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Valvular heart disease

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.

Recognizing Mitral Stenosis


Palpation:
Auscultation:
Small volume pulse
Tapping apex
palpable S1
+/- palpable
opening snap (OS)

RV lift
Palpable S2
ECG:

LAE, AFIB, RVH,


RAD

patophysiology

Right
Right Heart
Heart
Failure:
Failure:
Hepatic
Hepatic
Congestion
Congestion
JVD
JVD
Tricuspid
Tricuspid
Regurgitation
Regurgitation
RA
RA Enlargement
Enlargement

RV
RV Pressure
Pressure
Overload
Overload
RVH
RVH
RV
RV Failure
Failure

Pulmonary
Pulmonary HTN
HTN
Pulmonary
Pulmonary
Congestion
Congestion
LA
LA Enlargement
Enlargement
Atrial
Fib
Atrial Fib
LA
LA Thrombi
Thrombi
LA
Pressure
LA Pressure

LV
Filling
LV Filling

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

Complications
Atrial dysrrhythmias
Loud S1- as loud as
Systemic embolization (10-25%)
S2 in aortic area
o Risk of embolization is related to, age, presence of atrial fibrillation,
A2 to OS interval
previous embolic events
inversely proportional
Congestive heart failure
to severity
Diastolic rumble:
Pulmonary infarcts (result of severe CHF)
length proportional
Hemoptysis
to severity
0
In severe MS with low o Massive: 2 to ruptured bronchial veins (pulm HTN)
flow- S1, OS & rumble o Streaking/pink froth: pulmonary edema, or infection
may be inaudible

Endocarditis
Pulmonary infections

Physical Exam

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)

EKG

LAE
RVH
Premature contractions
Atrial flutter and/or fibrillation
o freq. in pts with mod-severe MS for several
years
o A fib develops in 30% to 40% of pts
w/symptoms

Common Murmurs
Systolic Murmurs

Aortic
stenosis

Mitral
insufficiency

Mitral valve
prolapse

Tricuspid
insufficiency

Auscultation-Timing of A2 to OS
Interval
Diastolic
Width of A2-OS inversely correlates
Murmurs
with severity
Aortic
The more severe the MS the higher
insufficiency
the LAP the earlirthe LV pressure
Mitral stenosis
falls below LAP and the MV opens

Role of Echocardiography

Diagnosis of
Diagnosis and
Mitral Stenosis
assessment of
concomitant

Assessment of
valvular lesions
hemodynamic
Reevaluation of
severity
o mean gradient,
patients with
known MS with
mitral valve
changing
area, pulmonary
symptoms or
artery pressure

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.

signs.
Assessment of
F/U of asymptomatic
right ventricular
size and function.
patients with
mod-severe MS
Assessment of valve
morphology to
determine

Therapy

Medical
o Diuretics for LHF/RHF
percutaneous
o Digitalis/Beta blockers/CCB: Rate
mitral balloon
control in A Fib
valvuloplasty
o Anticoagulation: In A Fib
ACC/AHA Class IIB
o Endocarditis prophylaxis
Patients in NYHA functional Class I,
moderate or severe MS (mitral valve area Balloon valvuloplasty
o Effective long term improvement
<1.5 cm 2 ),* and valve morphology
favorable for repair who have had
Surgical
recurrent episodes of embolic events on
o Mitral commissurotomy
adequate anticoagulation.
ACC/AHA Class III
o Mitral Valve Replacement
Patients with NYHA functional Class I-IV
Mechanical
symptoms and mild MS.
Bioprosthetic

suitability for

Mitral regurgitation
Etiology

Valvular-leaflets
Myxomatous

MV Disease
Rheumatic

Endocarditis

Congenitalclefts
Chordae

Fused/inflamma

Annulus
Calcification, IE
(abcess)
Papillary Muscles
CAD (Ischemia,
Infarction,
Rupture)
HCM
Infiltrative

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

tory
trauma
Degenerative
IE

disorders
LV dilatation &
functional
regurgitation

Chronic Mitral Regurgitation

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

Pulse:

brisk, low volume


Apex:
hype
rdynamic
later
ally displaced
palp
able S3 +/- thrill
late
parasternal lift 2
to LA filling
S 1 soft or
normal
S 2 wide
split (early A2)
unless LBBB

