(K7) Valvular Heart Disease

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Valvular Heart Disease

Department of Cardiology and Vascular Medicine


University of Sumatera Utara
Mitral Stenosis
Etiology
 Rheumatic fever  most common
 Rarely congenital

Mitral Stenosis 2
Pathophysiology
• Normal MVA 4-6 cm2
– Mild MS 2-4 cm2
– Severe MS < 1.0 cm2
• Restriction of blood flow
from LA to LV during
diastole.
• As HR increases, diastole
shortens disproportionately
and MV gradient increases.

Mitral Stenosis 3
Hepatic Congestion Pulmonary Congestion
JVD Pulmonary HTN

LA Enlargement
Tricuspid Regurgitation Atrial Fib
RA Enlargement LA Thrombi
↑ LA Pressure

RV Pressure Overload
↓ LV Filling
RV Failure

↓ Cardiac output
Mitral Stenosis 4
Natural history
• Progressive, lifelong disease
• Usually slow & stable in the early years.
• Progressive acceleration in the later years.
• 20-40 year latency from rheumatic fever to symptom
onset.
• Additional 10 years before disabling symptoms.

Mitral Stenosis 5
Clinical features
• Fatigue • Atrial fibrillation
• Palpitations • Systemic embolism
• Cough • Pulmonary infection
• SOB • Hemoptysis (massive or frothy sputum)
• Left sided failure • Right sided failure
– Orthopnea – Hepatic Congestion
– PND – Edema
• Palpitation • Worsened by conditions that  cardiac
output.
– Exertion,fever, anemia, tachycardia, Afib,
intercourse, pregnancy, thyrotoxicosis

Mitral Stenosis 6
Physical Examination
 Tapping apex beat that is not displaced.

 Loud S1.

 Opening snap (OS) after S2.

 Low rumbling mid-diastolic murmur heard best at the apex.

 Pulmonary hypertension
 Loud P2 (pulmonary component of second heart sound)

 There might be Right ventricular heave

 Tricuspid regurgitation may be present.

Mitral Stenosis 7
Auscultation

1 2 3 4

S1 S2 OS S1

1. S1 is accentuated and snapping


2. Opening snap (OS) after S2 (the more severe the MS,
the shorter S2-OS interval)
3. Low pitch diastolic rumble at the apex
4. Pre-systolic accentuation (if in sinus rhythm)
Mitral Stenosis 8
Electrocardiography
• P mitral  LA enlargement (if sinus rhythm)
• RV hypertrophy (if pulmonary hypertension)
• Atrial fibrillation is common

Mitral Stenosis 9
Mitral Stenosis 10
Chest Radiography
• LA enlargement
• Prominent pulmonal
segment
• Congestion

Mitral Stenosis 11
Management
Medical management
 Diuretics for LHF/RHF.
 Digoxin/β-blocker/CCB: rate control in AFib.
 Anticoagulation (warfarin): in AFib.
 Rheumatic fever prophylaxis
 Endocarditis prophylaxis

Balloon Mitral Valvuloplasty (BMV)


Indicated for those who have severe MS

Surgical
• Multiple severe valvular lesions or contraindications for BMV
– Mitral commissurotomy
– Mitral valve replacement (mechanical/bioprostethic)

Mitral Stenosis 12
Balloon Mitral Valvuloplasty
Contraindication:
 Marked mitral regurgitation
 Thrombus in LA
 Calcified or thickened rigid
leaflets

Mitral Stenosis 13
Mitral Regurgitation

Mitral valve apparatus :


 Mitral valve annulus
 Mitral valve leaflets
 Chorda tendineae
 Papillary muscle

Abnormality of any part of


the apparatus  Mitral
regurgitation

Mitral Regurgitation 14
Causes of MR
Site of pathology Pathology

Mitral annulus Senile calcification


Left ventricular dilatation and enlargement of the annulus
Abscess formation during infective endocarditis

