Valvular heart disease assessment of lesion severity

Valvular Heart DiseaseValvular Heart Disease
Assessment of Lesion severityAssessment of Lesion severity
Dr Awadhesh kumar sharma
DM Cardiology
PGIMER &Dr RML Hospital,New Delhi

 In managing the patient with valvular heart disease (VHD)
three major issues must be addressed:-
 Assessment of the severity of disease,
 The effect the disease is having or is likely to have on the
patient and his/her cardiovascular system
 The timing and type of intervention to be used to correct
the lesion.
Braunwald’s Heart Disease: A Textbook of Cardiovascular Medicine. 8th
ed. Philadelphia, PA: WB Saunders; 2007:1625-1712.

 The distinction between mild, moderate and severe disease
is thought crucial since it is believed that, in most cases,
mild and moderate disease are tolerated indefinitely
(unless severity worsens) and only severe disease (as
defined) causes symptoms and cardiac dysfunction.

 Classification of the severity of valve lesions should be
based on multiple criteria, including the initial findings on
the physical examination, which should then be correlated
with data from a comprehensive TTE.
 Intervention should primarily be performed on patients
with severe VHD

Classification of progression of VHD
J Am Coll Cardiol. March 2014.Online first.

OBJECTIVE ASSESSMENT OF DISEASE
SEVERITY
 The physical examination
 In this age of high-tech diagnostic modalities, the physical
examination, and the skill applied when performing it,
seem to be diminishing.
 However, the importance of the physical exam cannot be
overemphasized because it lays the Bayesian foundation
for all tests that follow.

Mitral stenosis (MS)
Etiology
 Most commonly rheumatic fever
——rheumatic heart disease （ RHD ）
 Symptoms commence mostly in 2nd~4th decade
 2/3 of all patients are female
 25% of all patients with RHD have pure MS
 40% have combined MS and mitral regurgitation (MR)
J Am Coll Cardiol. 1994;24:152-8.

Clinical features s/o severe MS
 PND
 Pulmonary edema
 Orthopnea
 Atrial fibrillation
 Ortner syndrome
 Short A2-OS interval
 Long duration of diastolic murmur

Laboratory examination
Electrocardiography (ECG)
Left atrial enlargement
Mitral valve P wave
P-wave duration in lead II ＞ 0.12 s
Large terminal negative P force in lead V1
Right ventricular hypertrophy
Arrhythmia
Premature atrial contraction → atrial fibrillation

Radiological findings
“Mitral valve heart”
Marked enlargement of LA
Enlargement of RV
Dilatation of PA
Pulmonary congestion
Interstitial edema (manifested as Kerley B lines)

Echocardiography
The most valuable technique for diagnosing MS,
and determining its severity
M-mode echoM-mode echo ：：
Thickened, calcified leaflets
open poorly, close slowly (EF slope↓)
The double peaks disappear
Both leaflets move anteriorly during early diastole
Two-dimensional echo:Two-dimensional echo:
Fusion, thickening, doming of the valve leaflets, and poor
leaflet separation in diastole; mitral orifice area↓
Eur J Echocardiogr. 2009;10:1-25.

Mitral stenosis
Moderate MS
Severe MS

Hemodynamic changes
MS involves mainly LA and RV
1. Effect of MS on left atrioventricular pressure
gradient and left atrial pressure (LAP)
MVA transvalvular gradient LAP
Normal 4 ～ 6cm2
Mild MS ＞ 1.5cm2
<5 mmHg ↑
Moderate 1.0 ～ 1.5cm2
5-10mmHg ↑↑
Severe ＜ 1.0cm2
≥10mmHg 25mmHg

Doppler echoDoppler echo ：：
Most accurate noninvasive technique for quantifying the
severity of MS
Spectrum Doppler: measure transvalvular gradient, MVA
Color Doppler: display high velocity color jet
Provide other important information
Cardiac chamber size (LA, RV)
Left ventricular contractility
Pulmonary arterial pressure
Other coexisted valvular or congenital abnormalities
Mural thrombi

