Cardiology lectures

•Valvular heart disease •Reading

•Heart failure – acute rheumatic
•Hypertension fever
– Arrhythmias(particula
•Ischemic heart disease rly atrial fibrillation)
•Cardiomyopathy – Congenital heart
•Endocardits diseases in adults
•Pericardial disease – Pulmonary
hypertension
– Cardiac tumor
– Cardiac manifestation
of systemic illness

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Valvular Heart Disease

Getnet Amberber- MD

2
 Overview of Valves
•Normal heart valves are thin and very pliable
•They open widely and allow blood to flow across them
with very low resistance (normally only 1-2 mmHg
pressure gradient required)
•Stenotic valves do not open normally and higher
pressure is required to open them
– Over time, the “upstream” pressure overloaded
chambers enlarge
– The process is generally progressive and severe
stenosis may eventually cause congestive heart failure

3
Major Factors That Affect Flow Across Any
Valvular Lesion
•The valve area

•The square root of the hydrostatic pressure gradient

across the valve

•The time duration of transvalvular flow (applies to

both systole and diastole)

4
 Adult Valvular Heart Disease

•Mitral Stenosis
•Mitral Regurgitation
•Aortic Stenosis
•Aortic Regurgitation

5
 Mitral Stenosis
•Causes:
– Rheumatic
• almost all cases in adults
– 50% of pts who have ARC don’t
remember it.
– Mitral Annular Calcification- massive
(rare)
– Congenital – rare
– SLE, RA
– infective endocarditis with large
vegetations
– cor triatriatum
– left atrial myxoma
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•Predominant MS occurs in ~ 40% of all patients with RHD
(90% of pts with RHD have mitral valve involvement)
•2/3 of MS- women

•pathology
– Commissural fusion, leading to bowing or doming in
diastole
– Thickening of leaflet tips, remainder of leaflet with
variable thickening
– Subvalvular aparatus typically affected: fusion,
shortening, fibrosis, calcification of chordae
– These all changes lead to narrowing at the apex of
the funnel-shaped valve -------"fish-mouth“ valve

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8
 Pathophysiology
Cardiac hemodynamic
•Primary hemodynamic consequence of MS is a pressure
gradient between the LA and LV in diastole

•The elevated LA pressure is reflected backward, causing an

increase in pulmonary venous, capillary, and arterial
pressures and resistance leading to poor pulmonary
complaince and exertional dyspnoea

•In patients with moderate MS, the CO is normal or almost so

at rest but rises subnormally during exertion

•In patients with severe MS, the CO is subnormal at rest and

may fail to rise or may even decline during activity
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Pathophysiology of Mitral Stenosis
Obstruction to LA emptying

Decreased LV filling Increased Increased

LA pressure LA size

Pulmonary Increased pulmonary Atrial fibrillation

edema venous pressure

Increased pulmonary
artery pressure

RV overload

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•Pulmonary hypertension results from:

1) passive backward transmission of the elevated LA

pressure;

2) pulmonary arteriolar constriction, which presumably

is triggered by LA and pulmonary venous hypertension
(reactive pulmonary hypertension)

3) interstitial edema in the walls of the small pulmonary

vessels;

4) organic obliterative changes in the pulmonary vascular

bed.
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 Pathophysiology: LV and RV function
•LV function is usually normal
– Decreased LVEF in about 1/3 of MS patients:
• Rheumatic carditis
• Chronic volume overloading
• Concomitant CAD
• Septal hypertrophy in patients with PHT

•RV function is normal in absence of pulmonary hypertension.

•Severe pulmonary hypertension will result in RV failure and

secondary abnormalities of LV function

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 Symptoms
•Afib
•Fatigue •Systemic embolism
•Palpitations •Pulmonary infection
•Cough •Right sided failure
•SOB – Hepatic Congestion
•Left sided failure – Edema
– Orthopnea •Worsened by conditions that
– PND  cardiac output.
•Hemoptysis- – Exertion,fever,
anemia, tachycardia, Afib,
intercourse, pregnancy,
thyrotoxicosis