Mitral valve leaflets Infective endocarditis


Rheumatic fever
Prolapsing (floppy) mitral valve
Congenital malformation
Connective tissue disorders-Marfan syndrom, Ehlers-Danlos
syndrome
Osteogenesis imperfecta, pseudoxanthoma elasticum
Chordae tendinae Idiopathic rupture
Myxomatous degeneration
Infective endocarditis
Connective tissue disorders
Papillary muscle Myocardial infarction
Infiltration-sarcoid, amyloid
myocarditis
Mitral Regurgitation 15
Most common etiology of MR:
• Mitral valve prolapse
• Ischemic heart disease
• Rheumatic heart disease
• Infective endocarditis

Mitral Regurgitation 16
Pathophysiology
Hepatic Congestion Pulmonary Congestion
JVD Pulmonary HTN

↑ LA volume
LA dilatation

Regurgitant
flow

↑ LV inflow
RV failure LV volume overload
LV dilatation
LV failure

Mitral Regurgitation 17
Acute vs. Chronic MR
Acute MR (e.g. IE, RHD)
• Normal LA size
• Increased LA pressure
• Acute pulmonary edema

Chronic MR (e.g. ischemic)


• Dilated LA
• LA pressure normal or slightly
increased
• Fatigue

Mitral Regurgitation 18
Examination
 Atrial fibrillation – irregularly irregular pulse

 Jugular venous distension

 Apex is downward & laterally displaced

 Pansystolic murmur at the apex, radiating to axilla

 Signs of congestive cardiac failure

 P2 loud & right ventricular heave (if PH)

Mitral Regurgitation 19
Auscultation

S1 S2 S1
Systolic Murmurs
• Aortic stenosis
• Mitral insufficiency
• Tricuspid insufficiency

Diastolic Murmurs
• Aortic insufficiency
• Mitral stenosis
Mitral Regurgitation S1 S2 20S1
• ECG: • CXR:
– LA enlargement – LVH
– AFib – LAE
– LVH / RVH / – Congestion
biventricular
hypertrophy

Mitral Regurgitation 21
Management
Medical management
Diuretics and ACE inhibitors to treat the congestive cardiac failure.
Other drugs for the primary disease (e.g. ischemic heart disease, RHD,
IE)

Surgical management
Patients are considered for surgery if the MR is severe. It is important
to act before irreversible left ventricular damage has occurred.
• Mitral valve repair
• Mitral valve replacement (mechanic / bioprostethic)

Mitral Regurgitation 22
Aortic Stenosis
• Valvular AS  most common form
– Senile calcification
– Bicuspid valve
– Rheumatic heart disease
• Subvalvular AS
– HCM
• Supravalvular AS
– Coarctation of aorta

Aortic Stenosis 23
Normal Bicuspid Calcified

Aortic Stenosis 24
Normal valves Aortic stenosis

Aortic Stenosis 25
Pathophysiology
Pulmonary Congestion

↑ LA pressure

↑ LV pressure
LVH Anginal symptoms
↑ LVEDP
LV dilatation

↑ Cardiac output
Aortic Stenosis 26
Natural History & Clinical Symptoms
• Asymptomatic for many years
• Symptoms develop when valve is critically narrowed
and LV function deteriorates
– Bicuspid AV 5th - 6th decade
– Senile AS 7th-8th decades
• Classic Symptoms:
– Angina pectoris
– CHF
– Syncope
– Sudden Death

Aortic Stenosis 27
Clinical features
 Angina – due to the increased myocardial work and
reduced blood supply (the coronary arteries may be
normal).
 Dyspnea – may lead to orthopnoea and paroxysmal
nocturnal dyspnoea as the left ventricle fails.
 Dizziness and syncope – especially on exertion (fixed
cardiac output).
 Sudden death.
 Systemic emboli.

Aortic Stenosis 28
Examination
 A slow rising, small volume pulse
 A low blood pressure.
 Heaving apex beat (rarely displaced)
 Ejection systolic murmur (diamond-shape) at the aortic
area radiating to the carotids + palpable thrill

S1 S2
 S2 single or paradoxically split
 Signs of left ventricular failure

Aortic Stenosis 29
Investigations
Electrocardiography: LVH

Chest radiography: LVH

Echocardiography

Cardiac catheterization

Aortic Stenosis 30
Management of Asymptomatic Patients
• Statin might be useful to delay calcification process
• Rheumatic fever prophylaxis
• Severe, asymptomatic AS  surgery??