Cardiac catheterization
Its value in assessment of patients with MS or
suspected MS has been largely superseded by
echocardiography
If surgery is planned, coronary angiography is
performed to ascertain whether or not bypass grafting
is indicated in patients at risk of having coexisting
coronary artery disease

2014 AHA/ACC Valvular Heart Disease
Guidelines
J Am Coll Cardiol. March 2014.Online first.

Mitral regurgitation (MR)
Etiology
Mitral valve apparatus and/or LV structural and
functional abnormality
RHD: common(1/3); + MS and/ or aortic valve disease
Mitral valve prolapse (MVP)
myxomatous degeneration, floppy and redundancy
Ischemic heart disease (or CAD)
papillary muscle dysfunction
Mitral annular calcification

Severe dilatation of LV
result in dilatation of the mitral annulus and
lateral movement of papillary muscle
Infective endocarditis
valve leaflets destruction, perforation, retraction;
valve closure interfered by vegetation
Other causes:
Rupture of the chordae
congenital abnormalities
obstructive hypertrophic cardiomyopathy

Hemodynamic changes
MR involves mainly LA and LV
Chronic MR
Compensation: MR→ LV volume↑→LV, LA↑→
LVEDV↑→ SV↑→ CO↑, EF↑
Decompensation:
Left HF, LAP and LVEDP↑ → pulmonary congestion,
pulmonary hypertension, right HF
(hepatomegaly, edema, and ascites)
CO↓
Acute MR
MR →LA, LV volume↑→LVEDP↑→LAP↑→
↓ pulmonary congestion, pulmonary edema
SV and CO↓

Clinical manifestations
Symptoms
Chronic MR
Mild— no symptom
Severe— left-sided heart failure
Weakness, fatigue (CO↓)
Dyspnea (pulmonary congestion)
RHD: symptoms occur late, once present, LV
dysfunction is usually irreversible
MVP: asymptomatic, or atypical chest pain,
palpitation, fatigue; in severe MR, left
HF occur at late stage
Acute Mild— mild exertional dyspnea
Severe— acute left HF, pulmonary edema,
or cardiac shock
Circulation. 2003;108:2432-2438.

Physical examination
Cardiac impulse at apex
Hyperdynamic
Displaced laterally, inferiorly (Chronic)
Changes of heart sounds
S1↓(RHD) or normal (MVP, CAD)
S3 (severe MR): prominent
Mid or late systolic click （ MVP ）
（ Acute: P2↑ ， S4 ）
Circulation. 2003;108:2432-2438.

Systolic murmur
RHD ： Pansystolic, blowing, high-pitched murmurPansystolic, blowing, high-pitched murmur
maximal at the apex
Anterior valve lesion, radiate to the axilla and back
Posterior leaflet abnormality, radiate to the base
MVP ： mid- to late-systolic murmur
Dysfunction of papillary muscles:
Variable (early, mid, late or holosystolic)
Rupture of the chordae: musical
(Acute MR: not pansystolic murmur, but lower-pitched,
decrescendo, and softer than the murmur of chronic MR)
Circulation. 2003;108:2432-2438.

Severe MR
 Hyperdynamic LV type apex
 Systolic thrill over apex
 S3
 Functional flow mid diastolic murmur
Circulation. 2003;108:2432-2438.

ECG
Chronic (severe) MR:
LA dilation, Atrial fibrillation
LV enlargement and non-specific ST-T changes
Acute MR: sinus tachycardia
Chronic (severe) MR:
Cardiomegaly with LA, LV↑; pulmonary congestion,
interstitial edema with Kerley B lines (left HF)
C-shaped calcification of mitral annulus
Acute MR:
Normal cardiac silhouette or mild LA dilation
overt pulmonary congestion, edema

Echocardiography
1 、 Display anatomy of the mitral valve apparatus
Useful in determining the etiology of MR (2D)
2 、 Confirm the existence of MR
Doppler (color, spectrum): reveal high-velocity jet into LA
during systole
Sensitivity~100%
Estimate the severity of MR
＜ 4 cm2 Mild
（ Color flow jet area ） 4~8 cm2 Moderate
＞ 8 cm2 Severe
3 、 Measure cardiac chamber sizes, evaluate LV
function, pulmonary artery pressure, provide data
concerning other valvular lesions