Murmer-Fixed MR:
pansystolic
loudest apex to
axilla
no post extrasystolic
accentuation
Murmer-Dynamic
MR(MVP)
mid systolic
+/- click
upright
S 3 / flow rumble if
severe

Acute Severe Mitral Regurgitation


Acute severe
dyspnea, CHF &
hypotension
LV size normal
LV may/may not
be hyperdynamic
Loud S1
Systolic murmur
may/may not be
pan-systolic
Inflow/rumble
S3 present-may
be only
abnormality

Recognizing Mitral Regurgitation

ECG:
LA enlargement
Afib
LVH (50% pts.
With severe MR)
RVH (15%)
Combined
hypertrophy (5%)

CXR:
LV
LA
pulmonary
vascularity
CHF
Ca++ MV/MAC

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

RV lift
TTE/TEE for
diagnosis
Chordal or
papilllary muscle
rupture/tear
Infarction with
papillary muscle
ischaemia or tear
Infectious
endocarditis with
leaflet perforation
or disruption or
chordal tear
Flail MV segment

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

Echo Indicators for Valve Replacement in


Asymptomatic Aortic & Mitral
Regurgitation
Type of
Regurgi
tation
Aortic
Mitral

LVESD
mm

EF %

FS

> 55
> 45

< 55
< 60

< 0.27
< 0.32

RECOMMENDED FREQUENCY OF ECHOCARDIOGRAPHY IN PATIENTS WITH


CHRONIC MITRAL REGURGITATION AND PRIMARY MITRAL-VALVE DISEASE.

SEVERITY OF
MITRAL
REGURGITATION

LEFT
VENTRICULAR
FUNCTION*

FREQUENCY OF
ECHOCARDIOGR
A-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 <0.65

Annually

Severe

Normal ESD and


EF

Annually

Severe

ESD >40 mm or
EF <0.65

Every 6 mo

Ejection Fraction (LVEF)

Strongest predictor of outcome following


surgery
Should be assessed quantitatively
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

MV Repair vs. Replacement

Lower operative mortality


Better late outcome
Curative
Avoids anticoagulation unless atrial fibrillation

Open Afib ablation

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

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
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

Valve replacement:
o Mortality 2-7%
o Anti-coagulation
o Decreased LVEF
Tissue prosthetic valve degeneration
Mechanical prosthetic valve dysfunction/
thrombosis

Valve repair
o Mortality 2-3%
o No anticoagulation (unless
Afib)
o Preservation of LVEF
Valve repair always preferable
o Feasible in 70-90% of patients

Aortic stenosis
Etiology
Young

patient think

congenital

Bicuspid

2% population

3:1
male:female
distribution
Co-existing
coarctation 6%
of patients

Symptoms

Asymptomatic
Common in asymptomatic adults
Characterized by
Grade I II @ LSB
Systolic ejection pattern

Rarely
Unicus
pid valve
Subaortic stenosis
o
Discrete
o
Diffuse (Tunnel)
Middle aged
patient(4&5th
decades) think
bicuspid or
rheumatic disease
Old patient think
degenerative
(6,7,8th decades)

Normal
Ao V

bicuspid

S1

Normal intensity & splitting of second sound (S2)


No other abnormal sounds or murmurs

No evidence of LVH, and no with Valsalva

normal greatric calcific valve

Physical Findings

S2

Recognizing Aortic Stenosis

Cardinal Symptoms
Chest pain (angina)
o Reduced coronary flow reserve
o Increased demand-high afterload
Syncope/Dizziness (exertional presyncope)
o Fixed cardiac output
o Vasodepressor response
Dyspnea on exertion & rest
Impaired exercise tolerance
Other signs of LV failure
Diastolic & systolic
dysfunction

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

Intensity DOES NOT predict severity


Presence of thrill DOES NOT predict severity
Diamond shaped, harsh, systolic crescendodecrescendo
Decreased, delay & prolongation of pulse
amplitude
Paradoxical S2
S3 (with left ventricular failure)

Echocardiogram

Prognosis
Symptom/Sign
Angina
Syncope
Congestive Heart
Failure

Live
expectancy
5 years
2-3 years
1-2 years

Therapy: Valve replacement for


severe aortic stenosis
Operative mortality (elderly) ~ 424%/Morbidity ~ 3-11%
Event rate in asymptomatic severe
AS ~ 1%/year

