Valvular Heart Disease

Hakim Alkatiri
Introduction
Mitral Stenosis
Mitral Stenosis
 Mitral Stenosis
Etiology
Symptoms
Physical Exam
Severity
Natural history
Timing of Surgery
 Mitral Stenosis: Etiology
Primarily a result of rheumatic fever
(~ 99% of MVs @ surgery show rheumatic
damage )
Scarring & fusion of valve apparatus
Rarely congenital
Pure or predominant MS occurs in
approximately 40% of all patients with
rheumatic heart disease
Two-thirds of all patients with MS are
female.
 Mitral Stenosis:
Pathophysiology

Normal valve area: 4-6 cm2

Mild mitral stenosis:
MVA 1.5-2.5 cm2
Mod mitral stenosis
MVA 1.0-1.5 cm2
Severe mitral stenosis
MVA < 1.0 cm2
 patophysiology
Right Heart Pulmonary HTN
Failure: Pulmonary
Hepatic Congestion Congestion
JVD LA Enlargement
Tricuspid Atrial Fib
Regurgitation LA Thrombi
RA Enlargement LA Pressure

RV Pressure
Overload
RVH LV Filling
RV Failure
 Mitral Stenosis: Symptoms
SOB
Systemic embolism
Palpitations Pulmonary infection
Cough Hemoptysis=Pecahnya
pemb.darah
Fatique Right sided failure
PND Hepatic Congestion
Edema
Orthopnoe Worsened by conditions that
cardiac output.
Exertion,fever, anemia,
tachycardia, , pregnancy,
thyrotoxicosis
 Recognizing Mitral
Stenosis
Palpation:
Small volume pulse Auscultation:
Tapping apex-palpable
Loud S1- as loud as S2 in
S1 aortic area
+/- palpable opening
A2 to OS interval inversely
snap (OS) proportional to severity
Diastolic rumble: length
RV lift
proportional to severity
Palpable S2 In severe MS with low
ECG: flow- S1, OS & rumble
LAE, AFIB, RVH, RAD may be inaudible

Wave Sound
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)
 Common Murmurs and
Timing (click on murmur to play)
Systolic Murmurs
Aortic stenosis

Mitral insufficiency

Mitral valve prolapse

Tricuspid insufficiency

Diastolic Murmurs
Aortic insufficiency

Mitral stenosis

S1 S2 S1
 Auscultation-
Timing of A2 to OS Interval
Width of A2-OS
Say Timing Severity Other
inversely correlates seconds of MS HSs
with severity Prrr 0.06 Severe
The more severe Pada .07-.08 Mod-
the MS the higher severe
Pata .08-.09 Mod
the LAP the
earlirthe LV Papa 0.10 Mild PK
0.1-0.110
pressure falls Tu- .12 A2-S3
below LAP and the huh 0.12-0.18
MV opens
 Mitral Stenosis: 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: 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
 Mitral Stenosis: EKG
LAE
RVH
Premature contractions
Atrial flutter and/or fibrillation
freq. in pts with mod-severe MS for several
years
A fib develops in 30% to 40% of pts
w/symptoms
A 75 year old woman with loud first heart
sound and mid-diastolic murmur
CXR
 Mitral Stenosis: Role of

Echocardiography
Diagnosis of Mitral Stenosis
Assessment of hemodynamic severity
mean gradient, mitral valve area, pulmonary artery
pressure
Assessment of right ventricular size and function.

