Valvular Regurgitation

Valvular Regurgitation

Susan A. Raaymakers, MPAS, PA-C, RDCS (AE)(PE)Assistant Professor of Physician Assistant Studies

Radiologic and Imaging Sciences - EchocardiographyGrand Valley State University, Grand Rapids, Michigan

[email protected]

Basic Principles

EtiologyCongenital Acquired abnormalities

Fluid Dynamics of Regurgitation

CharacterizedRegurgitant orifice areaHigh-velocity regurgitant jetProximal flow convergence areaDownstream flow disturbanceIncreased antegrade flow volume

Fluid Dynamics of RegurgitationRegurgitant orificecharacterized by high-velocity laminar

jet Related to instantaneous pressure

difference (∆P=4v2)

Upstream side of regurgitant acceleration proximal to regurgitant orifice PISA

Narrowest segment of the regurgitant jet occurs just distal to the regurgitant orifice reflects regurgitant orifice area Vena Contracta


Size, Shape and Direction of Regurgitant JetSize

Affected by physiologic and technical factorsRegurgitant volumeDriving pressureSize and shape of regurgitant orificeReceiving chamber constraintInfluence of coexisting jets or flowstreamsUltrasound system gainDepth Signal strength


Size, Shape and Direction of Regurgitant JetShape and Directions

Affected byAnatomy and orientation of regurgitant orificeDriving force across the valveSize and compliance of receiving chamber

Volume Overload

Total Stroke Volume Total volume of blood pumped by the ventricle in a single beat

Forward Stroke Volume Amount of blood delivered to the peripheral circulation

Regurgitant Volume Amount of backflow across the abnormal valve

Volume Overload

Chronic valvular regurgitationResults in progressive volume overload

of the ventricleVolume overload in LV results in LV

chamber enlargement with normal wall thickness (total LV mass is increased)Important clinical feature:

• An irreversible decrease in systolic function can occur in absence of symptoms

Detection of Valvular Regurgitation2D imaging

Indirect evidenceChamber dilation and function

Color flow imaging Flow disturbance downstream form regurgitant orifice Sensitive (90%) when correct settings are utilized Specific (nearly 100%) compared with angiography True positives and false positives

False positives due to mistaken origin or timingFalse negatives due to low signal strength or

inadequate images

Detection of Valvular RegurgitationContinuous-wave Doppler ultrasound

Identification of high velocity jet through regurgitant orifice

Advantage: Beam width is broad at the level of the valves

when studied from an apical approach

Valvular Regurgitation in Normal IndividualsPhysiologic

Small degree of regurgitation in normal individuals

No adverse implicationsTypically

Spatially restricted to area immediately adjacent to valve closure

Short in durationRepresents on a small regurgitant volumeMay be detected in 70 – 80% mitralMay be detected in 80 – 90% tricuspidMay be detected in 70 – 80% pulmonaryMay be detected in 5% aortic (increases with

age). • Clinical significance of AI is unknown

Approaches to Evaluation of the Severity of Regurgitation

Semi-quantitative measuresMild, moderate or severe utilizing

Color jet areaVena contracta widthPressure half-time (for aortic insufficiency)Distal flow reversals

Approaches to Evaluation of the Severity of Regurgitation

Quantitative measuresRegurgitant volume (RV)

Retrograde volume flow across the valveExpressed either as

• Instantaneous flow rate in ml/sec

• Averaged over the cardiac cycle in ml/beat

Calculated by• PISA

• Volume flow rates across the regurgitant and competent valve (Spectral Doppler Technique)

• 2D total left ventricular stroke volume minus Doppler forward stroke volume

Regurgitant fractionRF = RV/SV total

Regurgitant orifice area

Effective Regurgitant Orifice Area (EROA)

Application of continuity equation“what flows in must flow out”

Based on theory of conservation of mass

May be calculated utilizing Spectral Doppler techniqueApplication of the PISA method

Spectral Doppler Method

Spectral Doppler TechniqueRegurgitant volume through an incompetent valve is

equal to the flow at the regurgitant orifice Stroke volume may be calculated from the CSA and the VTI

RVol = EROA x VTIRJ RVol = Regurgitant volume (cc) EROA = Effective regurgitant orifice area (EROA) VTIRJ = Velocity time integral of the regurgitant jet (cm)

Rearrange equationEROA = RVOL/VTIRJ

Non-dynamic

Spectral Doppler Technique“Step by Step”

1. Calculate stroke volume (SV) through LVOT

2. Calculate stroke volume (SV) through MV

3. Calculate the regurgitant volume (cc)

4. Measurement of VTI of regurgitant signal

5. Calculate the effective regurgitant area (cm2)

Non-dynamic


1. Calculate stroke volume (SV) through LVOT Measure LVOT diameter from PLAX

Inner edge to inner edge CSA = 0.785 x D2

Measure the LVOT VTI from apical long axis or apical four chamber anterior tilt SV (cc) = CSA (cm2) * VTI (cm)


2. Calculate the stroke volume through the mitral valve Measure the mitral valve annulus

Apical four chamber at mid-diastole: inner edge to inner edge CSA = 0.785 x D2

Measure mitral annulus VTI PW Doppler at the level of the annulus

SV (cc) = CSA (cm2) * VTI (cm)


3. Calculate the regurgitant volume R Vol(MR) = SV (MV) – SV (LVOT)

4. Measurement of VTI of regurgitant signal Optimize CW Doppler spectrum of regurgitant signal


5. Calculate the effective regurgitant orifice area (EROA in cm2)

EROA = RVol(MR) ÷ VTI(MR)

Spectral Doppler TechniqueLimitations

Accuracy of measurements Inadequate spectral Doppler envelope for mitral

regurgitation VTI measurement

Significant learning curve May be considered time consuming and tedious

Spectral Doppler TechniqueClinical Significance of the EROA and Mitral Regurgitation

Color Doppler Imaging

Jet Area Screening for significant flow often based on flow

disturbance in receiving chamber Size of flow disturbance evaluated in at least two

views Important to evaluate color flow disturbance based on

cardiac cycle timing Size of jet relative to receiving chamber provides

qualitative index of regurgitant severity on scale of 0(mild) - 4+(severe)



Aortic Regurgitation Best evaluated from PLAX approach

Shorter distance from transducer to flow region of interest: better signal to noise ratio

Multiple flow directions within jet

Color Doppler Imaging - Mmode

Evaluation of exact timing of flow

In relation to QRS and valve opening and closure

Higher sampling rate

Vena Contracta

Narrowest diameter of the flow stream Reflects diameter of regurgitant orifice Relatively unaffected by instrument settings Recommended