Etiology
Valve gradient and area
LVH
Systolic LV function
Diastolic LV function
LA size
Concomitant regional wall motion
abnormalities
Coarctation associated with bicuspid AV

Natural History
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

sign
JVP-prominent A
wave
Carotiddelayed,anacrotc
A2 audible over
carotid

Correlation wi severity
No
Yes
If A2 transmitted to
carotids mean AV gradient
<50mmHg
Yes

Apex-sustained,
atrial kick
Enlarge, displaced
Thrill
Cardiomegaly
Soft S1
Paradoxical S2
S3, S4
SEM intensity
-late peak
ECG- LAE, LVH

Yes
No
Yes
Yes
Yes
Yes
No
Yes
Yes

Operative mortality of AVR in the elderly

~ 4-24%/year
Risk factors for
operative
mortality
Functional class
Lack of sinus
rhythm
HTN
Pre-existing LV
dysfunction

Aortic regurgitation
Concomitant surgical
procedures:CABG/MV
surgery
Previous bypass
Emergency surgery
CAD
Female gender

Prosthetic Valves
MECHANICAL
Durable
Large orifice
High thromboembolic potential
Best in Left Side
Chronic warfarin therapy

BIO-PROSTHETIC
Not durable
Smaller orifice/functional
stenosis
Low thromboembolic
potential
Consider in elderly
Best in tricuspid position

Aortic regurgitation
Etiology

Symptoms

Any conditions Acquired

Rheumatic
resulting in
heart disease
incompetent

Dilated aorta
aortic leaflets
(e.g.
hypertension..)
Congenital

Degenerative
Bicuspid valve

Connective

Dyspnea, orthopnea, PND


Chest pain.
Nocturnal angina >> exertional
angina
( diastolic aortic pressure and
increased LVEDP thus coronary
artery diastolic flow)

With extreme reductions in

Central Signs of Severe Aortic


Regurgitation
Apex:
Enlarged
Displaced
Hyper-dynamic
Palpable S3
Austin-Flint
murmur

Aortic diastolic
murmur
length correlates
with severity
(chronic AR)
in acute AR
murmur shortens

tissue disorders
diastolic pressures (e.g. < 40)
Aortopathy
o E.g.
may see angina

Cyst
ankylosing
ic medial
spondylitis,
necrosis
rheumatoid
arthritis,

Coll
Reiters
agen
Peripheral Signs of Severe
syndrome,
disorders
Aortic Regurgitation
Giant-cell
(e.g.
arteritis )

Quinckes

Durosiers sign:

Syphilis
Marfans)
sign: capillary
femoral
(chronic
pulsation
retrograde

Ehle
aortitis)
bruits

Corrigans
r-Danlos
Acute AI: aortic

Traubes sign:
sign: water

Ost
dissection,
hammer pulse
pistol shot
eogenesis
infective
femorals

Bisferiens
endocarditis,
imperfecta

Hills sign:BP
pulse (AS/AR
trauma

Pse
> AR)
Lower
extremity >BP

De
Mussets
udoxantho
Upper
sign: systolic
ma
extremity by
head bobbing
elasticum
o > 20 mm Hg

Muellers sign:
systolic
pulsation of
uvula.

o
o

Assessing Severity of AR

Assess severity by impact on peripheral


signs and LV
peripheral signs = severity
LV = severity
S3
Austin -Flint
LVH
radiological cardiomegaly

- mild AR
> 40 mm Hg
mod AR
> 60 mm Hg
severe AR

Echo Indications for Valve


Replacement in Asymptomatic AR
& MR
Type of
Regurg
itation
Aortic
mitral

LVESD
(mm)

EF (%)

FS

> 55
> 45

< 55
< 60

< 0.27
< 0.32

as
Aortic DP=LVEDP
in acute AR mitral pre-closure

Physical Exam
Widened pulse pressure

Systolic diastolic = pulse


pressure
High pitched, blowing, decrescendo diastolic
murmur at LSB
Best heard at end-expiration & leaning
forward
Hands & Knee position

S1
S1

S2

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

Indication for Valve Replacement in Aortic Regurgitation


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

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