Calculating (PISA)
 Apical 4Ch view
 Narrow sector width
 Minimise depth
 Zoom
 Adjust Colour Doppler
alaising velocity (20-40
cm/s)

PISA
 Measure the radius of the
hemisphere. (red/blue
interface)
– PISA radius =2πr2
(cm2
)
• Mild MR: <0.4
• Severe MR:>1.0

Colour Doppler Indicators of Mitral
Regurgitation Severity
Mild Moderate Severe
Colour Doppler
Jet area (cm2
) Nyquist
50-60cm/s
<4 >10
Ratio of jet area to left
atrial area (%)
<20 >40
Vena contracta width
(cm)
<0.3 >0.7
PISA radius (cm) at
Nyquist 40cm/s
<0.4 >1.0

Continuous wave and Pulse wave Doppler
 Continuous wave spectral
Strength
– Apical 4Ch view CW of
regurgitant jet
• Faint in mild mitral
regurgitation
• Denser in moderate
and severe
regurgitation.

Peak Mitral Valve E velocity
 Increased mitral valve E
velocity (>1.2m/s) may
indicate significant
regurgitation.
– Assumes ejection
fraction is>40%)
 Decreased mitral valve DT
(<150msec) may indicate
significant regurgitation.
– Assumes normal
diastolic LV function.

Pulmonary Vein Systolic Flow Reversal
 PW doppler 1cm into the
pulmonary veins
– Systolic S (systolic)
wave is normally larger
than the D (diastolic)
wave.
– If D wave is larger there
is blunting of forward
flow.
– S wave inversion
demonstrates systolic
flow reversal (indicative
of severe MR).

Limitation
 Eccentric jets may affect
pulmonary vein flow

Determination of Pulmonary Artery
Pressures at Rest and Exercise

Multimodality Indicators of Mitral
Regurgitation Severity
Mild Moderate Severe
Multimodality
Regurgitant volume
(mL/beat)
<30 30-59 >60
Regurgitant fraction
(%)
<30 30-49 >50
Effective regurgitant
orifice area (cm2
)
<0.20 0.20-0.39 >0.40

Regurgitant Volume, Regurgitant Fraction
and ERO
 Regurgitant volume
 Step 1
– A4ch view measure
diameter of the mitral
annulus.
• CSAMV=0.785 X
(mitral annulus
diameter)2

Regurgitant volume
 Step 2
– Apical 4Ch view measure
the VTI of the mitral inflow
(using PWD)
– Commonly at valve tip
level.
• VTIMV in cm
 Step 3. Stroke Volume
– SVMV(mL/beat) =CSAMV X
VTIMV

Regurgitant volume
 Step 4
– In PLAx measure the
diameter of the LVOT
(cm).
– Calculate CSA of the
LVOT (cm2
)
• CSALVOT = 0.785 x (LVOT
diameter)2

Regurgitant volume
 Step 5
– In the Ap5 Ch view
measure the VTI of the
LVOT outflow (using
PWD)
• VTILVOT (cm)
 Step 6. Stroke volume
– SVLVOT = CSALVOT x VTILVOT

Regurgitant Volume/Fraction
 Step 6
– Mitral regurgitant volume (RV)(mL)
• RV =SVMV – SVLVOT
– Mild MR:<30 Mod MR:31-59
– Severe MR:>60
 Step 7
– Mitral regurgitant Fraction (MF)(cm2
)
• RF = RV / SVMV (x100)
– Mild MR:<30 Mod MR:31-49
– Severe MR:>50

Regurgitant orifice area
 Step 8
– Measure the VTI of the
mitral regurgitation
VTIMR (cm) (using CWD)
– Calculate Regurgitant
Orifice Area (ROA) in
cm2
• ROA = RV / VTIMR
– Mild MR:<0.20
– Mod MR:0.21-0.39
– Severe MR:>0.40

Regurgitant Orifice Area
PISA method
 Step 1. Measure the radius
of the hemisphere.
(red/blue interface)
– PISA =2πr2
(cm2
)
– Calculate regurgitant
flow rate
– RFR mL/s =PISA X
aliasing velocity