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 Physical examination/Signs

Mitral faces :-malar flush Auscultation:

with pinched and blue •Loud S1- as loud as S2 in
facies aortic area
Palpation: •opening snap(OS)
•Small volume pulse •A2 to OS interval inversely
•Tapping apex-palpable S1 proportional to severity
•RV lift •Diastolic rumble: length
•Palpable S2 proportional to severity
•In severe MS with low
flow- S1, OS & rumble may
be inaudible

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Mitral Stenosis: Physical Exam

S1 S2 OS S1

•First heart sound (S1) is accentuated and snapping

•Opening snap (OS) after aortic valve closure
•Low pitch diastolic rumble at the apex
•Pre-systolic accentuation (esp. if in sinus rhythm)

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 DDX diastolic murmur at apex
•MS
•significant MR
•severe AR (Austin Flint murmur).
• TS
•Atrial septal defect
•Left atrial myxoma

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 Mitral Stenosis: Natural History
•Time to clinical presentation varies
– from a few years in countries with a high
prevalence of rheumatic fever to 20 years in countries
where rheumatic fever is rare
– 20-40 year latency from rheumatic fever to
symptom onset.
– Additional 10 years before disabling symptoms
•Progressive, lifelong disease,
•Usually slow & stable in the early years.
•Progressive acceleration in the later years

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 Mitral Stenosis: Complications
•Atrial dysrrhythmias
•Systemic embolization (10-25%)
– Risk of embolization is related to, age, presence of
atrial fibrillation, previous embolic events
•Congestive heart failure
•Pulmonary infarcts (result of severe CHF)
•Hemoptysis
– Massive: 20 to ruptured bronchial veins (pulm
HTN)
– Streaking/pink froth: pulmonary edema, or
infection
•Endocarditis
•Pulmonary infections
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 Investigations
•Chest x-ray-
– straightening of the upper left border of the cardiac
silhouette,
– prominence of the main pulmonary arteries,
– pulmonary congestion
– Barium swallow

•EKG
– LAE
– RVH
– Premature contractions
– Atrial flutter and/or fibrillation
•  freq. in pts with mod-severe MS for several years
• 80% of pts with MS &~ are in AF
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•Role of Echocardiography
– Diagnosis of Mitral Stenosis
– Assessment of hemodynamic severity
• mean gradient, MVA, pulmonary artery
pressure
– Assessment of right ventricular size and function.
– Assessment of valve morphology to determine
suitability for percutaneous mitral balloon
valvuloplasty
– Dx and assessment of concomitant valvular lesions
– Reevaluation of patients with known MS with
changing symptoms or signs.
– F/U of asymptomatic patients with mod-severe MS

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 Mitral Stenosis:Therapy
•Medical
– Penicillin prophylaxis for rheumatic MS
– Diuretics for HF
– Digitalis/Beta blockers/CCB: Rate control in A Fib
– Anticoagulation: In A Fib
– Endocarditis prophylaxis
•Balloon valvuloplasty for patients with MV score of < 8
– Effective long term improvement
•Surgical
– Mitral commissurotomy
– Mitral Valve Replacement
• Mechanical
• Bioprosthetic

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 Mitral regurgitation
•MR may result from an abnormality or disease
process that affects any one or more of the five
functional components of the MV apparatus
(leaflets, annulus, chordae tendineae, papillary
muscles, and subjacent myocardium)

•Can be acute or chronic

•Can be primary or secondary/functional

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 Mitral Regurgitation:
Etiology
•Valvular-leaflets •Annulus
– Myxomatous MV – Calcification, IE
Disease (abcess)
– Rheumatic – LV dilatation &
– Endocarditis functional regurgitation
– Congenital-clefts •Papillary Muscles
•Chordae – CAD (Ischemia,
– Fused/inflammatory Infarction, Rupture)
– Torn/trauma – HCM
– Degenerative – Infiltrative disorders
– IE •Trauma

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Etiology

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 Pathophysiology

•In acute severe MR

• the regurgitant volume is delivered into a normal-
sized LA having normal or reduced compliance=> LA
pressures rise markedly for any increase in LA volume.
=> elevated pulmonary venous pressures =>
pulmonary edema
• LV systolic function may be normal, hyperdynamic,
or reduced.