Perpendicular to jet width Zoom mode Narrow sector and depth

Non-dynamic

Proximal Isovelocity Surface Area Method (PISA)

Proximal Isovelocity Surface AreaBasic Principle

Based on conservation of energy PISA measurement analogous to calculation of

stroke volume proximal to a stenotic valve Variation of continuity equation

Flow rate proximal to a narrowed orifice is the product of the hemispheric flow convergent area and the velocity of that isovelocity shells Expressed by Q = 2r2Vr

Q = flow rate2r2 = area of hemispheric shell (cm2)Vr = velocity at the radial distance –

r(cm/s) Non-dynamic


Continuity principle: blood flow passing through a given hemisphere must ultimately pass through he narrowed orifice

Flow rate through any given hemisphere must equal the flow rate through the narrowed orifice

2r2Vr = A0*V0

• A0 = area of the narrowed orifice (cm2)• V0 = peak velocity through the narrowed

orifice (cm/s)

Rearrange the equation• A0 = (2r2Vr )/V0 Non-dynamic


Continuity principle: blood flow passing through a given hemisphere must ultimately pass through he narrowed orifice

Flow rate through any given hemisphere must equal the flow rate through the narrowed orifice

2r2Vr = A0*V0

• A0 = area of the narrowed orifice (cm2)• V0 = peak velocity through the narrowed orifice (cm/s)

Rearrange the equation• A0 = (2r2Vr )/V0

Proximal Isovelocity Surface Area(PISA) Application in Calculation of Effective Orifice Area (EROA)

Regurgitant valve acts as the narrowed orifice

Peak velocity is equivalent to the peak velocity of the regurgitant jet

Utilizing Doppler colorflow radius and velocity at the radial distance can be identified

Proximal Isovelocity Surface Area(PISA) Application in Calculation of Effective Orifice Area (EROA)

Adjustment of Nyquist limit enlarges size of shell for more accurate measurement Shift baseline to downward typically 20 to 40 cm/sec

The surface area of a hemisphere is calculated by the formula: Surface area = 2πr2

Multiplication of aliasing velocity with surface area yields regurgitant volume

Non-dynamic

Proximal Isovelocity Surface Area

Effective Regurgitant Orifice Area (ROA) EROA = RVmax /VMR

RVmax : Regurgitant Volume (cm3)

VMR : Velocity of mitral regurgitation (cm/sec)

Non-dynamic

Steps for Obtaining PISA Regurgitant Orifice Area

1. Zoom mitral valve

2. Decrease color scale to identify surface of hemisphere shell

3. Note alias velocity – color bar (Valiasing)

4. Measure alias from orifice to color change (r)

5. Regurgitant volume RVmax = 2 r2 x Valiasing

6. Measure peak mitral regurgitant velocity (VMR)

7. Effective Regurgitant Orifice Area EROA = RVmax/VMR

Steps for Obtaining PISA Regurgitant Orifice Area

Surface area = 2r2

2(0.67 cm)2 = 2.80 cm2

Regurgitant Volume Flow Rate

RVmax=Surface Area* Valiasing

2.80 cm2 * 26 cm/sec = 72.8 cm3/sec

Effective Regurgitant Orifice AreaEROA = RVmax/VMR

(72.8 cm3/sec) / (66.2 cm/sec) = 1.1 cm2

0.67cm

Simplified Method for Calculation of the Mitral Regurgitant Volume

May be employed when appropriate CW jet is unable to be obtained (i.e. eccentric jet)

Based on premise: Ratio of maximum MR velocity to VTI MR is equal to a

constant of 3.25

Regurgitant volume = (2r2Valiasing)/3.25 2r2 = area of hemispheric shell derived from the radius [r] (cm2)

Valiasing = aliased velocity identified as the Nyquist limit (cm/s)

3.25 constant

Clinical Significance of the PISA Radius and Valvular Regurgitation

Proximal Isovelocity Surface Area – EROA MV Considerations

Assumption is made that RVmax and VMR occur at the same position in the cardiac cycle

PISA is larger in large volume sets and smaller in smaller volume sets Also changes size in accordance with color Doppler scale

PISA should be recorded in a view parallel to flow stream typical apical four chamber

If PISA is hemi-elliptical or if valve is nonplanar, alternate approach or alternate corrections

PISA Limitations

Nonoptimal flow convergence

Phasic changes

Eccentric jets

Interobserver variability

Isovelocity surface not always hemisphere

PISA model is a sphere. Mitral regurgitant orifice may be irregular

Multiple regurgitant jets

May not be able to completely envelope the mitral regurgitation trace

Mitral flow rate will vary throughout systole

PISA – EROALimitations

Nonoptimal flow convergence

Suboptimal Flow Convergence

Flow: not symmetric

Suboptimal Flow Convergence

Perforated mitral leaflet - TEE

Continuous Wave Doppler Approach

Signal intensityProportional to number of

blood cells contributing to regurgitant signal

Compare retrograde to antegrade flow intensityWeak signal = mild regurgitationStrong signal = severe

regurgitationIntermediate signal = moderate

regurgitation


Antegrade flow velocityRegurgitation results in increase in antegrade

flow across the incompetent valveGreater the severity of regurgitation; the greater the

antegrade flow velocity• Consideration of co-existent stenosis


Time course (shape) of mitral regurgitant velocity curveDependent on time-varying pressure gradient

across regurgitant orificeRelated to pressure gradient

Normal LV systolic pressure = 100 – 140 mmHgNormal LA systolic pressure = 5 – 15 mmHgDifference therefore: 85 – 135 mmHg

• MR velocity is typically 5 – 6 m/sec

Continuous Wave Doppler ApproachTime course (shape) of

mitral regurgitant velocity curve

Normal LV systolic function: • Rapid acceleration to peak

velocity• Maintenance of high velocity in

systole• Rapid deceleration prior to

diastolic opening of the mitral valve

Increase in left atrial pressure results in late systolic decline in the instantaneous pressure gradient

Continuous Wave Doppler ApproachShape of aortic regurgitant curve

Dependent on time course of diastolic pressure difference

Normal low end-diastolic pressureAortic end-diastolic pressure is

normal (high pressure difference)Slow rate of pressure declineAcute AI results in more rapid velocity

decline in diastole

Continuous wave Doppler across AV

Decel = 270 cm/sec

Decel >500 cm/sec

With permission, Dunitz 2000

Distal Flow Reversals

Severe atrioventricular valve regurgitation may result inFlow reversal of veins entering atrium

Flow reversal in hepatic vein due to severe tricuspid regurgitation

Flow reversal in pulmonary veins on TEE due to severe mitral regurgitation

Distal Flow ReversalsSevere semilunar valve regurgitation

may result inFlow reversal of associated vessel

Abdominal flow reversal in diastole due to severe aortic regurgitation. Note moderate aortic regurgitation is limited to descending thoracic aorta

Aortic Regurgitation

Aortic ValveDiastole: free margins of the cusps coapt

tightly preventing the backflow of blood into the ventricle. “Y” shape in PSAX (sometimes referred to as

inverted Mercedes-Benz sign)

Systole: cusps open widely in a triangular fashion, with flexion occurring at the base.