Regurgitant orifice area
 Step 2. CWD of the mitral
regurgitation. Measure peak
velocity (VMR) in cm/s.
 Calculate Regurgitant
Orifice Area in cm2
.
– ROA =Regurgitant flow
rate / VMR

Common pitfalls
 Measuring regurgitant jet area or VC width on colour
doppler with inappropriate colour gain settings
 Underestimating severity of eccentric jets on CFD.
 Failure to align the doppler beam with regurgitant flow
during CW doppler interrogation.
 Inaccurate measurement of mitral valve orifice area or
LVOT diameter when calculating RV.
 Trying to calculate RV when there is coexistant aortic
regurgitation.
 Failure to average several readings when the patient is in
AF.

Radionuclide angiography and MRI
Evaluate LV function
Estimate the severity of regurgitation
The regurgitant fraction can be estimated from
the ratio of LV to RV (LV/RV) stroke volume
Confirm the diagnosis of MR and estimate
its severity, evaluate cardiac function and
pulmonary artery pressure
Coronary angiography is performed to
determine presence of CAD prior to surgery

Aortic stenosis (AS)
Etiology
RHD
Common, + AR and mitral valve disease
Degenerative calcific AS
Common in the elderly, accompanied by calcification of
the mitral annulus
Congenital abnormalities
Calcific stenosis of congenitally bicuspid aortic valve
Congenital aortic stenosis

Hemodynamic changes
Normal aortic orifice area (AOA): 3.0~4.0 cm2
AOA ≤1.0cm2, LVSP↑, with significant transvalvular gradient
Compensation
AS→LV pressure load↑
Concentric LVH→compliance↓→LVEDP↑→LAH
Maintain systolic wall stress and CO ↑LVEDV
Decompensation
LVEDV↑→wall stress↑, myocardial ischemia, fibrosis →
left HF

Classic symptom triad
 Dyspnea
 Angina
 Syncope

Classic symptom triad
 Once any of these classic symptoms develop,
prognosis dramatically worsens.
 Thus, within 5 years of the development of angina,
approximately 50% of patients will die unless aortic
valve replacement is performed.
 For syncope, 50% survival is 3 years
 For congestive heart failure, 50% survival is only 2
years unless the valve is replaced.
 Angina 5yrs, Syncope 3yrs, and CHF 2yrs.

Severe AS
 Triad of angina,dyspnoea and syncope
 Heaving apex
 Slow rising small volume pulse
 Reverse splitting of S2
 Long duration of systolic murmur
 Late peaking of murmur
 Presence of S4

ECG
Severe: LVH and secondary ST-T changes,
LA↑ ， arrhythmias
Normal size or slightly enlarged heart
Calcification of the aortic valve
Poststenotic dilatation of the ascending aorta
Pulmonary congestion

Echocardiography
Establish a diagnosis, and determine the severity
of AS
M-mode and 2D echo
Observe aortic valve opening, thickening and
calcification
Helpful in determining the etiology of AS
Also invaluable in detecting associated mitral
valve disease and in assessing LV performance,
hypertrophy, and dilatation

Doppler echo
Allows calculation of the aortic valve gradient
Estimate the severity of the stenosis
＜ 20 mmHg Mild AS
MPG 20~40 mmHg Moderate AS
＞ 40 mmHg Severe AS
Color Doppler flow imaging is helpful in the
detection and determination of the severity of any
accompanying aortic regurgitation

Enriquez-Sarano, M. et al. N Engl J Med 2004;351:1539-1546
Jet of Aortic Regurgitation, as Shown by Color-Flow Imaging

Classification of the Severity of Aortic Regurgitation

Quantitation of Aortic Regurgitation by the Convergence of the Proximal Flow

Determine the severity of AS by measuring systolic
LV and aortic pressure simultaneously, and
calculating the valve area
An average pressure gradient of ＞ 40mmHg or
peak pressure gradient of ≥ 70mmHg represent
severe AS
Coronary angiography is performed in most adults
to assess for concomitant coronary disease

