance
• Rheumatic valvular lesion
• Mitral valve alone 50%
• Mitral and aortic valve 40%
• Mitral, aortic and tricuspid 5%
• Aortic valve alone 2%
• Other combination 3%
• Grading of MS
• Normal 4-6cm
• Mild 2-4cm
• Moderate 1-2cm
• Severe <1cm
• Symptoms: dyspnea,hemoptysis and fatigue
in MS is attributable to either :
• A critical increase in transmitral flow,
• A decrease in the diastolic filling period
• Result in an increase in left atrial and
pulmonary venous pressures
• Rise in pulmonary vascular resistance and fall
in cardiac output .
• In AF there is:
• sudden increase in LAP
• rapid ventricular rate
• critical decrease diastolic time
• increase potential for thromboembolism

• The late stages of uncorrected MS may be complicated by:

• Development of pulmonary hypertension,
• Failure of the right side of the heart, with edema and ascites
• TR secondary to RV dilatation
• S1 is initially accentuated but becomes reduced as the
leaflets thicken.
• P2 becomes accentuated, and the splitting of S2
decreases as PUL HTN develop.
• An opening snap of the mitral valve often is heard at
the apex, where a diastolic filling murmur also is heard
• Mid diastolic murmur with presystolic attenuation at
apex.
• Graham steell murmur of PR secondary to pul.
Hypertension.
• CXRAY: normal size heart with enlarged left
atrium
• Signs of pulmonary hypertension
• ECG: LAE bifid p wave
• RVH Rt axis deviation Rwave in V1
• TREATMENT : LIFE STYLE, MEDICAL/SURGICAL
• LIFE STYLE: salt restriction
• Avoid strenous physical activities
• Nutritional effort
• Graduated compression stocking
• MEDICAL: Diuretics
• Digoxin
• Beta blocker
• Non dihydropyridine calcium blocker
• Anticoagulation
• Antiarrhytmic: Class 1A, 1C and 3
• SURGICAL
• Valvotomy: trans-septal
• open
• close
• Valve replacement
• Non-pharmacological treatment of AF:
• Catheter delivered radio-frequency ablation
• Dual-site atrial pacing
• Atrial cardioverters/defibrillators
• Surgical (Cox) maze procedure
 PROGNOSIS
• Survival is >80% at 10 years for untreated
patients who are asymptomatic or minimally
symptomatic at time of diagnosis
• 60% of such patients may not experience any
progression of symptoms over this time
frame .
• But 0-15% do Once limiting symptoms
develop25%
• The mortality of untreated patients with MS is attributable to:
• progressive heart failure in 60-70%
• systemic embolism in 20–30%
• pulmonary embolism in 10%
• infection in 1–5% (7, 8).
• Precipitants are: exercise,
• emotional upset,
• fever,
• pregnancy,
• atrial fibrillation, especially with a rapid ventricular response
 MITRAL REGURGITATION
clinical features may not occur until relatively
late in the natural history.
• the favourable loading conditions may obscure
the recognition of left ventricular contractile
dysfunction until relatively late in the natural
history
• The onset of symptoms may correlate with the
development of AF.
• Forceful displaced diffuse apical systolic thrill
• Soft S1 S3
• Pansystolic murmur that radiates to the axilla
• A short mid diastolic murmur may follow S3
• MR patients are less susceptible to
thromboembolism with AF, but are more
prone to infective endocarditis
• CXR: LAE and LVE
• ECG: bifid p wave and LVH
• ECHO:
• CARDIAC CATHERIZATION
• Surgery may be indicated when there is systolic dysfunction
• The outcome of mitral valve surgery are influenced by:
• age,
• severity of symptoms,
• coexistent coronary artery disease,
• Preoperative left ventricular function,
• type of surgery (repair vs. replacement),
• presence of AF .
• Drugs: B-Blocker, Diuretics, Digoxin, Spironolactone,Warfarin
ACEIs
• Prophylaxis against endocarditis
 MIXED MITRAL VALVE DISEASE
• One lesion may predominate, or the
components may be more closely balanced,
creating a hybrid natural history.
• Treatment must respect the inherent risks of
AF and thromboembolism with MS
• Chronic left ventricular volume overload of
MR. The combined use of diuretics and
vasodilators in
 AORTIC STENOSIS
• Aortic stenosis typically is associated with aortic
insufficiency.
• The valve commissures and cusps become adherent and
fused.
• The valve orifice becomes small with a round or triangular
shape.
• It leads to incr Left ventricular pressure and Left ventricular
hypertrophy.
• Relative ischaemia of myocardium
• Fall in BP
• Obstruction more severe in exercise
• Low vol. slow rising pulse
• Sustained apical beat with systolic thrill at
aortic area
• Ejection systolic murmur (diamond) radiate to
carotid
• Systolic ejection click
• Soft S2, single S2 reversed splitting of S2
• Prominent S4
• CXR relatively small heart with dilated
ascending aorta
• ECG: LVH LV strain pattern
• ECHO
• CARDIAC CATHETERIZATION