Semi-lunar valve

Aortic Cusps

Three Cusps named for the corresponding origins of the coronary arteries.

Folds of endocardium with a fibrous core attached to the aortic wall rather than the ventricular wall.

Base of the cusps is thicker and cusps themselves are thin and translucent.

Crescent and pocket shaped.

Equal in size.

Aortic Cusps

Free edge of each cusp curves upward from commissure and form a slight thickening at tip called Arantius nodule.

When valve closes: three nodes meet in center, allowing coaptation to occur

along three lines. “Y” shape in diastole.

Behind each cusp is its associated Sinus of Valsalva.

Aortic Cusps

Sinotubular junction

Sinus of Valsalva

Sinuses represent out-pouchings in the aortic root directly behind each cusps.

Function to support the cusps during systole and provide reservoir of blood to augment coronary artery flow during diastole.

Sinus and its corresponding cusp share the same name.

Noncoronary sinus is posterior and rightward just above the base of the interatrial septum.

M-mode Normal AV – Coaptation Point In Center Of Aortic Root

Parasternal Views

Apical views

Aortic valve in the far fieldPoor resolution of anatomic details

PARALLEL to flowBest view for measuring velocities across valve

AR jet

AS jet

Subcostal view

Often the view that “saves” the studyNon-coronary cusp is intersected by the

interatrial septum

Short axis Subcostal view - Non-coronary cusp intersected by

Interatrial septum

TEE views

Anterior root is at the bottom of the screen (reverse parasternal LAX view)

Leaflet at top of screen usually non-coronary (can be left coronary cusp)

Leaflet at bottom of screen is right coronary cusp

TEE - 137º

Non-dynamic

Aortic Cusps – Lambl’s Excrescences

Thin, delicate filamentous strands that arise from ventricular edge of aortic cusps.

Normal variants.

Seen increasingly with advancing age and improved image quality.

Aortic Cusps – Lambl’s Excrescences

Originate as small thrombi on endocardial surfaces

Have the potential to embolize to distant organs

10-56 Feigenbaum 21-9 Lambl TEE Feigenbaum

Aortic Insufficiency

Presence of AI should be assessed by Doppler

Flail AV leaflet will always produce AI

Direction of regurgitant jet may or may not produce MV or septal fluttering

Use TEE of abscess detection

Aortic RegurgitationHistory Exertional dyspnea

Fatigue

Palpitations

Chest pain (angina)

Dizziness

Syncope (uncommon)

Congestive Heart Failure (dyspnea on exertion, orthopnea, paroxysmal nocturnal dyspnea)

Right heart failure (e.g., jugular venous distention, hepatomegaly, peripheral edema, ascities, anasarca)

Aortic InsufficiencyComplicationsChronic AI;

Initially patients may appear asymptomatic and may later develop signs of CHF

Patients with bicuspid valve are at higher risk for endocarditis

LV volume overload (similar to MR)

Diastolic murmur at left sternal border (LSB) and apex (Austin-Flint murmurdiastolic rumble)

Acute AI; sudden onset of CHF may occur because the LA does not have time to enlarge


Etiology

• Inflammatory

• Structural

• Genetic

• Stress

Aortic Insufficiency (AI)Inflammatory

Rheumatic FeverAnkylosing SpondylitisRheumatoid ArthritisSystemic Lupus ErythematosusSyphilusPhen-fen

Aortic Insufficiency (AI)Structural

Atherosclerosis

Bicuspid or unicuspid aortic valve

Aortic dissection

Aortic valve prolapse

Infective endocarditis

Ventricular septal defect (perimembranous, outlet)

Sinus of Valvsalva aneurysm

Trauma

Catheter balloon valvuloplasty

Dilated root and effacement sinotubular junction

Non-dynamic

Preserved root - dilated ascending aorta

Non-dynamic

Aortic Valve Prolapse

Best seen in parasternal long axisDisruption of commissural support

DissectionDilatationPerimembranous VSDMyxomatous or congenitally abnormality

Aortic Valve Prolapse Right Coronary Cusp

Non-dynamic

Severe AR filling LVOT

Non-dynamic

Bicuspid Aortic Valve

10-47 Feigenbaum

Quadracusp Aortic Valve

http://video.google.com/videoplay?docid=-1101037639424512577#

Endocarditis

19-32a Feigenbaum

19-32b Feigenbaum

Rupture of Sinus of Valsalva Due to Endocarditis

13-17 Feigenbaum

Endocarditis

10.33a Feigenbaum

10.33b Feigenbaum

Aortic Dissection

Proximal extent usually 1 cm distal to sinotubular junction

Flap may extend to rootRupture into pericardial spaceDissect coronary (right > left)Disrupt AV architecture

Transthoracic very INSENSITIVE

TEE aortic dissection disrupting commissurebetween right and left coronary cusps

Non-dynamic

TEE Long Axis View – Dissection Flap In Aortic Root

Non-dynamic images

Marfan’s SyndromeConnective tissue multisystemic

disorder characterized by Skeletal changes (arachnodactyly,

long limbs, joint laxity, pectus)

Cardiovascular defects Aortic aneurysm which may dissectMitral valve prolapse

Ectopia lentis

Autosomal dominant inheritance, caused by mutation in the fibrillin-1 gene (FBN1) on chromosome 15q .