Assessment of valve morphology to determine

suitability for percutaneous mitral balloon valvuloplasty

Diagnosis 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
 Mitral Stenosis:Therapy
Medical
Diuretics for LHF/RHF
Digitalis/Beta blockers/CCB: Rate
control in A Fib
Anticoagulation: In A Fib
Endocarditis prophylaxis
Balloon valvuloplasty
Effective long term improvement
Balloon Mitral valvuloplasty
 Mitral Stenosis:Therapy
Surgical
Mitral commissurotomy
Mitral Valve Replacement
Mechanical
Bioprosthetic
 Recommendations for Mitral Valve
Repair for Mitral Stenosis
ACC/AHA Class I
Patients with NYHA functional Class III-IV symptoms,
moderate or severe MS (mitral valve area <1.5 cm
2 ),*and valve morphology favorable for repair if
percutaneous mitral balloon valvotomy is not available
Patients with NYHA functional Class III-IV symptoms,
moderate or severe MS (mitral valve area <1.5 cm
2 ),*and valve morphology favorable for repair if a left
atrial thrombus is present despite anticoagulation
Patients with NYHA functional Class III-IV symptoms,
moderate or severe MS (mitral valve area <1.5 cm
2 ),* and a non-pliable or calcified valve with the
decision to proceed with either repair or replacement
made at the time of the operation.
 Recommendations for Mitral Valve
Repair
ACC/AHA for Mitral Stenosis
Class IIB
Patients in NYHA functional Class I, moderate
or severe MS (mitral valve area <1.5 cm 2 ),*
and valve morphology favorable for repair who
have had recurrent episodes of embolic events
on adequate anticoagulation.
ACC/AHA Class III
Patients with NYHA functional Class I-IV
symptoms and mild MS.
*The committee recognizes that there may be a variability in the
measurement of mitral valve area and that the mean trans-mitral
gradient, pulmonary artery wedge pressure, and pulmonary artery
pressure at rest or during exercise should also be considered.
Mitral Regurgitation
 Mitral Regurgitation
Etiology
Symptoms
Physical Exam
Severity
Natural history
Timing of Surgery
 Mitral Regurgitation:
Etiology
Annulus

Valvular-leaflets Calcification, IE
(abcess)
Myxomatous MV
Disease Papillary Muscles
Rheumatic CAD (Ischemia,
Endocarditis Infarction, Rupture)
Congenital-clefts HCM
Infiltrative disorders
Chordae
Fused/inflammatory
LV dilatation &
trauma functional
Degenerative
regurgitation
IE
 MR Etiology:Surgical series
MVP(20-70%)
Ischemia (13-40%)
RHD (3-40%)
Infectious endocarditis(10-12%)
 MR Pathophysiology
Chronic LV volume overload -
compensatory LVE initially maintaining
cardiac output
Decompensation (increased LV wall
tension) -CHF
LVE annulus dilation increased
MR
Backflow LAE, Afib, Pulmonary HTN
 MR Symptoms
Similar to MS
Dyspnea, Orthopnea, PND
Fatigue
Pulmonary HTN, right sided failure
Hemoptysis
Systemic embolization in A Fib
 Recognizing Chronic
Mitral Regurgitation
Pulse: Murmer-Fixed MR:
brisk, low volume pansystolic
Apex: loudest apex to axilla
hyperdynamic no post extra-systolic
accentuation
laterally displaced
palpable S3 +/- thrill
Murmer-Dynamic
late parasternal lift 2
MR(MVP)
to LA filling mid systolic
S 1 soft or normal +/- click
upright
S 2 wide split (early
A2) unless LBBB
S 3 / flow rumble if
severe

Wave Sound
 Recognizing Acute Severe
Mitral Regurgitation
Acute severe dyspnea, RV lift
CHF & hypotension TTE/TEE for diagnosis
LV size normal Chordal or papilllary
LV may/may not be muscle rupture/tear
hyperdynamic Infarction with
Loud S1 papillary muscle
ischaemia or tear
Systolic murmur
Infectious
may/may not be pan-
endocarditis with
systolic leaflet perforation or
Inflow/rumble disruption or chordal
S3 present-may be tear
only abnormality Flail MV segment
 Comparing AS and MR

