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 MV’s @ 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
 Fatigue
 Palpitations  Systemic embolism
 Pulmonary infection
 Cough  Hemoptysis
 SOB  Right sided failure
 Left sided failure • Hepatic Congestion
• Edema
• Orthopnea
 Worsened by conditions
• PND that  cardiac output.
 Palpitation • 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
snap (OS) inversely proportional to
 RV lift severity
 Palpable S2  Diastolic rumble: length
proportional to severity
ECG:  In severe MS with low
 LAE, AFIB, RVH, RAD flow- S1, OS & rumble
may be inaudible
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
inversely correlates Say Timing Severity Other
seconds of MS HS’s
with severity Prrr  0.06 Severe
 The more severe Pada .07-.08 Mod-
the MS the higher severe
the LAP the Pata .08-.09 Mod

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
 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 for Mitral Stenosis
ACC/AHA 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
• Myxomatous MV (abcess)
Disease  Papillary Muscles
• Rheumatic • CAD (Ischemia,
• Endocarditis Infarction,
• Congenital-clefts Rupture)
• HCM
 Chordae
• Infiltrative
• Fused/inflammato disorders
ry
• trauma  LV dilatation &
• Degenerative
functional
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
• no post extra-systolic
• hyperdynamic
accentuation
• laterally displaced
• palpable S3 +/- thrill
 Murmer-Dynamic
• late parasternal lift 2
MR(MVP)
to LA filling • mid systolic
• +/- click
 S 1 soft or normal
•  upright
 S 2 wide split (early
A2) unless LBBB  S 3 / flow rumble if
severe
 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
 Systolic murmur ischaemia or tear
may/may not be pan- • Infectious
systolic endocarditis with
 Inflow/rumble leaflet perforation
 S3 present-may be or disruption or
only abnormality chordal tear
• Flail MV segment
 Comparing AS and MR

Systolic Murmurs
 Aortic stenosis

 Mitral insufficiency

 Mitral valve prolapse

 Tricuspid insufficiency

Diastolic Murmurs
 Aortic insufficiency

 Mitral stenosis

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-
REGURGITATION FUNCTION* PHIC FOLLOW-UP

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
male:female decades) think
distribution bicuspid or rheumatic
disease
 Co-existing
Old patient think
coarctation 
degenerative (6,7,8th
6% of patients decades)
 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)
 Recognizing Aortic
Stenosis
Sign Correlation
with Severity
JVP-prominent A wave No
Carotid-delayed, anacrotic Yes
A2 audible over carotids If A2 transmitted to carotids mean AV
gradient  50 mm Hg and stenosis not severe
Apex- sustained, atrial kick Yes
-enlarged, displaced Yes
Thrill No
Cardiomegaly- Clinical/CXR Yes
Soft S1 Yes
Paradoxical S2 Yes
S3, S4 Yes
SEM- intensity No
- late peak Yes
ECG- LAE, LVH Yes
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  Acquired
resulting in • Rheumatic heart
incompetent aortic disease
leaflets • Dilated aorta (e.g.
hypertension..)
 Congenital
• Degenerative
• Bicuspid valve
• Connective tissue
 Aortopathy disorders
• Cystic medial necrosis  E.g. ankylosing
• Collagen disorders (e.g. spondylitis, rheumatoid
Marfan’s) arthritis, Reiter’s
syndrome, Giant-cell
• Ehler-Danlos arteritis )
• Osteogenesis • Syphilis (chronic
imperfecta aortitis)
• Pseudoxanthoma  Acute AI: aortic
elasticum
dissection, infective
 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
 Quincke’s sign:  Durosier’s sign:
capillary pulsation femoral retrograde
 Corrigan’s sign: water bruits
hammer pulse  Traube’s sign: pistol
 Bisferiens pulse shot femorals
(AS/AR > AR)  Hill’s sign:BP Lower
 De Musset’s sign: extremity >BP Upper
systolic head bobbing extremity by
• > 20 mm Hg - mild AR
 Mueller’s sign: systolic
• > 40 mm Hg – mod AR
pulsation of uvula
• > 60 mm Hg – severe
AR
 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
 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
• Austin-Flint murmur shortens
murmur as Aortic
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
Medical  Surgery BEFORE LV dysfunction
TX:25
 Symptomatic
Bonow RO,(Poor prognosis)
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).