Management of Symptomatic Patients


• ACE-I, diuretics might be given cautiously (reduce
preload & reduce arterial pressure  reduce cardiac
output)
• Rheumatic fever prophylaxis
• Balloon aortic valvuloplasty
• Surgery (aortic valve replacement)
• Transcatheter Aortic-Valve Implantation (TAVI)

Aortic Stenosis 31
Aortic regurgitation
Aortic regurgitation (AR) may be due to an abnormality of
the valve cusps themselves or dilatation of the aortic root
and therefore the valve ring.

Pathophysiology
The regurgitation of blood back into LV

 increased end diastolic volume

 LV works harder to increase stroke volume

 LV hypertrophy & LV dilatation

 LV failure

Aortic Regurgitation 32
Causes of AR
Type of disease Cause
Valve disease Congenital
rheumatic fever
Infective endocarditis
Rheumatoid arthritis
SLE
Connective tissue disease (e.g.
Marfan syndrome,
pseudoxanthoma elasticum)
Aortic root disease Marfan syndrome
Osteogenesis imperfecta
Type A aortic dissection
Ankylosing spondylitis
Reiter’s syndrome
Aortic Regurgitation 33
Psoriatic arthritis
Aortic Regurgitation 34
Clinical features
 A collapsing high-volume pulse (waterhammer pulse)

 Wide pulse pressure on measuring blood pressure

 Downward and laterally displaced apical impulse

 Soft-pitched, blowing early diastolic murmur, best heard at the


left upper sternal edge with the patient sitting forward and in
full expiration (severity of AR correlates with murmur duration)

 Austin Flint murmur heard when the regurgitant jet causes


vibration of the anterior mitral valve leaflet. The murmur is
similar to that of MS but with no opening snap

Aortic Regurgitation 35
Peripheral signs of Severe AR
• Quincke’s sign: capillary • Durosier’s sign: femoral
pulsation of nailbed retrograde bruits
• Corrigan’s sign: water • Traube’s sign: pistol shot
hammer pulse sound at femoral artery
• Bisferiens pulse (AS/AR >
• Hill’s sign:BP Lower
AR)
extremity > BP Upper
• De Musset’s sign: systolic
extremity by
head bobbing
– > 20 mm Hg – mild AR
• Mueller’s sign: systolic
– > 40 mm Hg – mod AR
pulsation of uvula
– > 60 mm Hg – severe AR

Aortic Regurgitation 36
Prognosis
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

TX: Medical  Surgery BEFORE LV dysfunction


Aortic Regurgitation 37
Investigations
 Electrocardiography: LVH
 Chest radiography: LVH
 Echocardiography
 Cardiac catheterization

Aortic Regurgitation 38
Management
Medical management
Diuretics and ACE-I to treat cardiac failure
It is, however, important to make the diagnosis and
surgically treat this condition before the left ventricle
dilates and fails.
Surgical management
Aortic valve replacement is considered if the patients is
symptomatic or if there are signs of progressive left
ventricular dilatation. The aortic root may also need to
be replaced if it is grossly dilated.

Aortic Regurgitation 39
Tricuspid regurgitation
Causes
Mostly secondary to dilatation of the right ventricle. This
may be due to any cause of RV failure or pulmonary
hypertension.
Occasionally, tricuspid valve is affected by infective
endocarditis (usually in intravenous drug abusers).
Rarer causes include congenital malformations and the
carcinoid syndrome.

Tricuspid regurgitation 40
Clinical features
The symptoms and signs are due to the backpressure
effects of the regurgitant jet into the right atrium, which
are transmitted to the venous system causing a
prominent v wave in the jugular venous waveform.
Fatigue and discomfort due to ascites or hepatic
congestion are the commonest feature. Patients usually
present with symptoms of the disease causing the
underlying right ventricular failure;the TR is often an
incidental finding.
Management
The mainstay of management is medical with diuretics and
angiotensin-converting enzyme inhibitors to treat the
right ventricular failure and fluid overload. Tricuspid valve
replacement is considered in very severe cases.