 Symptomatic patient that are not candidates for
surgery:
diuretics and ACEIs with caution;
• digoxin if systolic dysfunction;
• beta-blockers and other negative
inotropic effects should be avoided;
• CX angina,syncope, heart failure
• AF is an uncommon complication of isolated
aortic stenosis,
• RISK FACTOR for progression:
• smoking,
• hyperlipidaemia,
• elevated creatinine,
• Hypocalcaemia,
• GRADING OF AORTIC STENOSIS
• Mild:>1.5cm- <2cm
• Moderate: 1-1.5cm
• Severe:<1cm
• Survival without valve replacement after the
onset of angina, syncope, or heart failure is
generally measured at five, three, and two
years respectively
 AORTIC REGURGITATION
• Chronic, severe AR usually result in:
• Increase in left ventricular end-diastolic volume,
• Increase in chamber compliance,
• Eccentric and concentric hypertrophy.
• Preload reserve is maintained
• Ejection performance is normal,
• Enormous increase in stroke volume allows preservation
of forward output.
• Left ventricular afterload progressively increases.
• Volume and pressure overload.
• The rate of progression to systolic dysfunction
has been estimated at less than 6% per year.
• Thus, these patients can be safely and
expectantly followed.
• Asymptomatic patients with left ventricular
dysfunction, however, develop symptoms at a
rate of >25% per year
• Symptomatic patients with severe AR have an
expected mortality that exceeds 10% per year .
CLINICAL FEATURES
• Large vol. collapsing pulse ,wide pulse presure
• Displaced diffuse forceful apex beat
• High pitch early diastolic murmur at LSE
• Ejection systolic murmur at base into neck
• Autin flint mid diastolic murmur at apex beat
• CXR LVE dilated ascending aorta
• ECG volume overload tall R wave deeply inverted
T wave in v5-6 and deep S wave in v1-2
• ECHO
• TREATMENT
• Surgery: Aortic valve replacement
• Tissue or mechanical
• Antibiotic prophylaxis
• Clinical and noninvasive variables associated with
poor outcomes include:
• Age,
• Coexistence of coronary artery disease,
• Severity of symptoms,
• Resting ejection fraction,
• End-systolic dimension,
• End-diastolic dimension,
• AF.
MIXED AORTIC STENOSIS/REGURGITATION
• Management of patients with mixed aortic valve disease
depends, in part, on the dominant lesion.
• Symptoms may develop and indications for surgery may
be met before the traditional anatomic (valve area) and
haemodynamic (ejection fraction) thresholds are reached.
• The nondominant lesion may exacerbate the
pathophysiology imposed by the dominant lesion.
• Diuretic, digoxin and/or vasodilator therapies may be
favourable
• Beta-blockers should be avoided.
 MULTIVALVULAR HEART DISEASE
• In many patients with chronic RHD both the mitral and
aortic valves may be involved, often with mixed lesions in
one or both locations.
• In general, management should be predicated on the
identification of the dominant valve lesion and location,
• Proximal valve lesion(s) may mask the presence and
significance of the more distal valve lesion(s).
• Common combinations are:
• Aortic regurgitation with mitral stenosis, .
• Mitral stenosis with tricuspid regurgitation ,
• Aortic stenosis with mitral regurgitation.
 PREGNANCY IN RHD PATIENT
• The haemodynamic changes that occur during
pregnancy present a challenge to the cardiovascular
system in women with RHD
• It may threaten the well-being and survival of the
patient and fetus.
• The changes can worsen prior haemodynamic
alterations and this situation poses a special
therapeutic problem.
• The relevant haemodynamic changes are an
increasing heart rate.
• During labour, delivery and the postpartum,
these haemodynamic alterations suffer
sudden and severe changes that can cause
life-threatening complication in these patients.
• Sometimes, subclinical RHD becomes
apparent for the first time during pregnancy.
• ACEIs should not be use in pregnancy.
 DIAGNOSIS
• Laboratory
• Throat culture
• Rapid antigen detection test
• Anti streptococcal antibody
• Acute phase reactant
• Heart reactive antibody: tropomyosin
• Rapid detection test for D8/17
 Chest xray
• Echo:MR are annular dilatation,
• Elongation of the chordae to the anterior leaflet,
• Posterolaterally directed MR jet.
• Stenosis : diffusely thickened valve leaflets,
• fusion of the commissures and chordae
tendineae.
• Increased echodensity.
• :
• Heart catheterisation: evaluate chronic RHD
for balloon stenotic mitral valve
• ECG: sinus tachycardia/bradycardia
• Heart block
• ST segment elevation
• atrial flutter, multifocal atrial tachycardia, or
atrial fibrillation .
• ECG: sinus tachycardia/bradycardia
• Heart block
• ST segment elevation
• Atrial flutter,
• Multifocal atrial tachycardia, or
• Atrial fibrillation .