Cath data
 “Pull back” tracing can be used in pt with NSR but not
accurate in irregular rhythms or low-out put states.
 In low cardiac output, the stenosis may be severe, with a
mean gradient <50mm Hg per echo.
 Gorlin equation can be used to calculate AVA from
pressure gradients, independent of CO.
 AVA= (1000)(CO)
(44)(SEP)(HR)(√∆P)

Aortic regurgitation (AR)
Etiology
Primary disease of the aortic valves
and/ or aortic root

Aortic valve disease
① RHD ： most common, about 2/3
+ AS and/or mitral valve disease
② Infective endocarditis
③ Congenital deformity: bicuspid valves
④ Myxomatous degeneration of the aortic valve
Aortic root dilatation
① Marfan syndrome
② Aortic dissection (involve annulus or leaflets)
③ Syphilitic aortitis
Clinical practice: aortic regurgitation. N
Engl J Med. 2004;351:1539-1546.

Valvular Abnormalities leading to AR
Nodular Rheumatic Disease Aortic Root Dilation
Endocarditis

Hemodynamic changes
Chronic AR
Compensation ：
AR→LV volume↑→ LV↑, LVEDV↑→ SV↑(CO)
Decompensation:
LV systolic dysfunction→ LV failure (EF↓, LVESV↑)
Acute AR
AR →LV volume↑→ LVDP↑→ LAP↑
↓ ↓
CO↓ pulmonary congestion
pulmonary edema
Engl J Med. 2004;351:1539-1546.

Clinical manifestations
Symptoms
Chronic AR
Asymptomatic for many years
Palpitation, precordial discomfort, head pounding
(related to SV↑)
LV failure (dyspnea, fatigue): occur at late stage
Angina pectoris or chest pain: less common
Acute AR
mild—no symptom
severe—Acute LV failure and hypotension
(pulmonary edema)
Engl J Med. 2004;351:1539-1546.

Physical examination
Chronic, severe AR
① Peripheral arterial signs: Owing to wide pulse pressure:
SBP↑, DBP↓
Water-hammer pulseWater-hammer pulse (rapid rise and fall)
“Pistol shot soundsPistol shot sounds” (booming systolic & diastolic sounds
heard over femoral artery)
Duroziez’s signDuroziez’s sign (systolic, diastolic murmur over partially
compressed femoral artery)
Quincke’s signQuincke’s sign (subungual capillary pulsations)
de Musset’s signde Musset’s sign (head bobs with each heartbeat )
② Apical impulse: diffuse and forceful, displaced laterally and
inferiorly (hyperactive, enlarged LV)
③ Heart sound: An S3 gallop is common with LV failure
Engl J Med. 2004;351:1539-1546.

④ Heart murmurs
Aortic diastolic murmur:Aortic diastolic murmur:
High-pitched, blowing, decrescendo pattern
When AR is due to primary valvular disease, the diastolic
murmur is best heard along the left sternal border in the
3rd and 4th intercostal spaces
However, when it is due mainly to dilatation of the ascending
aorta, the murmur is often more readily audible along the
right upper sternal border
Austin-Flint murmur:
apical mid or late diastolic low-pitched murmur:
common in severe AR, owing to partial closure of MV by
the regurgitant jet
Circulation. 2005;112(1):125-134.

Ejection systolic murmur:
common
harsh
at the base of the heart
accompanied by a systolic thrill
Acute AR
S1 soft or absent ， P2↑ ， S3 and S4
AR murmur: lower pitched and shorter than
that of chronic AR
Austin-Flint murmur: brief
Circulation. 2005;112(1):125-134.

ECG
Acute: sinus tachycardia; nonspecific ST-T changes
Chronic: LV enlargement and hypertrophy, arrhythmias
Circulation. 2005;112(1):125-134.