Tricuspid regurgitation 41
Thank You
Features indicating severity of valve
disease
Valve disease Features

MS Proximity of opening snap to second heart sound and duration of murmur
Valve area assessed on echocardiography
Evidence of pulmonary hypertension on echocardiography and cardiac
catheterization

MR Symptoms and signs of pulmonary oedema


Size of regurgitant jet and poor left ventricular function on echocardiography
Evidence op pulmonary hypertension on echocardiography and cardiac
catheterization

AS Presence of symptoms


Low- volume pulse and BP
Severity of aortic gradient and poor left venticular function on
echocardiography or cardiac catheterization

AR Signs of LVF


Left ventricular function and size of regurgitant jet on echocardiography or
cardiac catheterization
Overview of other valve lesions
Valve lesion Cause Clinical features Management

Tricuspid Rheumatic fever; rare Venous congestion – JVP Treat pulmonary


raised, large a waves, ascites, hypertension, valve
stenosis hepatomegaly, peripheral replacement
oedema, soft deastolic
murmur at left lower sternal
edge
Pulmonary Congenital If mild asymptomatic, if Pulmonary valvuloplasty or
malformation- severe- RVF and cyanosis, Pulmonary valve
stenosis Noonan’s syndrome, ejection systolic murmur in the replacement
maternal rubella pulmonary area (second left
syndrome, carcinoid ICS), wide splittting of second
syndrome heart sound

Pulmonary Dilatation of the valve RVF in severe cases, low- Treat underlying disease
ring secondary to pitched diastolic murmur in
regurgitation pulmonary pulmonary area, Graham
(PR) hypertension, infective Steel murmur- in severe PR
endocarditis the murmur is high pitched
due to the forceful parasternal
edge(i.e. similar to that in
aortic regurgitation but whith
signs of severe pulmonary
hypertension and RVF)
Normal Valve Function

• Maintain forward flow


and prevent reversal
of flow.
• Valves open and
close in response to
pressure differences
(gradients) between
cardiac chambers.
Abnormal Valve Function
• Valve Stenosis
– Obstruction to valve flow during that phase of the cardiac
cycle when the valve is normally open.
– Hemodynamic hallmark -“pressure gradient” ~ flow// VA
• Valve Regurgitation, Insufficiency, Incompetence
– Inadequate valve closure--- back leakage
• A single valve can be both stenotic and regurgitant;
but both lesions cannot be severe!!
• Combinations of valve lesions can coexist
– Single disease process
– Different disease processes
– One valve lesion may cause another
– Certain combinations are particularly burdensome (AS &
MR)
Mitral Valve Competence:

• Integrated function of
several anatomic
elements
– Posterior LA wall
– Anterior & Posterior
valve leaflets
– Chordae tendineae
– Papillary muscles
– Left ventricular wall
where the papillary
muscles attach
Mitral Valve Disease: Etiology

 Mitral Stenosis  Chronic Mitral Regurgitation


 Rheumatic - 99.9%!!!  Ischemic Heart disease
 Congenital  Papillary ms dysfunction
 Prosthetic valve stenosis  Inferior & posterior MI
 Mitral Annular  Mitral Valve prolapse
Calcification  Infective endocarditis
 Left Atrial Myxoma  Rheumatic
 Prosthetic
 Acute Mitral Regurgitation
 Mitral annular calcification
 Infective endocarditis
 Cardiomyopathy
 Ischemic Heart disease
 LV dilatation
 Papillary ms rupture
 IHSS
 Mitral valve prolapse
 Chordal rupture
 Chest trauma
Mitral Regurgitation-
Pathophysiology