Marfan’s Syndrome

Arachnodactyly in an 8-year-old girl with Marfan’s syndrome

Marfan Syndrome

20.22a Feigenbaum

20.22b Feigenbaum

Marfan’s Syndrome

10.31b Feigenbaum

Aortic Insufficiency (AI)Stress

Systemic hypertension (dilated root due to hypertension is the most common cause of AI)

Renal failure

Type A Aortic Dissection

20.30a Feigenbaum

20.30b Feigenbaum

“Renal” Heart

22.7 Feigenbaum

Aortic Insufficiency (AI)M-Mode, 2D Criteria and Doppler Criteria

AI - M-Mode Criteria

MV fluttering in early diastole Austin-Flint murmurDiastolic septal fluttering depends on direction of jet

Chronic AI Increased LV size with minimal LVH Normal or hyperdynamic LV systolic function In decompensated state, LV systolic function may be depressed.

Presence of “B” bump (Increased LV end diastolic pressure) associated with acute AI.

Premature AV opening in acute AI

Aortic Insufficiency2D Criteria

Valve Anatomy Flail, Bicuspid, Endocarditis, Prolapse

Chronic AI; enlarged LV cavity with minimal LVH – normal or hyperdynamic LV function unless decompensated

Ascending aorta size usually increased; identify aortic aneurysms (ascending, arch, descending)

Reverse doming of anterior mitral valve leaflets is associated with severe AI

Non-dynamic

Aortic InsufficiencyDoppler Criteria

Evidence of diastolic turbulence beginning at aortic valve closure

Patients with severe aortic insufficiency may demonstrate a reversed diastolic flow by PW Doppler in the abdominal or thoracic aorta.

Color flow mapping of flow disturbance into LV may disclose severity.

Color flow may be useful in quantitating severity based on width of flow disturbance to width of LVOT in parasternal long-axis view.

Aortic InsufficiencyDoppler Criteria

Doppler cursor is parallel to flow, “Normal” peak velocity of an aortic regurgitant jet is

3.0 to 5.0 m/sDue to the pressure difference between the aorta and LV

during diastole.

Spectral Doppler display signal intensity Should be considered in evaluating the degree of AI. Compare the forward aortic flow with the signal

strength of the AI jet.


10.5 Feigenbaum


Aortic Valve Prolapse - 2D Criteria Parasternal long-axis view: posterior placement of aortic

leaflet(s) into LVOT during diastole.

May be noted in association with MV or TV prolapse.

Right coronary cusp prolapse may occur with membranous ventricular septal defect.

M-Mode is not diagnostic; may see echo in LV outflow tract during diastole.

Sinus of Valsalva aneurysm

Non-dynamic

Aortic Insufficiency - Flail Aortic Leaflet2D Criteria

In PLAX, loss of leaflet coaptation and erratic echoes in LVOT

PSAX-Ao may disclose leaflet(s) involved. Perforations in leafletsAortic ring abscess due to endocarditis

Flail Aortic Leaflets - M-Mode Criteria

Course flutter of closed aortic leaflets during diastole.

Erratic systolic motion of closed aortic leaflet(s).

When AI is present, associated diastolic fluttering of MV and/or septum.

Enlarged LV chamber with hyperdynamic LV systolic function.

Premature closure of AV in acute AI.

Left Ventricular Response

Chronic volume overloadProgressive dilation and increased sphericity of LV Initially LV systolic function remains normal

Stroke volume is ejected across the aortic valve into the high-impedence systemic vasculature therefore not hyperdynamic

Long asymptomatic periodChronic gradual increasing AI

LV remains compliant in diastole: end-diastolic pressure remains normal

Over time LV systolic dysfunction occurs in presence of significant regurgitation

Diastole Systole

LV Dysfunction Secondary to AI

10-35 Feigenbaum

Left Ventricular Response

Acute Aortic RegurgitationShort interval from set of volume overload to clinical

presentationVolume overload is poorly tolerated due to the normal

left ventricular size and the constraining effects of the pericardium.Mitral regurgitation

Left ventricular pressure increases rapidly.

Premature closing of MV, which can be recorded using M-mode imaging.

Acute AI

Usually caused by endocarditis

Disruption or destruction of aortic leaflets

and/or aortic dissection

Annular and/or root dilation

Acute AI

Acute AI may also be caused by:

Trauma

Effect of AI on mitral valve

10.030 Feigenbaum

Severity of Aortic Regurgitation


Semi-quantitative measurementNo gold standard

Invasive measurement is qualitativeVentricular opacification following aortic root

injection with IV dye


Size of the color flow jetLength of jet dependent on ultrasound machine settings

GainPulse repetition frequencyTransmission frequency

Length of jet dependent on ventricular compliance

Severe AR - broad jet extends into LV cavity


Width of jet compared to LVOT diameterMeasured in parasternal long axis viewOr in TEE longitudinal plane

<25% - mild AR25-40% moderate>40% severe

Mild AR - jet ratio <25%

Severe AR - jet ratio >60%

Grading Aortic Regurgitation by Regurgitant Jet Area/LVOT Area (PLAX)

10.44a 10.44b 10.44c

Feigenbaum

≥ 65% Regurgitant Jet Area/LVOT Area (PLAX)

10.36 Feigenbaum

View Dependent Color Flow Doppler EvaluationBoth Images Obtained From Same Patient

10.48a Feigenbaum

10.48b Feigenbaum

Severity of Aortic Regurgitation Short axis area of regurgitation

Dependent on level of short axis imageShort axis of the LVOT, not aortic sinuses

Color M-mode

Continuous wave Doppler across AV

Deceleration slope of AR spectral envelopePressure gradient = 4 V 2

Fall in velocity during diastole related to decrease in pressure gradient

Flat slope indicates no change in gradient during diastole = mild AR

Deceleration SlopeGrading of AR (AI)

<200 cm2/sec = mild200 - 350 cm2/sec = moderate>350 cm2/sec = severe

Pressure half time also may be usedDependent on ventricular complianceEccentric jets may be difficult to assess

Diastolic Reversal of Flow

Sample volume in descending thoracic aorta from suprasternal notch

Also in abdominal aorta from subcostal position

Reversal of flow in diastole from abdominal aorta

Indications for Surgery AR

SymptomsEnd-systolic internal dimension > 55 mm

May not be applicable in women - use smaller LVIDD

Fall in ejection fractionDiastolic dimension > 70 mm associated

with sudden death

Mitral Regurgitation

Mitral Valve Apparatus

Left atrial wallMitral annulusAnterior and posterior

leafletsChordaePapillary musclesLeft ventricular

myocardium underlying the papillary muscles


Occurs during systole, which at normal heart rates constitutes approximately 1/3 of the cardiac cycle.


Hemodynamically significant mitral regurgitation results in volume overload.

Subsequent left ventricular dilation and left atrial dilation.