•In chronic MR
– LV “unloads” itself into left atrium
• Chronic left atrial overload

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 conti…
•Chronic overload on left ventricle  heart failue
•Volume of regurgitant flow determined by:
– Ventriculo-atrial gradient
– Diastolic time
– Size of the regurgitant orifice
•LVE – » annulus dilation – » increased MR
•Backflow – » LAE, Afib, Pulmonary HTN

•Since EF rises in severe MR in the presence of normal LV

function, even a modest reduction in this parameter
(<60%) reflects significant dysfunction.

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Pathophysiology of Mitral Regurgitation
Backward flow of blood from LV to LA (Systolic)

Left atrial enlargement

Increased
LA volume and
pressure
Increased
pulmonary
Increased LV filling venous pressures
(Increased LVEDV)

Pulmonary
edema
Increased SV

Blood ejected into aorta

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 Natural History
•Chronic MR (variable course)

•Chronic MR may be protected from pulmonary

congestion by dilated, highly compliant left atrium

•Acute MR usually with fulminant pulmonary edema

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 MR Symptoms
•Similar to MS
•Dyspnea, Orthopnea, PND
•Fatigue
•Pulmonary HTN, right sided failure
•Hemoptysis
•Systemic embolization in A Fib

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 Recognizing Chronic
Mitral Regurgitation
•Pulse: •Murmer-Fixed MR:
– brisk, low volume – pansystolic
•Apex: – loudest apex to axilla
– hyperdynamic •Murmer-Dynamic MR(MVP)
– laterally displaced – mid systolic
– palpable S3 +/- thrill – +/- click
– late parasternal lift 2 –  upright
to LA filling •S 3 / flow rumble if severe
•S 1 soft or normal
•S 2 wide split (early A2)
unless LBBB

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 Assessing Severity of Chronic
Mitral Regurgitation
Measure the Impact on the LV:
•Apical displacement and size
•Palpable S3
•Longer/louder MR murmer (chronic MR)
•S3 intensity/ length of diastolic flow rumble
•Wider split S2 (earlier A2) unless HPT
narrows the split

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 Recognizing Mitral
Regurgitation
•ECG:
– LA enlargement •CXR:
– Afib –  LV
– LVH (50% pts. –  LA
With severe MR) –  pulmonary
– RVH vascularity
– Combined
hypertrophy

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 MR Echocardiography

•Baseline evaluation to identify etiology, quantify

severity of MR
•Assess and quantify LV function and dimensions
•Annual or semi-annual surveillance of LV function,
estimated EF and LVESD in asymptomatic severe MR
•To establish cardiac status after change in
symptoms
•Baseline study post MVR or repair

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 Treatment

•Depends on cause, type, severity

•Medical
– Vasodilators
• for acute MR - to reduce the regurgitant fraction and
increase forward flow,
• for chronic ,isolated severe MR use if there is
systemic HTN
– Diuretics for treatment of congestion( HF)
– Anticoagulation for atrial fib
– Penicillin – for rheumatic fever recurrence prophylaxiss
– ??SBE Prophylaxis – prevent endocarditis
– avoid isometric forms of exercise in severe MR

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 Treatment
• Surgical (repair or replacement of the valve )
– Acute severe MR- repair of valve
– Indications for MV surgical treatment of chronic MR depends on
symptom, LVEDV, and EF
 Surgery is indicated in severe MR
 Symptomatic
 Asymptomatic severe MR
 Progressive LV dysfunction(LVEF < 60% and/or
ESLV > 40 mm)
 recent-onset AF and pulmonary hypertension(PA
pressure 50 mmHg at rest or 60 mmHg with exercise.)

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Aortic Stenosis

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 Aortic Stenosis
•Etiology
– Bicuspid Valve
• Usually asymptomatic until > 30 yrs
• Associated aortic coarctation (40%)
• becomes stenotic later in life
– Unicuspid Valve
• Generally repaired in early childhood
– Subvalvular (membrane or ridge)
 Degenerative (“senile”)
 calcification of leaflets and commisures(=30% of
persons >65 years exhibit aortic valve sclerosis, 2% exhibit
frank stenosis)
 Chronic inflammatory process?
 Rheumatic AS: is almost always associated with involvement
of the mitral valve and with AR
 Fibrosis and calcification of commisures
 Degeneration of prosthetic valves (especially bioprosthetic)

