Echocardiographic assessment of Aortic
Dr Prathap Kanagala
BSE Education Committee
East Midlands Deanery
My sincere thanks to Dr Andrew R. Houghton (Consultant Physician
& Cardiologist) and the Department of Medical Physics, Grantham
& District Hospital for their valuable input in preparing this
coronary artery bypass graft
ventricular end diastolic diameter
ventricular end diastolic pressure
ventricular end diastolic volume
ventricular end systolic diameter
ventricular outflow tract
M-mode motion mode
proximal isovelocity surface area
regurgitant orifice area
relative wall thickness
ventricular septal defect
velocity time integral
1. To understand the epidemiology, aetiology, pathophysiology
and prognosis of aortic regurgitation
2. To review the qualitative and quantitative echocardiographic
methods available to assess severity
3. To appreciate the role of echocardiography in management
The incidence of clinically significant AR increases with age,
typically peaking between the 4th and 6th
decades of life. AR is more common in males. Reported prevalence is
4.9%, with moderate to severe cases accounting for 0.5%.
The causes of AR can be broadly categorised into disease
affecting: the valvular apparatus (e.g. rheumatic, myxomatous), the
aortic root (e.g. Marfan's syndrome, sinus of valsalva
aneurysm) or both (e.g. ankylosing spondylitis, bicuspid aortic
valve). In developing countries, rheumatic disease remains
the leading cause of AR. In the Western World however, bicuspid
valves and aortic root abnormalities predominate.
Valvular pathologies result in alterations in leaflet
flexibility and shape with resultant inadequate coaptation.
Regurgitation also results from leaflet perforation as seen in
endocarditis or trauma. In aortic root disease, annular dilation
causes malcoaptation as the valve leaflets become stretched further
apart. In addition, a false channel created by dissection may
directly distort valve structure causing flail leaflets.
Causes of Aortic
Connective tissue disease e.g. Rheumatoid Arthritis, Systemic
*Trauma - leaflet rupture / perforation
VSD - supracristal type associated with cusp prolapse
Cystic medial necrosis
Ehler's Danlos syndrome
Sinus of Valsalva aneurysm
*Conditions associated with acute
Acute AR is a medical emergency.
Untreated, LVEDP rises rapidly and effective stroke volume cannot
be maintained despite intrinsic compensatory mechanisms (increasing
heart rate and contractility) attempting to cope with the
regurgitant volume (preload). Pulmonary oedema, cardiogenic
shock and death usually develop quickly.
Chronic AR however allows the LV to adapt and
remodel, delaying the onset of symptoms. A summary of the changes
Left ventricular volume and pressure overload
Increase in LV wall stress
Compensatory hypertrophy (concentric and eccentric) in an
attempt to normalise wall stress
Systolic hypertension (often) as a consequence of increased
Pulse pressure widening as aortic diastolic blood pressure
drops due to regurgitation back into the LV
During initial stages, the regurgitant volume increases
LVEDV without an increase in LVEDP as the LV dilates and compliance
Despite the compensatory mechanisms however, LVEDP eventually
rises as systolic dysfunction supervenes and heralds the onset of
symptoms. The end-stage heart often resembles a spherical, dilated
LV with increased mass - the so called cor bovinum (bovine
or ox heart).
Acute AR is associated with high mortality rates without
immediate surgical intervention. In chronic AR, predictors of poor
outcome include increasing age, severe AR, symptoms, EF<50% and
The echo study should aim to confirm diagnosis, establish
aetiology, categorise severity and consequences of AR.
Two dimensional imaging
2D imaging provides useful information regarding valve anatomy,
valvular structure & deformity, aortic root dimensions and the
adaptive LV response to regurgitant volume.
Valve anatomy: Is the valve tricuspid? Is there evidence of
eccentric coaptation? (unicuspid, biscuspid, quadricuspid)
Valve structure: Is there cusp thickening, calcification?
Are other valves affected? (rheumatic) Is there evidence
of perforation or vegetations? (endocarditis)
Valve function: Are the cusps thickened with redundant
leaflets? Is there diastolic sagging into the LVOT?
(myxomatous) Is leaflet motion restricted? (co-existent
aortic stenosis) Is there leaflet prolapse? (false channel
secondary to aortic dissection)
Aortic Root: Is there dilation with maintenance of normal
contours and narrowing at the sinotubular junction?
(degenerative disease) Is there effacement i.e. enlargement of
the sinuses of valsalva accompanied by loss of narrowing at the
sinotubular junction? (Marfan's syndrome) Is the aortic
root extensively calcified? (syphilis) Is there evidence
of a false channel / dissection flap? (aortic dissection)
Left Ventricle: Is there concentric hypertrophy i.e.
increased LV mass & relative wall thickness? (typically
seen with isolated hypertension and pressure overload) Is there
eccentric hypertrophy i.e. increased LV mass but normal relative
wall thickness? (typically as a consequence of volume
overload) Is the LV dilated? (suggestive of chronicity of
AR and increasing severity) Is LV function diminished?