• MR: Leakage of blood


into LA during systole
• 10 Abnormality -Loss of
forward SV into LA
• Compensatory
Mechanisms
– Increase in SV (& EF)
– Forward SV + regurgitant
volume
– LV (LA) dilatation
– Left Ventricular Volume
Overload (LVVO)
Chronic Mitral Regurgitation –
Left Ventricle Volume Overload
• LVVO
– LV dilatation
– Eccentric hypertrophy
• Increased LA pressure
• Pulmonary HTN
• Dyspnea
• Atrial arrhythmias
• Low output state
Pathophysiology –Acute vs Chronic
Mitral Regurgitation
• Acute MR
– Normal (noncompliant) LA
– Increase LA pressure
– large “V” waves
– Acute Pulmonary Edema
• Chronic MR
– Dilated, compliant LA
– LA pressure normal or
slightly increased
– Fatigue, low output state
– Atrial arrhythmias- a. fib.
• Most patients fall between
these two extremes!!
Mitral Regurgitation:
Physical Findings
• Auscultatory Findings
– S1 – soft or normal
– P2 – increased
– Holosystolic blowing murmur @ apex
• MVP – mid-systolic click
• IHSS – murmur increases with Valsalva
• Acute MR – descrescendo systolic murmur
– S3 gallop & diastolic flow rumble
• Hyperdynamic Left Ventricle
– Brisk carotid upstrokes
– Hyperdynamic LV apical impulse
– LA lift; RV tap
Mitral Stenosis -Pathophysiology
• Restriction of blood flow
from LALV during
diastole.
• Normal MVA 4-6cm2.
– Mild MS 2-4cm2.
– Severe MS < 1.0cm2.
• MV Pressure gradient –
• MV grad ~ MV flow//MVA.
– Flow = CO/DFP (diastolic
filling period).
• As HR increases, diastole
shortens disproportionately
and MV gradient increases.
Relationship between MV gradient
and Flow for different Valve Areas
• Cross hatched area
indicates range of normal
resting flow.
• The vertical line represents
the threshold for developing
pulmonary edema.
• Pressure gradient increases
as flow increases:
– to a small degree with
normal valve area(4-6cm2).
– to greater degrees with
smaller valve areas.
– in severe stenosis, a
significant gradient is
present at rest.
Mitral Stenosis-Pathophysiology
• MV gradient Incr LA pr
• Pulmonary HTN
– Passive
– Reactive- 2nd stenosis
• RV Pressure Overload
– RVH
– RV failure
– Tricuspid regurgitation
– Systemic Congestion
• Paradoxes of MS
– Disease of Pulm Arts & RV
– LV unaffected (protected)
– As RV fails, pulmonary
symptoms diminish
Mitral Stenosis- Clinical Symptoms
• Symptoms related to severity of
MVA reduction-
• Symptoms unrelated to severity
of MS-
– Atrial fibrillation
– Systemic thromboembolism
• Symptoms due to Pulmonary
HTN and RV failure-
– Fatigue, low output state
– Peripheral edema and
hepato-splenomegaly
– Hoarseness –recurrent
laryngeal nerve palsy
Mitral Stenosis: Physical Findings
• Auscultatory findings
– S1 – variable intensity; increased early, progressively decreases
– OS –opening snap, variable intensity
– A2-OS interval – varies inversely with severity of MS; shortens as
MVA diminishes
– Low-pitched diastolic rumble @ apex
• Duration of murmur correlates with severity of MS
• Pre-systolic accentuation
– Increased P2
• Body habitus – thin, asthenic, female
• Low BP
• LA lift & RV tap
Mitral Valve Disease – Echo findings
• Mitral Stenosis
– Thickened, deformed MV
leaflets
– 2D MVA
– Doppler Gradient
– Associated LAE, RVH,
PHTN, TR,MR, LV function
• Mitral Regurgitation
– Determine etiology –
leaflets, chordae, MVP, MI
– Doppler severity of MR jet
– LV function
Mitral Valve Disease : Treatment