Systolic Murmurs
Aortic stenosis Wave Sound

Mitral insufficiency
Wave Sound

Mitral valve prolapse

Wave Sound

Tricuspid insufficiency

Diastolic Murmurs
Aortic insufficiency
Wave Sound

Mitral stenosis
Wave Sound

S1 S2 S1
 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

 Recognizing Mitral
Regurgitation
ECG: CXR:
LA enlargement LV
Afib LA
LVH (50% pts. pulmonary
With severe MR) vascularity
RVH (15%) CHF
Combined Ca++ MV/MAC
hypertrophy
(5%)
CXR
 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
 MR Echocardiography
Etiology:
flail leaflets (chord/pap rupture)
thick (RHD)
post mvt of leaflets (MVP)
vegetations(IE)
Severity:
regurgitant volume/fraction/orifice area
LV systolic function
increased LV/LA size, EF
MR Echo/Doppler
 MR Stages
LV size and function defined by echo
Stage 1-compensated:

End-diastolic dimension less 63mm, ESD less

42mm
EF more than 60
Stage 2-transitional
EDD 65-68mm, ESD 44-45mm, EF 53-57
Stage 3-decompensated
EDD more than 70mm, ESD more than 45mm,
EF less than 50
 Echo Indicators for Valve
Replacement in Asymptomatic
Aortic & Mitral Regurgitation
Type of LVESD EF FS
Regurgitati mm %
on

Aortic > 55 < 55 <0.27

Mitral > 45 < 60 < 0.32

 RECOMMENDED FREQUENCY OF ECHOCARDIOGRAPHY
IN PATIENTS WITH CHRONIC MITRAL REGURGITATION
AND PRIMARY MITRAL-VALVE DISEASE.

SEVERITY OF LEFT FREQUENCY OF

MITRAL VENTRICULAR ECHOCARDIOGRA-
FUNCTION* PHIC FOLLOW-UP
REGURGITATION

Mild Normal ESD and EF Every 5 yr

Moderate Normal ESD and EF Every 1 2 yr

Moderate ESD >40 mm or EF Annually

<0.65
Severe Normal ESD and EF Annually

Severe ESD >40 mm or EF Every 6 mo

<0.65
*ESD denotes end-systolic dimension and EF ejection fraction. Otto C.M. NEJM
345:10.
 Mitral Valve Surgery
Only effective treatment is valve
repair/replacement
Optimal timing determined:
Presence/absence of symptoms
Functional state of ventricle
Feasability of valve repair
Presence of Afib/PHTN
Preference/expectations of patient
 Surgical Therapy - Timing
Surgery reduces morbidity and
mortality from severe MR but
exposes patient to risk of surgery
and prosthetic valve
Surgery should be performed before
onset of severe symptoms or
development of LV contractile
dysfunction
 Ejection Fraction (LVEF)
Strongest predictor of outcome following
surgery
Should be assessed quantitatively
MUGA or Echo
Surgery indicated if LVEF is below normal
(60%)
If EF normal, follow every 6 to 12 months
If EF <30%, medical management (valve
repair experimental in this setting)
 Mitral Regurgitation
ACC/AHA recommendations
Surgery Recommended in patients
who are
Symptomatic

Asymptomatic with

Any LV dysfunction
Atrial fibrillation
Pulmonary hypertension
Reparable valves
Recurrent VT
 Indications for Surgery
Isolated,Severe Chronic MR
Definite (major criteria):
NYHA Class III or IV heart failure (any
duration)
EF <60%
EF >60% but decreasing on serial
measurements
LVIDs >45mm
ESVI >50cc/m2
 Indications for Surgery
Isolated,Severe Chronic MR
Emerging (minor criteria):
Any symptoms of heart failure
or sub optimal exercise tolerance test
Flail mitral leaflet
Left atrial diameter >45mm
Paroxysmal atrial fibrillation
Abnormal exercise end-systolic volume
index or ejection fraction
 MV Repair vs. Replacement
Lower operative mortality
Better late outcome
Curative
Avoids anticoagulation unless atrial
fibrillation
Open Afib ablation
MV Repair vs. Replacement (2)
Valve replacement: Valve repair
Mortality 2-7% Mortality 2-3%
Anti-coagulation No anticoagulation
Decreased LVEF (unless Afib)
Tissue prosthetic Preservation of
valve degeneration LVEF
Mechanical Valve repair always
prosthetic valve preferable
dysfunction/ Feasible in 70-90%
thrombosis of patients
Aortic Stenosis
 Aortic Stenosis
Etiology
Physical Examination
Assessing Severity
Natural History
Prognosis
Timing of Surgery
 Aortic Stenosis - Aetiology