• HISTOLOGY: verrucous lesions at the line of closure.

• Aschoff bodies are found in the pericardium, myocardium, and endocardium.
• nodules of scar tissue.
• Anitschkow cells are plump macrophages within Aschoff bodies
• fibrinous and serofibrinous exudates (bread and butter pericarditis)

• :
 MEDICAL THERAPY
• Primary prophylaxis:
• Penicillin V is the drug of choice.
• Tetracyclines and sulfonamides should not be.
• For recurrent case a second 10-day course of the same antibiotic
can be repeated.
• Alternate drugs include: narrow-spectrum cephalosporins,
amoxicillin-clavulanate,
• dicloxacillin,
• erythromycin, or other macrolides for 10 d.
• Secondary prophylaxis:
• IM 0.6-1.2 million units of benzathine penicillin G 3-4wkly
• Prophylaxis before surgical intervention to prevent IE
• Antiinflammatory drugs: aspirin(6-8wks)
• Prednisolone(2-6wks)
• Digoxin,
• Diuretics,
• ACEIs
• Supplemental oxygen,
• Bed rest, An injection of 0.6-1.2 million units of
benzathine
• Sodium and fluid restriction.
• Indication for treatment in carrier
• Outbreaks of rheumatic fever or poststreptococcal
glomerulonephritis
• Family history of rheumatic fever
• Outbreaks of group A streptococcal pharyngitis in a closed
community
• When considering tonsillectomy for chronic group A
streptococcal carriage
• Multiple episodes of documented group A streptococcal
pharyngitis within a family despite appropriate therapy
• Following group A streptococcal toxic shock syndrome or
necrotizing fasciitis in a household contact
• Mitral valve repair for MR;
• posterior collar annuloplasty,
• commissurotomy,
• cusp level chordal shortening,
• cusp thinning,
• cleft suture,
• cusp excision or plication
• For MS:
• mitral valvulotomy,
• percutaneous balloon valvuloplasty,
• mitral valve replacement
 COMPLICATION
heart failure,
atrial arrhythmias,
pulmonary edema,
recurrent pulmonary emboli,
infective endocarditis,
intracardiac thrombus ,
systemic emboli
Rheumatic Heart Disease
Prevention and control
Not controlling RHD – some cost
comparisons
Total population of Nigeria 180,000,000

Estimated population 0.05% (conservative)

prevalence of advanced RHD

Total advanced RHD 90,000

population in need of surgery

Surgical cost per patient N5 Million (~13,500 USD)

Follow-up cost per patient per 500 USD (~N185,000)

year
Cost of preventing advanced 4 USD x 12 = $48 (<50 USD /
RHD per patient per year <N20,000) per year

Cost of primary prevention <5USD (<N2,000)

per sore throat episode
 PROGNOSIS
• Mortality rate decreased to almost 0% by the 1960s in the
United States;
• It has remained 1-10% in developing countries.
• Before penicillin, 60-70% of patients developed valve disease as
compared to 9-39% of patients since penicillin was developed
• Incidence of residual RHD at 10 years is 34% in patients without
recurrences but 60% in patients with recurrent rheumatic fever.
• Disappearance of the murmur happens within 5 years in 50% of
patients.
• Significant numbers of patients experience resolution of valve
abnormalities even 5-10 years
 CONCLUSION
• Without doubt, appropriate public health
control programs and optimal medical care
reduce the burden of disease .
• The economic effects of the disability and
premature death caused by these diseases are
felt at both the individual and national levels
• Through higher direct and indirect health-care
costs these can de reduced
• THANK YOU FOR LISTENING