Consequentially there is elevation of left atrial pressure, which is transmitted in pulmonary congestion.

Mitral RegurgitationSigns and Symptoms

Shortness of breath, especially with exertion or when lying down

Fatigue, especially during times of increased activity

Cough, especially at night or when lying down Heart palpitations — sensations of a rapid,

fluttering heartbeat Swollen feet or ankles Heart murmur Excessive urination

Mitral Regurgitation- Acute

Acute severe mitral regurgitation often results in acute pulmonary congestion.

Left atrial size is normal. Left ventricular sysotolic function is hyperdynamic

Most common cause of acute MR:Rupture of chordae tendineae due to mitral valve

prolapseAcute ischemia Infarction Infective endocarditis

Mitral Regurgitation-Chronic

Chronic mitral regurgitation may be tolrated for decades

Left ventricular size is dilated, left ventricular function is hyperdynamic early, may be normal or depressed with long-standing regurgitation, enlarged LA

EtiologyMyxomatous valve diseaseAnnular dilatation

Mitral RegurgitationEtiologies

Rheumatic mitral valve diseaseMitral valve prolapseMyocardial infarction (papillary muscle dysfunction)Ruptured chordae tendineaeFlail mitral leafletMitral valve vegetationsDilated cardiomyopathiesLeft ventricular outflow tract obstructions Use of certain appetite suppressantsCalcification of the mitral annulusTumors of the mitral valveAnnular DehiscenceRadiation damage

Rheumatic Heart Disease

Non-dynamic

Mitral Valve Prolapse

Non-dynamic


11.72a-72b Feigenbaum


11.80a Feigenbaum


Ruptured Papillary Muscle Due to Coronary Artery Disease

15.44 Feigenbaum

Ruptured Chordae Tendineae

Data source : Arizona Society of Echocardiography Image Library

Standard real-time B-scan Duplex scan: color Doppler super-imposed on real-time B-scan

Diagnosis: Severe mitral regurgitation due to flail posterior MV leaflet. Underlying pathology: Mitral valve prolapse with ruptured chordae tendinae.

Flail Mitral LeafletRupture of the supporting apparatus of the mitral valve allowing the tip of the leaflet to project into the left atrium in systole

The most frequent etiologies are : Chordal rupture complicating mitral valve prolapse syndrome Infective endocarditis Papillary rupture caused by acute myocardial infarction. Primary degeneration of the chordae is a cause of spontaneous

rupture.

11.81b Feigenbaum

Flail Mitral Leaflet

Yale Atlas of Echo- Flail Mitral Valve

Mitral Valve Vegetations/Infections

Mitral Valve Vegetations/Infections

Mitral vegetations

Found on the upstream side of valves such as the left atrium in mitral valvular vegetation.


13.3a & b Feigenbaum

Dilated Cardiomyopathies

Dilated Cardiomyopathy

Hypertrophic Cardiomyopathy Idiopathic Hypertrophic Subaortic Stenosis (IHSS)

IHSS

Appetite Suppressants

Common name: Fen-Phen(fenfluramine, phentermine, dexfenfluramine)

Use of Fenfluramine or dexfenfluramine for more than four months may have an increased risk of valvular heart disease.

Fenfluramine and dexfenfluramine are no longer marketed in the U.S. as of 1997 and have no current FDA labels.

Calcification of the Mitral Annulus

Mitral annulus area normally is smaller in systole than in diastole.

Increased rigidity of the annulus impairs systolic contraction of the annulus leading to mitral regurgitation.

Appearance on 2D imaging as area of increased echogenicity on left ventricular side of annulus immediately adjacent to attachment point of the posterior leaflet.

Commonly seen in elderly subjects and in younger patients with renal failure or hypertension.

11.89 Feigenbaum

Tumor of mitral valve/Papillary Fibroelastoma

Unlike vegetations: fibroelastomas are more often found on the down stream side of the valve

Usually of no clinical significance but may cause mitral regurgitation

21.6 Feigenbaum

Annular Dehiscence

Infrequent sequela of blunt trauma.

Presumed mechanism Sudden dramatic increase in

pressure against a closed mitral valve resulting in tearing of the posterior leaflet from the mitral valve annulus

19.31b Feigenbaum

Radiation Damage

Note Pathologic echo density of

the anterior mitral leaflet

Reduced mobility of the portion of the mitral valve

Increased echo densities in the aortic valve,

Which is also a consequence of radiation therapy in these two relatively young patients.

11.095a Feigenbaum


JetsCentral

Bileaflet prolapseRheumatic disease

PeripheralVegetationsUnicuspid prolapseFlail


Color Doppler is primary tool for detection and quantification

Recognition of expected timing of regurgitation is critical.


Doppler evaluation of mitral regurgitation

Not all color Doppler signals appearing within the LA represent mitral regurgitation


Normal posterior motion of the blood pool caused by mitral valve closure.

Pulmonary Vein Flow

11.40 Feigenbaum


Reverberation from aortic flow

11.39 Feigenbaum


Characteristics of True Mitral Insufficiency/Regurgitation

Evidence of proximal flow acceleration (proximal isovelocity surface area (PISA)

Flow conforms to the appearance of a true “jet” or ejection flow with a vena contracta

Downstream (left atrial) appearance is consistent with a volume of blood being ejected through a relatively constraining orifice


Characteristics of True Mitral Insufficiency/Regurgitation (cont.)

Flow signal is appropriately confined to systole

Color Doppler signals are appropriate in color for the anticipated direction and/or reveal the appropriate variance or turbulence encoding

PW and CW Doppler confirms origin, timing and direction of blood flow


PhysiologicSpacially restricted to the area immediately

adjacent to valve closureShort in durationRepresents only a small regurgitant volumeWhen meticulously sought MR can be detected

in 70%-80%.

Determination of Mitral Regurgitation Severity

Determination of Mitral Regurgitation

Color Flow DopplerSize of the flow disturbance relative to the chamber

receiving the regurgitant jet in at least two views.Severity scale of 0(mild) to 4+(severe)Limitation: Variation with technical and physiological factors

Continuous Wave-DopplerSignal intensityShape of velocity curveLimitation: Qualitative

Vena Contract WidthWidth of regurgitant jet at originLimitation: Small values, careful measurement needed

Determination of Mitral Regurgitation…continued

PISACalculation of RV (regurgitant volume) and ROA

(regurgitant orifice area)Less accurate with eccentric jets

Volume Flow at Two SitesCalculation of RV (regurgitant volume) and ROA

(regurgitant oriface area).Limitation: Tedious

Distal Flow ReversalsPulmonary Vein reversal in DopplerLimitation: Qualitative, affected by LA pressure

Continuous Wave

Signal intensity Proportional to the number of blood cells contributing to

the regurgitant signalWeak signal reflects mild regurgitation, whereas a

signal equal to intensity to the antegrade (forward) flow reflects severe regurgitation

Time course (shape) of the velocity curveAcute MR: increase in end-systolic left atrial pressure

results in last-systolic decline in the instantaneous pressure gradient. Waveform appears more early slanted “V” than an equal “V”.