Congenital 1st-3rd decade

Valve degeneration and calcification
Rheumatic - 4th decade
Bicuspid valve; 1%, males>females, 5-6th decades
Tricuspid valve - 7-8th decades, 1-2% incidence
 Aortic Stenosis - Etiology
Young patient Rarely
Unicuspid valve
think congenital Sub-aortic stenosis
Bicuspid Discrete
Diffuse (Tunnel)
2% population

Middle aged
3:1
patient(4&5th decades)
male:female think bicuspid or
distribution rheumatic disease
Co-existing
Old patient think
degenerative (6,7,8th
coarctation decades)
6% of patients
 Aortic Stenosis: Etiology
Congenital bicuspid valve is the most
common abnormality
Rheumatic heart disease and
degeneration with calcification are found
as well

Normal Bicuspid Ao V Normal geriatric

calcific valve
Bicuspid Aortic Valve
Aortic Stenosis: Asymptomatic
Common in asymptomatic adults
Characterized by
Grade I II @ LSB
Systolic ejection pattern

S1 S2
Normal intensity & splitting of second sound (S2)
No other abnormal sounds or murmurs
No evidence of LVH, and no with Valsalva
 Aortic Stenosis: Symptoms
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
 Common Murmurs and
Timing (click on murmur to play)
Systolic Murmurs
Aortic stenosis

Mitral insufficiency

Mitral valve prolapse

Tricuspid insufficiency

Diastolic Murmurs
Aortic insufficiency

Mitral stenosis

S1 S2 S1
 Aortic Stenosis: Physical
Findings

S1 S2 S1 S2
Mild-Moderate Severe
 Aortic Stenosis: Physical
Findings
Intensity DOES NOT predict severity
Presence of thrill DOES NOT predict
severity
Diamond shaped, harsh, systolic
crescendo-decrescendo
Decreased, delay & prolongation of pulse
amplitude
Paradoxical S2
S4 (with left ventricular hypertrophy)
S3 (with left ventricular failure)
An 83 year old man with
exertional dyspnea
 Severity of Stenosis
Normal aortic valve area 2.5-3.5 cm2
Mild stenosis 1.5-2.5 cm2
Moderate stenosis 1.0-1.5 cm2
Severe stenosis < 1.0 cm2
Onset of symptoms
~0.9 cm2 with CAD
~0.7 cm2 without CAD
 Echocardiogram
Etiology
Valve gradient and
area
LVH
Systolic LV function
Diastolic LV function
LA size
Concomitant regional
wall motion
abnormalities
Coarctation associated
with bicuspid AV
 Aortic Stenosis: Prognosis

Symptom/Sign Live
expectancy
Angina 5 years
Syncope 2-3 years
Congestive Heart Failure 1-2 years