• Mitral Stenosis • Chronic Mitral Regurgitation


– Medical Rx for Class I & II – Medical Rx for mild to mod
• HR control – Dig & BB MR with vasodilators,
• Anticoagulation diuretics, anticoagulation
– Afib, >40yrs, LAE, MR,
prior embolic event – Surgical Rx –ideally before
– Surgical Rx -Class III &IV LV systolic function
Balloon Mitral Valvuloplasty declines.
• Commissural fusion • MV replacement
• pliable, noncalcified leaflets • MV ring & CABG
• No MR of LA thrombus • MR repair – associated with
Mitral Valve Surgery improved long-term LV
• Open commissurotomy funvtion
• MV replacement – MVP, ruptured chords,
infective endocadritis, pap
ms rupture.
Balloon Mitral Commissurotomy
Aortic Valve Disease: Etiology

• Aortic Stenosis • Chronic Aortic Insufficiency


– Degenerative calcific • Aortic leaflet disease
(senile) – Infective endocarditis
– Congenital – Uni or bicuspid – Rheumatic
– Bicuspid Aortic valve
– Rheumatic
– Prolapse & congenital VSD
– Prosthetic
– Prosthetic
• Aortic root disease
– Aortic aneurysm/dissection
• Acute Aortic Insufficiency – Marfan’s syndrome
– Infective endocarditis – Connective tissue disorders
– Acute Aortic Dissection – Syphilis
• Marfan’s Syndrome – HTN
• Chest trauma – Annulo-aortic ectasia
Aortic Stenosis - Pathophysiology

• Normal AVA 2.5-3.0cm2


– Severe AS <1.0cm2
– Critical AS <0.7cm2;
<0.5cm2/m2
• Hemodynamic Hallmark
– Systolic pressure
gradient
– AV grad ~ AV flow//AVA
• AV flow = CO/SEP
(systolic ejection period)
– 50-100mmHg gradients
are common in severe AS
Relationship between AV gradient
and Flow for different Aortic valve
areas.
• Like Mitral Stenosis –
as flow increases so
does the gradient.
• Unlike Mitral Stenosis –
– Resting flows are higher
• smaller AV area
• shorter SEP
– Larger gradients
– Significant (>50mmHg)
gradient can be present
at rest in asymptomatic
individuals.
Pathophysiology of Aortic Stenosis –
Left Ventricle Pressure Overload
• Chronic LV Pressure
Overload Concentric LVH
• “Stiff” noncompliant LV
– Increased LVEDP
– Increased LV mass Increased
MVO2
• Well tolerated for decades
– LV fails CHF
• Atrial fibrillation
– Poorly tolerated
• Loss of atrial “kick”
• Rapid HR
• Acute pulmonary edema and
hypotension.
Aortic Stenosis: Natural History &
Clinical Symptoms
• Asymptomatic for many • Natural History Studies-
years – Pts grad 25mmHg –20%
• Symptoms develop when chance of intervention in 15
valve is critically narrowed years
and LV function deteriorates – Pts with asymptomatic
severe AS require close f/u
– Bicuspid AV 5th - 6th decade
– Gradient progression
– Senile AS 7th-8th decades
• 6-10mmHg/yr
• Classic Symptom Triad
– Risk Factors
– Angina pectoris – 5 years • Age > 70
– CHF 1-2 years • CAD, hyperlipidemia
– Syncope 2-3 years • Chronic renal failure
– Sudden Death
Aortic Stenosis: Physical Findings
Severity of AS Mild Moderate Severe

Carotid pulse normal Slow rising Parvus et Tardus


LV apical normal heaving Heaving &
impulse sustained
Auscultation
S4 gallop - +/- ++
Systolic + +/- -
ejection Click
SEM, peaking Early systole midsystole mid-to-late
systole
S2 normal Normal or Single or
single paradoxical
Aortic Insufficiency-
Pathophysiology
• 10 abnormality – LVVO
• Severity of LVVO
– Size of regurgitant orifice
– Diastolic pressure gradient
between Ao & LV
– HR or duration of diastole
• Compensatory Mechanisms
– LV dilatation & eccentric
LVH
– Increased LV diastolic
compliance
– Peripheral vasodilation
LV Volume vs Pressure Overload