Vena Contracta

11.42 Feigenbaum

Distal Flow Reversals

Significant volume of flood is displaced by the regurgitant resulting in flow reversal seen in the pulmonary veins entering the left atrium

Reversal of normal patterns of systolic inflow of pulmonary veins.

Determination of Mitral Regurgitation

PISA (Proximal Isovelocity Surface Area)The highest velocity of blood flow occurs

proximal to the valve planeSeries of isovelocity “surfaces” leading to the

high velocity jet in the regurgitant orifice

Decision Making Repair or Replacement

Most important factor: left ventricular size and function

Progressive dilatation, an end-systolic dimension of greater than 45 mm or any reduction of left ventricular function may prompt surgical intervention regardless of symptomatic status.

Posterior leaflet prolapse and annular dilatation are most amendable to repair, others require more complex procedures with lower likihood of successful repair.

Intraoperative Evaluation of Mitral Repair

Transesophageal Echo is used during operations.

Baseline images are obtained in the operating room to reconfirm regurgitant severity.

After valve repair, the patient is weaned from cardiopulmonary bypass and valve anatomy and regurgitation is re-evaluated.

Intraoperative Evaluation of Mitral Repair

If significant residual mitral regurgitation is present,Second bypass pump may be done to allow a

second attempt at repair or mitral valve replacement.

Complications may include: Left ventricular outflow tract obstructionFunctional mitral stenosisWorsening of left ventricular systolic function.

Actually young hairy man. Antibiotics prior to dental cleanings is no longer indicated in patients with mitral valve prolapse.

Tricuspid Regurgitation

Anatomy of the Tricuspid Valve

Anatomy of the Tricuspid Valve

Atrioventricular valve that prevents backflow of blood from the right ventricle into the right atrium.

Composed of:tricuspid annulusleaflet tissuechordae tendinaepapillary muscles

Tricuspid Annulus

Make-up of the tricuspid valve is similar to mitral valvular composite but is less strong

Shape is roughly triangular

Largest valvular orifice of the heart

Tricuspid Valve Leaflets

Three leaflets of the tricuspid valve

Named based upon the physical location in relation to the right ventricular walls Anterior Medial Inferior (posterior)

Leaflets composed of collagenous material surrounded by endocardium

Basal zones are thicker than the tips, which possess indentations or commissures, which attach to chordae tendinea

Chordae Tendinae

Support the leaflets and prevent them from prolapsing during systole

Strong, fibrous, collagenous structures which arise from papillary muscles and insert on the ventricular side of the valve leafletsPrimarySecondaryTertiary

Papillary Muscles

Two major papillary muscles Less prominent than those of the left ventricle Named for their location within the ventricle

Anterior papillary muscle Largest Located on the anterolateral wall of the ventricle Supplies chordae to the anterior leaflet

Posterior (sometimes called inferior) Located on the inferoseptal wall Muscle is smaller and frequently has two or three head Supplies chordae to the inferior leaflet

Unique Feature of the Right VentricleMedial or septal leaflet receives its chordae directly from

the ventricular septum, found only in the RV

Normal Valve Area of the Tricuspid Valve

7-9 cm2

Tricuspid Valve Views

RVIT PSAX-Ao

Apical 4 Subcostal Long Axis

M-Mode Tricuspid Valve

Transesophageal Echocardiogram 110 degree view at the base of the heart

12.24 Feigenbaum

M-Mode Tricuspid Valve


Disorder involving backflow of blood From the right ventricle to the right atrium during contraction of the

right ventricle.

May be acute, chronic, or intermittent

The most common cause of tricuspid regurgitation Not damage to the valve itself

Enlargement of the right ventricle, which may be a complication of any disorder that causes right ventricular failure


Common abnormality in the adult population

Caused by two general mechanismsFunctionalAnatomic

Functional (secondary) – Structurally Normal Tricuspid Valve

Pulmonary hypertension due to left heart failure

Cor pulmonalePrimary pulmonary hypertensionRight heart pathological conditions

Pulmonic stenosis, Eisenmenger’s syndrome

Constrictive pericarditis

Anatomic (primary) – Abnormal Tricuspid Apparatus Rheumatic heart disease Infective endocarditis Tricuspid valve prolapse Tricuspid annular dilatation/calcification Ruptured chordae tendinae Papillary muscle dysfunction Carcinoid syndrome Ebstein’s anomaly Catheter induced (e.g. pacemaker wire) Prosthetic heart valve Systemic lupus erythematosus Trauma Tumor Orthotopic heart transplantation Endomyocardial fibrosis Physiologic

Symptoms

Usually well toleratedWeaknessFatigueCongestive heart failure

DyspneaOrthopneaParoxysmal nocturnal dyspneaPulmonary edema

Tricuspid Valve Prolapse

Tricuspid RegurgitationComplications

Severe right heart failureRenal failure when severe congestion is

present

Chest X-Ray

Right atrial enlargementRight ventricular enlargementLeft heart enlargement

Suggests functional tricuspid regurgitationPulmonary congestion

Suggests functional tricuspid regurgitationPulmonary artery dilatation

Suggests functional tricuspid regurgitationProminent superior vena cava/right innominate

vein

http://www.yale.edu/imaging/findings/enlarged_heart/index.html

Cardiac Catheterization

Right ventriculography to determine presence and severity

Increased right atrial pressure and right ventricular diastolic pressure

Kussmaul’s signIncreased right atrial pressure with inspiration

Treatment

NoneTricuspid regurgitation may be well tolerated for

yearsEndocarditis prophylaxisDigitalis/diureticsVasodilators in patients with pulmonary

hypertensionAnticoagulation

Right heart failure

Treatment

Tricuspid valve excisionDrug addition with infective endocarditis

AnnuloplastyCarpentier ringKay ringDural ring

Tricuspid valve replacementUsually with a tissue valve to reduce the risk of

thrombus formation

M-Mode Criteria of Tricuspid Regurgitation

Right ventricular overload pattern

Increased D-E amplitude of the anterior tricuspid valve leaflet

Increased E-F slope of the anterior leaflet of the tricuspid valve leaflet

B “bump” or “notch” of the anterior tricuspid valve leaflet indicated increased right ventricular end-diastolic pressure (≥9 mmHg)