Therapy: Valve replacement for severe aortic stenosis

Operative mortality (elderly) ~ 4-24%/Morbidity ~ 3-11%
Event rate in asymptomatic severe AS ~ 1%/year
 Natural History of Aortic
Stenosis
Heart failure
reduces life
expectancy to less
than 2 years
Angina and syncope
reduce life
expectancy between
2 and 5 years
Rate of progression
@ 0.1 cm2/year
 Operative mortality of AVR
in the elderly
~ 4-24%/year Aortic regurgitation
Risk factors for Concomitant
surgical
operative mortality
procedures:CABG/M
Functional class V surgery
Lack of sinus Previous bypass
rhythm
Emergency surgery
HTN
CAD
Pre-existing LV
Female gender
dysfunction
 Prosthetic Valves
MECHANICAL BIO-PROSTHETIC
Durable Not durable
Large orifice Smaller
orifice/functional
High stenosis
thromboembolic
Low
potential thromboembolic
Best in Left Side potential
Chronic warfarin Consider in elderly
therapy Best in tricuspid
position
Aortic Regurgitation
 Aortic Regurgitation
Etiology
Physical Examination
Assessing Severity
Natural History
Prognosis
Timing of Surgery
 Aortic Regurgitation:
Etiology
Any conditions resulting Acquired
in incompetent aortic Rheumatic heart disease
leaflets Dilated aorta (e.g.
hypertension..)
Congenital Degenerative
Bicuspid valve Connective tissue disorders
Aortopathy E.g. ankylosing
Cystic medial necrosis spondylitis, rheumatoid
arthritis, Reiters
Collagen disorders (e.g. syndrome, Giant-cell
Marfans) arteritis )
Ehler-Danlos Syphilis (chronic aortitis)
Osteogenesis imperfecta Acute AI: aortic
Pseudoxanthoma dissection, infective
elasticum endocarditis, trauma
 Aortic Regurgitation:
Symptoms
Dyspnea, orthopnea, PND
Chest pain.
Nocturnal angina >> exertional angina
( diastolic aortic pressure and increased
LVEDP thus coronary artery diastolic flow)
With extreme reductions in diastolic
pressures (e.g. < 40) may see angina
 Peripheral Signs of Severe
Aortic Regurgitation
Quinckes sign: Durosiers sign:
capillary pulsation femoral retrograde
Corrigans sign: water bruits
hammer pulse Traubes sign: pistol
Bisferiens pulse shot femorals
(AS/AR > AR) Hills sign:BP Lower
De Mussets sign: extremity >BP Upper
systolic head bobbing extremity by
> 20 mm Hg - mild AR
Muellers sign: systolic > 40 mm Hg mod AR
pulsation of uvula > 60 mm Hg severe
AR

Wave Sound
 Aortic Regurgitation:
Physical Exam
Widened pulse
pressure
Systolic diastolic =
pulse pressure
High pitched, blowing,
decrescendo diastolic
murmur at LSB
Best heard at end-
expiration & leaning S1 S2 S1
forward
Hands & Knee position Wave Sound
 Central Signs of Severe
Aortic Regurgitation
Apex: Aortic diastolic
Enlarged murmur
Displaced length correlates
with severity
Hyper-dynamic (chronic AR)
Palpable S3 in acute AR
murmur shortens
Austin-Flint
as Aortic
murmur DP=LVEDP
in acute AR - mitral
pre-closure
 Assessing Severity
of AR
Assess severity by impact on
peripheral signs and LV
peripheral signs = severity
LV = severity
S3
Austin -Flint
LVH
radiological cardiomegaly
 Aortic Regurgitation:
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

TX: Medical Surgery BEFORE LV dysfunction

Bonow RO, et al, JACC. 1998;32:1486.
 Echo Indications for Valve
Replacement
in Asymptomatic AR & MR

Type of LVESD EF FS
Regurgitati mm %
on

Aortic > 55 < 55 <0.27

Mitral > 45 < 60 < 0.32

Indication for Valve Replacement in
Aortic Regurgitation
ACC/AHA Class I
Symptomatic patients with preserved LVF
(LVEF >50%)
Asymptomatic patients with mild to moderate
LV dysfunction (EF 25-49%)
Patients undergoing CABG, aortic or other
valvular surgery
ACC/AHA Class II a
Asymptomatic patients with preserved LVEF
but severe LV dilatation (EDD>75 mm or ESD
> 55mm)
Indication for Valve Replacement in
Aortic Regurgitation
ACC/AHA Class II b
Patients with severe LV dysfunction (EF < 25%)
Asymptomatic patients with normal systolic
func-tion at rest (EF >0.50) and progressi ve LV
dilata-tion when the degree of dilatation is
moderatelysevere (EDD 70 to 75 mm, ESD 50
to 55 mm).
ACC/AHA Class III
Asymptomatic patients with normal systolicf
unction at rest (EF >0.50) and LV dilatation
when the degree of dilatation is not severe
(EDD <70 mm, ESD <50 mm).