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 AS
•Left ventricular out flow obstruction can be caused by
– Valvular aortic stenosis- most common cause-
• Approximately 80% of adult patients with
symptomatic valvular AS are male
– Supravalvular aortic stenosis- majority of patients (60
to 75 percent) have an hourglass deformity, consisting of
a discrete constriction of a thickened ascending aorta at
the superior aspect of the sinuses of Valsalva
– Subvalvular aortic stenosis- include a thin membrane
(the most common lesion), thick fibromuscular ridge,
diffuse tunnel-like obstruction, abnormal MV
attachments, and occasionally, accessory endocardial
cushion tissue
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 Pathophysiology
•normal aortic valves area is 3.0-4.0 cm2.
•Obstruction to LV outflow produces a systolic pressure
gradient between the LV and aorta
•Significant gradient usually doesn’t occur until valve area
has ’d from ~ 3.0 cm2 to < 2.0 cm2
•Symptoms “usually” not seen until the valve area is < 1
cm2
•Progression ~ 0.1 cm2/year
•This leads to concentric hypertrophy of the LV
maintaining normal CO for many years; however, excessive
hypertrophy becomes maladaptive, and LV function
declines
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Pathophysiology of Aortic Stenosis
Aortic Stenosis

Obstruction to LV Ejection

Pressure Gradient Created Across the Valve

Chronic LV Pressure Overload

LV Hypertrophy
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 Aortic Stenosis: Symptoms
•May be a long asymptomatic period
•Symptomatic
– Usually have severe AS with AVA of 1 cm2 or less
•Cardinal Symptoms
– Chest pain (angina)
• Reduced coronary flow reserve
• Increased demand-high afterload
– Syncope/Dizziness (exertional pre-syncope)
• Fixed cardiac output
• Vasodepressor response
– Dyspnea on exertion & rest
– Impaired exercise tolerance
•Other signs of LV failure
– Diastolic & systolic dysfunction

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 Aortic Stenosis: Physical Findings
•Pulse, and BP are normal until late in the course of the
disease
– Pulsus Parvus et Tardus (The peripheral arterial pulse
rises slowly to a delayed sustained peak)
– Narrow pulse pressure
•LV impulse is usually displaced laterally. A double apical
impulse(Sustained Bifid LV impulse)
•carotid systolic thrill
•Paradoxical spliting of the second heart sound
•S3 (with left ventricular failure)
•S4 (with left ventricular hypertrophy)

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 Aortic Stenosis: Physical Findings
“Diamond” shaped, harsh, systolic crescendo-decrescendo, loudest
at the base of the heart), may radiate to the carotids
May sometimes be transmitted to the apex, be confused
with murmur of MR (Gallavardin effect)

Intensity DOES NOT predict severity

Presence of thrill DOES NOT predict severity

S1 S2 S1 S2
Mild-Moderate Severe
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 •Angina -5 yr survival
•Syncope -3 yr survival
•Congestive Heart Failure -1-2 yr survival

prognosis

Age
Based on data obtained at postmortem examination in patients before surgical treatment
Ross J Jr, Braunwald E: Aortic stenosis. Circulation 38[Suppl V]:61, 1968 44
 Investigations

•ECG- LV hypertrophy, ST- •Echocardiogram

T changes (LV strain
pattern)
•Chest x-ray-
– LV hypertrophy causes
only rounding of the apex,
– advanced disease may
show LV dilatation,
pulmonary congestion, LA,
PA and RV enlargement
– Etiology
– Valve gradient and
area
– LVH
– Systolic LV function
– Diastolic LV function
– LA size
– Concomitant regional
wall motion abnormalities
– Coarctation
associated with bicuspid
AV

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 Treatment
•Medical
– Avoid strenuous exercise in severe AS
– Avoid dehydration and hypovolemia
– Penicillin prophylaxis for rheumatic AS
– Diuretics for LHF/RHF
– Digitalis/Beta blockers/CCB: Rate control in A Fib
– Anticoagulation: In A Fib
– ???Endocarditis prophylaxis
– Vasodilator - may be unwise(SO AVOID) in pts with
severe AS
 Since there is a risk that this will
reduce aortic pressure and coronary perfusion
without an equivalent reduction in the left
ventricular afterload
•Surgical- valve replacement based on indications
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 Aortic regurgitation
•Caused by primary valve disease or by primary aortic root disease.