This implies haemodynamically severe AR although alternative causes
of impaired function should be borne in mind.
Note Relative wall
thickness (RWT) = 2 x posterior wall thickness ÷ LVEDD. In the
presence of increased LV mass, RWT greater than 0.42 indicates
concentric hypertrophy. On the other hand, RWT less than 0.42
defines eccentric hypertrophy.
Vena Contracta (Quantitative)
VC width is the narrowest portion of
colour flow at or just below the level of the
Calculation: Measure in parasternal windows since better axial
resolution is offered compared to apical windows. Use zoom &
colour M-mode to minimise errors in measurement.
Limitations: VC width is not reliable if there are multiple jets
or the jet is irregularly shaped. VC is valid for eccentric
jets however, if measurements are made perpendicular to the
direction of the jet rather than to the long axis of the LVOT.
Dealing with relatively small values of VC width (usually < 1cm)
also means that even small measurement errors may result in large
percentage errors and thus over/underestimating the degree of
Jet width / LVOT height (Quantitative)
The regurgitant jet width to LVOT diameter ratio refers to the
maximal proximal jet width measured
in the LVOT.
Calculation: Similar to VC width measurements, use parasternal
windows with zoom & colour M-mode to maximise axial and
Limitations: Regurgitant jets expand unpredictably below
the valve orifice often with differing shapes and are therefore a
potential source of error. Measurement too far below the valve
tends to overestimate severity as the jet spreads out. In
addition, central jets may overestimate (and conversely eccentric
jets may underestimate) severity.
Jet area / length in LV cavity
Calculation: In apical views, measure how far the regurgitation
extends into the LV cavity using colour & PW Doppler.
Regurgitation reaching the end of the anterior mitral valve leaflet
is indicative of moderate severity. Jets extending beyond and into
the body of the LV indicate severe disease. Set a Nyquist limit
(aliasing velocity 50-60 cm/sec) and optimise colour gain such that
random colour speckle from non-moving regions is just
Limitations: Colour Doppler is heavily dependent on PRF
and colour gain. Jet area includes both turbulent (aliased) and
laminar flow which may result in overestimation of central jets.
Increasing the scale may underestimate jet area. The length of the
regurgitant jet is similarly influenced by the above factors.
PISA or flow convergence (quantitative)
Whilst this method is theoretically measurable (as in MR
assessment) and has been shown to provide accurate quantification
in severity of AR, it is not routinely practiced. Limitations
include suboptimal images in the presence of aortic valvular
calcification and underestimation in aortic aneurysms. Validity is
questionable for multiple/eccentric jets.
CW & PW Doppler
Pressure half-time and jet deceleration rate
Calculation: In apical 5- or 3-chamber views, align CW Doppler
(aided by colour flow mapping) along the direction of the jet as it
originates from the regurgitant orifice. Measure peak velocity and
the slope of the flat part of the spectral trace i.e.
deceleration slope. Pressure half-time corresponds to the rate
of deceleration of the jet i.e. time taken for pressure across the
aortic valve to fall by half. Typically, with increasing severity
of regurgitation, aortic diastolic pressure falls more rapidly.
Therefore, the late-diastolic velocity is lower and a steep
deceleration slope & short pressure half-time result.
Limitations: Factors affecting the significance of pressure
half-time values include changes in LV compliance (e.g.
chronic AR), LV diastolic pressure (e.g. systolic dysfunction,
ischaemia) and aortic diastolic pressure (e.g. sepsis, patent
ductus arteriosus, vasodilators).
Acute versus Chronic severe
Pressure half-time is more useful as a marker of severity in
acute regurgitation since LV compliance will not have adapted so
quickly. With chronic cases, LV function and aortic compliance
change to accommodate the larger regurgitant volumes. These
processes slow down the equalisation of trans-aortic pressures and
lead to misleadingly longer pressure half-time values.
Similarly, normal LV dimensions, often with vigorous function
point towards acute regurgitation. In chronic cases, a dilated LV
with eccentric hypertrophy often results due to the process of LV
remodelling. Systolic function may also become impaired.
Other relevant pointers of acute onset include evidence of
dissection, endocarditis and trauma.