Color M-mode may be useful in determining the presence, timing and duration of tricuspid regurgitation when combined with PISA

2D Criteria for Tricuspid Regurgitation

Anatomic basis for the presence of tricuspid regurgitationTricuspid valve vegetation, ruptured chordae tendinae

Right atrial dilatation with systolic expansion

Right ventricular diastolic expansion

Right ventricular dilatation

Right ventricular volume overload pattern

2D Criteria for Tricuspid Regurgitation - continued

D-shaped left ventricle during ventricular diastole indicating a right ventricular diastolic volume overload

Globular (spherical)-shaped right ventricle which may form the cardiac apex

Dilated tricuspid valve annulus (≥3.0 cm in systole, ≥3.2 cm in diastole) indicates severe tricuspid regurgitation

2D Criteria for Tricuspid Regurgitation - continued Dilated inferior vena cava with lack of inspiratory collapse (normal 1.2 to 2.3

cm)

Dilated hepatic veins (normal: 05 to 1.1 cm)

Dilated superior vena cava/innominate vein

Systolic bowing of the interatrial septum toward the left atrium

Systolic reflux of saline contrast into the inferior vena cava and hepatic vein may indicate significant tricuspid regurgitation May also be visualized by color flow Doppler

Determine right atrial dimension, area and volume

Determine right ventricular end diastolic, end systolic dimensions, volumes and ejection fraction

PW Doppler - Inflow

Up to 93% of normal patients appear to have tricuspid regurgitation; calculate the duration and length of the regurgitant

Increased tricuspid E velocity may indicate significant tricuspid regurgitation

Laminar tricuspid regurgitation flow may denote significant regurgitationAssociated with lack of tricuspid valve leaflet coaptation

Important to Note

Tricuspid regurgitation is a volume overload of the right heart

Most common etiology of tricuspid regurgitation is pulmonary hypertension due to left heart pathology 90% incidence when systolic pulmonary artery pressure is >40 mmHg

Classic clinical triad of prominent jugular distension, holosystolic murmur at the lower sternal border increasing with inspiration and a pulsatile liver is present in only 40% of patients with severe tricuspid regurgitation

Myxomatous, redundant appearance of the involved tricuspid valve leaflet(s)

Tricuspid annular dilatation (normal 2.2 cm ± 0.3) – apical four chamber

Important to Note - Continued

Tricuspid regurgitation is the most common physiologic regurgitationNormal tricuspid valve apparatusNormal chamber dimensionsPeak tricuspid regurgitation (2.0 m/s ± 0.2) Small regurgitant jet area are indicators of

physiologic flow

Significant Tricuspid Regurgitation

Regurgitant jet area ≥0.9 cm2Right atrial area ›30 cm2Proximal jet jet width ≥0.8 cmSystolic flow reversal in the hepatic veinsParadoxical septal motion Diastolic septal flatteningInferior vena cava diameter ≥2.1 cmLack of inferior vena cava respiratory

variation

Secondary Effects of TR

Moderately severe tricuspid regurgitation.

Dilated right ventricle and diastolic flattening of the ventricular septum consistent with a right ventricular volume overload.

12.33 Feigenbaum

Mild Tricuspid Regurgitation

Apical four-chamber view Apical four-chamber view recorded in a patient with mild recorded in a patient with mild to moderate tricuspid to moderate tricuspid regurgitation. Note the color regurgitation. Note the color Doppler signal filling Doppler signal filling approximately 25% of the right approximately 25% of the right atriumatrium

Dilated Cardiomyopathy

12.30a Feigenbaum 12.30b Feigenbaum

Flail Tricuspid Leaflet Due to Trauma (MVA)

12.31a Feigenbaum

12.31b Feigenbaum

Marfan Syndrome• Myxomatous changes Myxomatous changes

• Tricuspid valve Tricuspid valve withwith pronounced pronounced bileaflet prolapse bileaflet prolapse ((small arrowssmall arrows) )

• Incidental note:Incidental note:• Prominent Prominent

Eustachian valve Eustachian valve ((EVEV))

12.32 Feigenbaum

Carcinoid Heart Disease Presence of Carcinoid Tumors Found predominantly in the

gastrointestinal tract

Tumors produce vasoactive substances that ultimately cause endothelial damage to the right side of the heart

Primary tumors can be small, with hepatic metastases noted in most patient who demonstrate cardiac involvement

Involvement of the heart occurs late in the progression of the disease in nearly half of those with carcinoid syndrome

Carcinoid heart disease. Insert shows pulmonary stenosis. The leaflets of the tricuspid valve are thickened. The valve is predominantly incompetent and causes pulmonary regurgitation. Fibrous plaques are deposited on the lining of the right ventricle and pulmonary trunk.

Carcinoid Heart DiseaseClinical Symptoms

Episodes of facial flushing with stimuliAbdominal painDiarrheaRenal and hepatic failureHepatomegaly is usually associated with later

stages of the disease

Cardiac signs include Elevated venous pressureSystolic and diastolic murmurs

Carcinoid Heart Disease2D Echocardiographic SignsDistinctive and are usually restricted to the right

heart

Findings include:Dilation of the right ventricle with abnormal septal

motion, indicative of right ventricular volume overload

Thickened tricuspid valve leaflets that are retracted, with foreshortened chordae

Tricuspid valve leaflets usually do not coapt completely and remain open throughout the cardiac cycle

Carcinoid Heart DiseaseTricuspid Doppler Signs

Tricuspid regurgitation, most prevalent finding

Increased diastolic velocities across the tricuspid valve

Carcinoid

Complete failure of coaptation of the leaflets, which results in severe tricuspid regurgitation, confirmed in an apical four-chamber view with color flow Doppler imaging

12.41 Feigenbaum

Epstein’s Anomaly

Congenital Anomaly

Apical displacement of one or more leafletsMost often septal leaflet is involvedDegree of displacement is extremely variable

Epstein’s should be considered when separation between mitral and tricuspid valve is > 1cm

Results in atrialization of a portion of the right ventricle.

Normal

Ebstein’s Anomaly

Note: apical apical displacement of the displacement of the septal leafletseptal leaflet

Epstein’s Anomaly

• Marked distortion of right ventricular and right atrial geometry.