47
Pathophysiology of Aortic Regurgitation
Backward flow of blood from aorta into LV (Diastolic)

Rapid fall of aortic Increased

pressure during diastole LV volume
and pressure
Increased
LA pressure
Increased SV
(Frank-Starling Mechanism)
Increased
pulmonary
Peak systolic pressure venous pressure
increased because of
increased SV ejected into aorta
Pulmonary
edema

Increased diastolic
Increased pulse pressure wall-tension produces
eccentric hypertrophy
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• Pathphysiology
– Increased total stroke volume
– Increased LVEDV
– Increased LV pre and after load
– Finally adaptive measures fail
» LV function declines
» SV and EF decline

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•Acute AR: nl LV poorly tolerates sudden increase
LVEDV  massive increase LVEDP leading to pulm
edema, hypotension +/- cardiogenic shock

•Chronic AR: LV overload  LV dilatation, eccentric

hypertrophy, insidious prog to CHF (decades, typically)

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•In advanced stages there may be considerable
elevation of the LA, PA wedge, PA, and RV pressures
and lowering of the forward CO at rest

•Myocardial ischemia may occur in patients with AR

because myocardial oxygen requirements are
elevated by LV dilatation, hypertrophy, and elevated
LV systolic tension

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Eccentric Hypertrophy

52
 Symptoms
•Approximately ¾ of patients with predominant valvular AR
are men;
– women predominate among patients with primary
valvular AR who have associated rheumatic mitral valve
disease.
•Patients may remain asymptomatic for decades
•Patients may complain of pounding and uncomfortable sense
of heart beat, palpitation
•Dyspnea, orthopnea, PND
•Chest pain.
– Nocturnal angina >> exertional angina
– ( diastolic aortic pressure and increased LVEDP thus 
coronary artery diastolic flow)

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 Peripheral Signs of Severe
Aortic Regurgitation

•Quincke’s sign: capillary pulsation

•Corrigan’s sign: water hammer pulse
•De Musset’s sign: systolic head bobbing
•Mueller’s sign: systolic pulsation of uvula
•Durosier’s sign: femoral retrograde bruits
•Traube’s sign: pistol shot femorals
•Widened pulse pressure
– Systolic – diastolic = pulse pressure

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•Becker's sign — Visible pulsations of the retinal arteries
and pupils.
•Mayne's sign — More than a 15 mmHg decrease in
diastolic blood pressure with arm elevation from the
value obtained with the arm in the standard position.
•Rosenbach's sign — Systolic pulsations of the liver.
•Gerhard's sign — Systolic pulsations of the spleen.
•Hill’s sign: BP Lower extremity >BP Upper extremity by
– > 20 mm Hg - mild AR
– > 40 mm Hg – mod AR
– > 60 mm Hg – severe AR

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 Central Signs of Severe
Aortic Regurgitation
•Apex:
– Enlarged
– Displaced
– Hyper-dynamic
– Palpable S3
– Austin-Flint murmur- a
soft, low-pitched, rumbling
mid-diastolic murmur at the
apex (produced by the
diastolic displacement of the
anterior leaflet of the mitral
valve by the AR stream )
•Aortic diastolic murmur
– High pitched,
blowing, decrescendo
,diastolic murmur at
LSB
– Best heard at end-
expiration & leaning
forward
– length correlates
with severity (chronic
AR)
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 Comparing AS and MR

Systolic Murmurs
•Aortic stenosis
•Mitral insufficiency
•Mitral valve prolapse
•Tricuspid insufficiency
Diastolic Murmurs
•Aortic insufficiency
•Mitral stenosis

S1 S2 S1
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 Assessing Severity
of AR
•Assess severity by impact on peripheral signs
and LV
–  peripheral signs =  severity
–  LV =  severity
– S3
– Austin -Flint
– LVH
– radiological cardiomegaly

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 Natural history
Asymptomatic %/Y
•Normal LV function (~good prognosis)
– Progression to symptoms or LV dysfunction <6
– Progression to asymptomatic LV dysfunction < 3.5
– 75% 5-year survival
– Sudden death <
0.2
•Abnormal LV function
– Progression to cardiac symptoms 25
•Symptomatic (Poor prognosis)
– Mortality > 10

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Laboratory
•ECG- signs of LV hyperthrophy with strain
•Echocardiography
•Chest X-ray