Feature LVPO (AS) LVVO (MR,AI)


LV Volume normal Dilated**

Wall thickness Conc. LVH Normal to slightly


increased
LV compliance “stiff” Increased
noncompliant compliance
LV diastolic Pr increased Normal to slightly
increased
LV systolic Pr Increased** Normal to slightly
increased
LVEF normal increased
Acute vs Chronic AR
Pathophysiology and Clinical Presentation
• Acute Aortic Regurgitation
– Sudden AoV incompetence
– Noncompliant LV
– Acute Pulmonary Edema
– Emergency AVR
• Chronic Aortic Regurgitation
– Long asymptomatic phase
– Progressive LV dilatation
– DOE, orthopnea, PND
– Frequent PVC’s
Chronic Aortic Regurgitation:
Physical Findings
• Widened Pulse Pressure > 70mmHg (170/60)
• Low diastolic pressure <60mmHg
• Hyperdynamic LV –
– DeMusset’s signs
– Corrigan’s pulse
– Quincke’s pulsations,
– Durozier’s murmur
• Auscultation:
– Diminished A2
– Descrescendo diastolic blowing murmur @ LSB
– Austin-Flint murmur – diastolic flow rumble @ apex
• Due to interference with trans-mitral filling by impignement from aortic
regurgitant jet.
• DDx - mitral stenosis(increases intensity with amyl nitrite)
Aortic Valve Disease:
Diagnostic Testing
• Aortic Stenosis • Aortic regurgitaiton
• EKG- NSR, LVH with strain, • EKG- LVH without strain
LAE,LAD
• CXRay-
• CXRay – frequently normal
– Chronic AI – “cor bovinum”
• 2D-ECHO
– Acute AI – pulmonary
– Aortic cusps –thickened,
edema with nl heart size
calcified, decreased
mobility • 2D ECHO
– Assessment of LVH & LV – Assess Ao valve and root
systolic function – Assess LV
– Concomitant MR, AR function/dilatation
– Doppler assesment of AoV • LVES dimension>55mm
gradient
– Doppler severity of
– Planimetry of AV area
regurgitant jet
Relationship between AV gradient
and Flow for different Aortic valve
areas.
• Like Mitral Stenosis –
as flow increases so
does the gradient.
• Unlike Mitral Stenosis –
– Resting flows are higher
• smaller AV area
• shorter SEP
– Larger gradients
– Significant (>50mmHg)
gradient can be present
at rest in asymptomatic
individuals.
Balloon Aortic Valvuloplasty
• Indications for BAV in critical Aortic Stenosis
– Younger patients with congenital AS and predominant
commissural fusion
– Bridge to eventual AVR
– Moderate to severe heart failure/cardiogenic shock
– Extremely high risk for AVR
– Urgent/emergent need for noncardiac surgery
– Patient with limited lifespan – cardiac or noncardiac
– Patient refuses surgery
Aortic Valve Surgery: Ross
Procedure
• Autotransplant of pulmonic
valve to the aortic position
• Reimplantation of the
coronary arteries
• Homograft valve in the
pulmonic position
• Indications
– Younger patients
– No anticoagulation
– Requires similar sized aortic
and pulmonic roots
Valvular Heart Disease

The End
Mitral Valve Competence:

• Integrated function of
several anatomic
elements
– Posterior LA wall
– Anterior & Posterior
valve leaflets
– Chordae tendineae
– Papillary muscles
– Left ventricular wall
where the papillary
muscles attach
Case 1
• Pria 30 thn
• Mudah capai
• Apex 1 cm lateral LMCS
• Pansystolic murmur, thrill
• Ronki basah halus 1/3 lap paru,
Edema pretibial minimal
• EKG P mitral, LVH
• CXR: CTR 53%, apex lateral
downward
• Diagnosa??
Case 2
• Pria 35 tahun
• Riwayat syncope saat main bola
• Apex kuat angkat, 1 cm med LMCS
• Ejection systolic murmur, thrill
• EKG LVH
• CXR: CTR 47%
• Diagnosa??

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