Acute AR: cardiac size normal or slightly enlarge,signs of pulmonary congestion,
pulmonary edema
Chronic: LV enlargement, associated with dilatation of the ascending aorta
Severe, aneurysmal dilatation of the aorta suggests aortic root disease
Marfan syndrome)
Pulmonary congestion （ LV heart failure ）
Chronic Acute
LVE with normal pulmonary
vasculature
Normal size LV with pulmonary
vascular congestion

Echocardiography
Confirm diagnosis, estimate severity, identify the cause
2-D echo:
Structural changes of the valve leaflets and/or aortic root
M mode echo:
Diastolic fluttering of the anterior leaflet of the mitral
valve is an important echocardiographic finding in AR
Serial assessments of LV size and function
Doppler echo:
Sensitive, accurate noninvasive technique for detecting AR
LVOT diastolic regurgitant jet, estimate the severity of AR
Quantify the severity of AR
Evaluate the coronary and aortic root anatomy
J Am Soc Echocardiogr.2003;16:777-802.

AMVL fluttering
Color Flow – top mild, bottom moderate

Regurgitant jet width/LVOT diameter ratio greater
than or equal to 60 percent

Vena contracta greater than 6 mm

Regurgitant jet area/LVOT area ratio greater than
or equal to 60 percent

Holodiastolic flow reversal in the descending
thoracic or abdominal aorta

vitrag24-www.medicalgeek.com
Assessing Severity of AR
 Assess severity by impact on peripheral signs and LV-
 Duration of murmur >2/3 of diastole
 Bisferiens pulse
 Hills sign>60 mmHg
 Apical impulse down & out
 Austin flint murmur
 Marked peripheral sign
Circulation. 2005;112(1):125-134.

Features AS > AR AR > AS
Symptoms:
Anginal pain, blackout
Palpitation
+++
+
+
+++
Pulse Low volume
Bisferians pulse
High volume
Corrigan’s pulse
Pulse pressure Normal to low Wide
Peripheral signs +/- +
Apex Heaving Hyperdynamic
Thril Always systolic Rarely
S3 Absent May be present
S4 May be present Absent
Ejection click Present Rare
Diastolic murmur Very short Classic murmur of AR
Systolic murmur Classic murmur of AS Function systolic murmur
+/-
Chest X-Ray Calcification + Cardiomegaly
ECG Pressure overload Volume overload

Tricuspid stenosis
 Uncommom valvular lesion
 Rheumatic heart disease
 Congenital TS
 Carcinoid syndrome

Severe TS
 Giant a wave in JVP
 Duration of diastolic murmur over tricuspid
valve
 Signs of right heart failure
N Engl J Med. 1997;337:32-41.

 ECG-
 Absence of evidence of RVH
 Right atrial abnormality
 Chest X ray
 Prominence of right atrium and SVC
N Engl J Med. 1997;337:32-41.

Tricuspid regurgitation
 Primary disorders of the tricuspid apparatus
 Rheumatic disease
 Prolapse
 Congenital disease (Ebstein’s)
 IE
 Radiation
 Carcinoid
 Blunt chest wall trauma
 RV endomyocardial biopsy related trauma
 Intra-annular RV pacemaker or implantable cardioverter-
defibrillator leads.
N Engl J Med. 1997;337:32-41.

 Approximately 80% of cases of significant TR are
functional in nature and related to tricuspid
annular dilation and leaflet tethering in the setting
of RV remodeling due to pressure and/or volume
overload.

Pulmonary stenosis
 Pulmonic stenosis is essentially a congenital
disorder.
 Less common etiologies include carcinoid
and obstructing vegetations or tumors.
 Assessment with TTE alone is usually
sufficient for diagnosis and clinical decision
making.
N Engl J Med. 1997;337:32-41.

Pulmonary regurgitation
 Mild-to-moderate PR seen on echocardiography is
common and does not require further follow-up or
intervention if asymptomatic with normal RV size and
function.
 Significant PR in patients is uncommon.
 Primary PR that follows in the wake of childhood surgery
for tetralogy of Fallot or other congenital lesions may
progress insidiously

 We urgently need research on almost every aspect of VHD
to ensure that patients who already have VHD receive
optimal therapy and to prevent VHD in those at risk.
 Approaches to improving outcomes in patients with VHD
include –
1) National and international registries and RCTs
2) Continuous evaluation of outcomes data at each Heart
Valve Center of Excellence
3) Focus on patient-centric care with involvement of the
patient in the decision-making process.

Valvular heart disease assessment of lesion severity

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