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 Treatment
•Medical
– Afterload reduction: ACEI, nifedipine,
hydralazine
– Use BB cautiously, if at all, given prolonged
diastole and therefore  regurg volume
•Surgical
– AVR – 4% mortality alone, 6.8% with CABG
– LV dysfunction often irreversible, despite AVR

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Treatment
•Acute AR- surgery is required urgently
•Chronic AR- avoid isometric exercise
•Treat hypertension with vasodilators
•Surgical treatment –valve replacement
– Indications

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Prosthetic Heart Valves

63
 Prosthetic Valves
•MECHANICAL •BIO-PROSTHETIC
– Durable – Not durable
– Large orifice – Smaller
orifice/functional
– High
stenosis
thromboembolic – Low thromboembolic
potential potential
– Best in Left Side – Consider in elderly
– Chronic warfarin – Best in tricuspid
therapy position

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•EXTRA SLIDES

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69
 Surgical Treatment

Indication for operation in patients with

•severe AS (valve area <1.0 cm2 or 0.6 cm2/m2 body surface area)
who are-
– symptomatic,
– Asymptomatic
• LV dysfunction (EF <50%),
•Severe or moderately severe stenosis
– who undergo coronary artery bypass grafting or aortic
root reconstruction.

70
 AVR Indication

•severe AR
• symptomatic patients irrespective of LV function.
• asymptomatic patients with progressive LV
dysfunction defined by an
– LVEF <50%,
– LV end-systolic dimension >55mm or
– LV diastolic dimension >75 mm, or
– end-systolic volume >55 mL/m2.

71
ACUTE RHEUMATIC FEVER

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 Definition

Acute rheumatic fever (ARF) is a multisystem

disease resulting from an autoimmune reaction to
infection with group A β hemolytic streptococci.

Any part of the body can be affected ,almost all

manifestation resolve completely except cardiac
valvular damage (RHD).

73
Epidemiology
ARF is a disease of child age group 6 – 15 yrs.
ARF uncommon < 5 yrs. And recurrence very rare after 34 yrs.

Pharyngitis

80 % viral 20 % bacterial

15% GABHS 5% other

bact.

.3 – 3 % ARF
74
 Pathobiology

agent host environ

-ment
-GABHS
->100 subtypeof M protein
Heart-myosin -Extent of immune
Heart valve- laminin response to pharyngitis
Synovia- vimentin -Genetic susceptibility
Skin-keratin -Prior history of RF
Brain- lysoganglioside

-Over crowding
-low socioeconomic status

75
 Diagnosis
•Modified Jones criteria –2002-03
•Essential criteria –
•major- 1.carditis – 1.+ve throat
2.polyarthritis culture
3.chorea
4.erythema marginatum – 2.+ve
5.subcutenous nodule streptococcal antigen
• minor- 1.fever test
2.polyarthralgia
3.elevated ESR – 3.increase ASO
4.prolong PR interval titer

76
2002-03 WHO criteria for the diagnosis
of RF and RHF
Diagnostic Categories
•Primary episode of
rheumatic fever
•Recurrent attack of RF in a
pt. without stablished RHD
•Recurrent attack of RF in a
pt. with stablished RHD
•Rheumatic chorea OR
insidious onset rheumatic
carditis.
Criteria
•2 major or 1 major plus 2
minor plus evidence of GAS
Infection.
•Same as above
•2minor manifestation plus
evidence of GAS infection.
•No other major
manifestations or evidence
of GAS infection
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 Continue….
Diagnostic categories Criteria
•Chronic valve lesion of RHD •Do not require any other
(pts presenting for first time criteria to be diagnose as
with pure MS or mixed having RHD
mitral valve disease and/or
aortic valve disease.)

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79
Arthritis

•Manifest in the 60 – 75% of pt.

• Painful, migratory, and limited to the major joint
of extremities
• Inflammation in 1 joint lasts for 1-2 week and
polyarthritis as whole resolve in 1 month or less.
•Tenderness out of proportion to other findings.
•Arthritis can overlap carditis but both
manifestations inversely related in severity.
• Very good response to salicylates.
80
Carditis

Manifest as valvulitis – (MR and/or AR) ,myocarditis or

pericarditis.
 40 – 60% result in RHD
 Soft blowing pansystolic murmur of MR is hallmark of carditis
in RF.
 HF due to the MR not due to myocardial involvement.
 Pericarditis cause friction rub and sometime pleuritic chest pain.
 Myocardial inflammation can cause conduction defect and heart
block.
There is a linear relationship b/w severity of MR during the first
episode of RF and subsequent RHD.