Regurgitant Volume / Regurgitant Fraction /
Regurgitant Orifice Area
Calculation: The volume of blood entering the LV via the mitral
valve during diastole should equal the volume leaving the LV via
the LVOT during systole (stroke volume). In AR, LV outflow exceeds
mitral inflow since LVOT outflow also comprises blood that has
entered the LV via AR during diastole. Therefore, Aortic
Regurgitant Volume (ml) = Stroke volume of LVOT -
Stroke Volume of MV in the absence of significant MR or a
Stroke volume of LVOT
= cross sectional area of LVOT x VTI of LVOT
= 0.785 x (LVOT diameter) 2 x VTI of LVOT
Measure LVOT diameter in Parasternal long axis view
Measure VTI using PW Doppler in Apical 5- chamber
Stroke volume of MV
= cross sectional area of MV annulus x VTI of MV
= 0.785 x (MV annulus diameter) 2 x VTI of MV
Measure MV annulus diameter in Apical 4-chamber
Measure VTI using PW Doppler in Apical 4-chamber view at
mitral annulus level
Regurgitant Fraction (%) = (Regurgitant Volume ÷ Stroke
Volume of LVOT) x 100
Regurgitant Orifice Area is the average size of the orifice in
the aortic valve during diastole through which regurgitation
Regurgitant Orifice Area (cm2) = Regurgitant
Volume ÷ VTI of AR Doppler trace
Measure VTI of the AR Doppler trace using CW Doppler in Apical
3- or 5-chamber views
Limitations: The above Doppler derived flow calculations are
fraught with potential pitfalls. Calculations are not valid in the
presence of more than mild mitral regurgitation. In addition, even
small errors in measurements of either LVOT/MV annulus diameters
are greatly magnified as the results are squared.
CW Doppler AR jet density (qualitative)
The intensity of the regurgitant signal seen on CW spectral
display in apical 3- or 5-chamber views reflects the volume of
regurgitation compared to forward flow through the aortic
valve. Whilst a weak regurgitant signal compared to forward
flow is consistent with minimal AR, greater degrees of
regurgitation produce equal density of retrograde and antegrade
flow signals. Reliable discrimination between moderate and
severe grades of regurgitation however is not possible based on
signal intensity alone.
Diastolic flow reversal - Descending Aorta
Calculation: Using a suprasternal view, PW Doppler interrogation
of the upper descending aorta may detect brief (early) reversal of
diastolic aortic flow even in normal individuals. As regurgitation
becomes more severe however, flow reversal occupies a greater
period of diastole and indeed diastolic flow velocities increase.
Descending thoracic aortic holodiastolic flow reversal indicates at
least moderate regurgitation.
Limitations: Varying degrees of flow reversal may also be seen
with age related changes in rigidity and diminishing compliance of
the aortic wall.
Severity of AR (BSE Education
Committee Guidelines for Valve Quantification)
VC width (cm)
Jet width/LVOT diameter (%)
Regurgitant Volume (ml/beat)
Regurgitant Fraction (%)
Regurgitant Orifice Area (cm2)
VTI diastolic flow reversal (cm) (upper descending
Pressure Half Time (ms)
Mild to moderate AR may be managed with annual review and echo
assessment every 2 years. Severe AR & normal LV function
typically necessitates 6 monthly patient review (annual if stable).
Dilated aortic roots require echo monitoring on an annual basis or
more frequently if rapid rate of growth is seen.
Whilst standard anti-heart failure medication is the mainstay of
medical therapy, the use of vasodilators in asymptomatic patients
is unproven. Additionally, beta-blockers may be helpful in peri-
& post-operative patients with Marfan's syndrome.
Surgical options include valve replacement or repair with
grafting of the aortic root as appropriate.
Surgical indications include:
1. Acute symptomatic AR
2. Chronic severe AR
Asymptomatic patients with LVEF = 50%
Asymptomatic patients with LVEF > 50% and severe LV
dilation (LVEDD > 70mm, LVESD > 50mm)
Patients undergoing other surgery (CABG, ascending aorta, other
3. Regardless of severity of AR, patients with aortic root
Aortic Root > 45mm in Marfan's syndrome
Aortic Root > 50mm in Bicuspid valves
Aortic root > 55mm in other patients
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guide. London: Hodder Arnold, 2009. ISBN: 978-0-3409-4688-6.
2. The Task Force on the Management of Valvular heart
Disease of the European Society of Cardiology. Guidelines on the
management of valvular heart disease. Eur Heart J 2007; 28:
3. Maurer G. Aortic Regurgitation. Heart 2006;
4. Otto CM. Textbook of Clinical Echocardiography,
3rd edn. Edinburgh: Elsevier Saunders, 2004. ISBN-13:
5. Zoghbi WA, Enriquez-Sarano M, Foster E, et al.
American Society of Echocardiography: recommendations for
evaluation of the severity of native valvular regurgitation with
two-dimensional and Doppler echocardiography. J Am Soc Echocardiogr
Last Updated (Fri 08 November 2013)