• The approximate position of the mitral anulus is noted by the broad arrow at the lower right.

• Septal leaflet of the tricuspid valve: apically displaced from the anulus by approx 3 cm

• Lateral leaflet is tethered to the right ventricular wall along much of its length (small arrows).

• Also pathologically elongated.

12.43 Feigenbaum

Pacemakers

Stiffer, larger diameter leads used for implantable defibrillators may interrupt normal coaptation to a greater degree

Typically does not result in significant TR

Fibrosis combined with pacemakers may result in more significant regurgitation

Pacemakers

• Pacemaker wire has restricted motion of the tricuspid valve

• Moderate tricuspid regurgitation

Non-dynamic

Bi-Ventricular Pacemaker

Pulmonic Valve

Pulmonic Valve

Similar to aortic valveTrileafletInserted into pulmonary artery annulus

distal to the right ventricular outflow tract

Pulmonic Valve Views

PSAX-Ao RVOT

Subcostal Short-Axis

Etiology of Pulmonic Regurgitation

Pulmonary hypertension Causing regurgitation secondary to dilatation of the valve ring Most common Referred to as high pressure pulmonary disease

Infective endocarditis Second most common cause

Rheumatic heart disease

Myxomatous degeneration

Etiology – Cont.

Idiopathic dilatation of the pulmonary arteryConnective tissue disorders (e.g. Marfan’s

syndrome)Congenital abnormalities

e.g. tetralogy of Fallot, ventricular septal defect, valvular pulmonic stenosis, congenital agsence of the pulmonic valve

IatrogenicPost surgical repairs for congenital heart disease

Etiology – Cont.

Pulmonary artery catheterCarcinoid heart diseaseSyphilisTuberculosisChest traumaProsthetic heart valvePhysiologic

History/Physical Examination

May tolerated for years w/o difficultySevere hemodynamic changed due solely to

pulmonary regurgitation is rareDyspneaFatiguePalpable right ventricular impulse along left

sternal borderRight heart failure

e.g. jugular venous distention, hepatomegaly, peripheral edema, ascites, anasarca

Complication

Right heart failure

Treatment

Pulmonary regurgitation is generally well tolerated

Endocarditis prophylaxisDigitalis (right heart failure)Valvuloplasty/valve replacement

M-Mode Criteria


Right ventricular volume overload pattern Right ventricular dilatation with paradoxical septal motion

Fine diastolic flutter of the tricuspid valve

Diastolic flutter of the pulmonic valve

Premature opening of the pulmonic valve due to severe acute pulmonary regurgitation Defined as pulmonic valve opening on or before the QRS complex

Evidence of pulmonary hypertension

2D Criteria

Anatomic basis for the presence of pulmonary regurgitation

Evidence of pulmonary hypertension Common cause


Right ventricular volume overload pattern Right ventricular dilatation with paradoxical septal motion

Right ventricular diastolic expansion

D-shaped left ventricle due to right ventricular volume overload

Pulmonary valve ring/artery dilatation

Right atrial dilation

Pulsed Wave Doppler

Up to 87% of normal patients appear to have pulmonary regurgitationLength and duration of the regurgitant jet differentiate

between true and physiologic regurgitation<1 cm in length and non-holodiastolic in duration with

normal pulmonary artery pressures implies physiologic regurgitation

Peak velocity across the RVOT is increased with significant pulmonary regurgitation

Increased RVOT velocity time integral (VTI) with significant pulmonary regurgitation

Color Flow Doppler

Holodiastolic flow reversal in main pulmonary artery and its branches may indicate severe pulmonary regurgitation

Continuous Wave Doppler

Compare the pulmonary regurgitation Doppler spectral display with the pulmonic outflow Doppler spectral display strength

Steep slope with cessation of flow at or before end diastole may indicate severe pulmonary regurgitationShortened pressure half-time

Pulmonary Regurgitation Severity Scales PW and ColorPhysiologic

Normal pulmonic valve and pulmonary artery Normal chamber dimensions Normal pulmonary artery pressures <1 cm in length and not holodiastolic in duration

Borderline 1 to 2 cm in length and holodiastolic in duration

Clinically significant > 2 cm in length with a peak velocity ≥1.5 m/sec and

holodiastolic in duration

Pulmonary Regurgitation Severity Scale CW Spectral Strength of Regurgitant Jet

Grade 1+ (mild)

Grade 2+ (moderate)

Grade 3+ (moderate severe)

Grade 4+ (severe)

Spectral in tracing stains sufficiently for detection, but not enough for clear delineation

Complete spectral tracing can just be seen

Distinct darkening of spectral tracing is visible but density is less than antegrade flow

Dark-stained spectral training

Important to Note

Significant pulmonary hypertension is a right heart pressure overload

The velocity of pulmonic regurgitation varies with respirationWhen determining the mean pulmonary artery

pressure and pulmonary artery end diastolic pressure, 3 to 5 beats should be averaged

Eccentric Jet PI

Parasternal short-axis view recorded at the base of the heart in a patient with minimal pulmonary valve insufficiency originating at the lateral aspect of the cusp commissure.

Because this jet originates immediately adjacent to the aorta (Ao), it could be confused for an aorta-pulmonary fistula.

Note, however, the exclusively diastolic flow, which would not be expected in the presence of the true shunt.

12.13 Feigenbaum

Mild Pulmonic Insufficiency/Regurgitation

12.14a Feigenbaum

Moderate Pulmonic Insufficiency/Regurgitation

12.14b Feigenbaum

Severe Pulmonic Insufficiency/Regurgitation

12.14c Feigenbaum

Sources

Azis F, Baciewicz F. (2007). Texas Heart Institute Journal. 34(3) 366-8.

Feigenbaum H, Armstrong W. (2004). Echocardiography. (6th Edition). Indianapolis. Lippincott Williams & Wilkins.

Goldstein S., Harry M., Carney D., Dempsey A., Ehler D., Geiser E., Gillam L., Kraft C., Rigling R., McCallister B., Sisk E., Waggoner A., Witt S., Gresser C.. (2005). Outline of Sonographer Core Curriculum in Echocardiography.

Otto C. (2004). Textbook of Clinical Echocardiography. (3rd Edition). Elsevier & Saunders.

Reynolds T. (2000). The Echocardiographer's Pocket Reference. (2nd Edition). Arizona. Arizona Heart Institute.

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Valvular Regurgitation

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