81
Sydenham's chorea

• Purposeless, rapid, involuntary, nonrepetitive, jerky

dance like movements.
• Milk maid grip.
• Lizard tongue.
• Raising of hand above the head.
• 5 – 35% pt. of RF
• Prior to puberty F>>>M, after puberty no male
involvement.
• Risk of developing subsequent RHD is 50%.

82
 Erythema marginatum

 5 – 13% of RF
 Begin 1-3 cm, pink to red, nonpruritic, macule or
papule.
 Trunk and proximal limb but never on face.
 Central clearing in serpegious fashion
 Exacerbate by heat.
 Also can seen in sepsis, drug reaction,
glomerulonephritis, JRA, Lyme disease.
 Occur in conjunction with milder form of carditis.
 May lasts for months or years.
83
 Subcutaneous nodules

 0 – 8% of pt. of RF
 External surface of elbow, knee, ankles, knuckles, scalp
and spinal process.
 Firm, nontender, free from attachment of underlying skin.
 Strongly support the severity of carditis
 Resolve within weeks to 1 or 2 months.
 Not diagnostic for rheumatic fever can seen with other
autoimmune disorder.

84
Recommended test in case of possible
acute rheumatic fever..
CBC
ESR
CRP
BLOOD CULTURE
ECG
X-RAY CHEST PA VIEW
2D-ECHO
THROAT SWAB CULTURE FOR GAS (gold standard)
ASO TITRE (rising) much specific for RF

85
 Treatment of ARF

 First line of symptomatic therapy is antiinflammatory

agent ranging from salicylates to steroid.
 Naproxen can be alternative for Aspirin.
 Bed rest in carditis pts.
 Effective antibiotic treatment acutely (starting less than
10 days.)almost completely eliminates risk of the dis.

86
 Treatment

•Aspirin and steroids are the two anti-

inflammatory agents of choice for
treatment of acute rheumatic fever.
•Both drugs suppress inflammation,
joint manifestations as well as acute
phase reactions.

87
 Treatment
•There is a little or doubtful effect on
erythema marginatum, subcutaneous
nodules, chorea as well as on long term
complication of arthritis.
•Aspirin is effective for arthritis but steroids
are far superior to aspirin in case of severe
carditis.

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 Treatment
•ASA Dose: 4-8 g/d PO divided q4-6h; until
all symptoms have resolved and APRs have
returned to normal
• Prednisone -- Used in carditis and CHF.
High-dose prednisone is administered for 2-3
wk, then tapered over 3 wk..
– Dose :40-60 mg PO qd for 2-3 wk initially,
then discontinue by gradual taper over 3 wk

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 Treatment of GABHS Infection

Benzathine 1.2 million U. One time Acutely

penicillin G IM one
Penicillin V 500 mg oral BD 10 days

Amoxicillin 500 mg oral TDS 10 days

Erythromycin 250 mg oral BD 10 days

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 Antibiotics
•The roles for antibiotics are to
(1)initially treat GAS pharyngitis(Primary prevention),
(2) prevent recurrent streptococcal pharyngitis, RF, and
RHD(Secondary prevention), and
(3) provide prophylaxis against bacterial endocarditis.

•Erythromycin -- for patients who are allergic to

penicillin.
•Other options include clarithromycin, azithromycin, or a
narrow-spectrum cephalosporin (ie, cephalexin).
• As many as 15% of penicillin-allergic patients also are
allergic to cephalosporins

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 Primordial prevention

1. Improvements in socioeconomic status.

2. Prevention of overcrowding.
3. Prevention of under nutrition and malnutrition.

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Primary prevention

Effective eradication of GABHS from the pharynx

define the role of primary prevention.

Penicillin V 500 mg oral BD 10 days

Benzathine penicillin 1.2 million unit one time

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Secondary prevention

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 Furthue reading
•Harison`s PIM 18TH ED
•AHA and WHO guidelines

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