Aortic Insufficiency
Lori Heller, MD
Swedish Heart and Vascular Institute
Swedish Medical Center
Acting Instructor, University of Washington
Seattle, WA
Aortic Valve Anatomy
ME SAX view of the aortic
valve and its location in the
center of the heart
The aortic valve is a semilunar trileaflet valve with three symmetric
cusps of similar size. Each cusp has a small fibrous nodule at the
center of the coaptation edge called the node of Arantius. The
plain of the aortic valve is oblique with the right posterior side angled inferiorly.
The aortic leaflets attach from the
ventricular wall (yellow arrows) to the
STJ (red dotted line). This area makes
up the aortic root.
The aortic valve is contained within the aortic root which extends from
the basal attachment of the leaflets within the LV to the distal
attachment of the leaflets at the sinotubular junction. The root provides
the supporting structures for the leaflets of the aortic valve and forms
the bridge between the LV and the ascending aorta.
The tips of the aortic leaflets protrude into the lumen of the aorta. The three cusps of the valve are
named according to their relationship to the coronary arteries: the left cusp adjacent to the left
coronary artery, the right cusp adjacent to the right coronary artery. The third cusp is not associated
with a coronary artery and is therefore called the non-coronary cusp.
At the mid portion of the aortic root are the three sinuses of Valsalva which are outpouchings directly
behind each cusp. They serve to absorb some of the stress associated within the high pressure system as
well as facilitate the smooth closing of the aortic valve and provide a reservoir of
blood for coronary blood flow during diastole. Each sinus is associated with an
aortic cusp, two of which are associated with coronary arteries. The coronary
arteries originate from the center of the superior aspects of the sinuses just
below the STJ.
Etiology of Aortic Insufficiency
The two major causes of isolated AR are conditions affecting primarily the valve and conditions affecting
the aorta and secondarily causing valve incompetence.
Leaflet Damage
Bicuspid Valve
Endocarditis
Rheumatic Valve Disease
Traumatic Rupture
Failed Surgical Valve
Balloon Valvulotomy
Rheumatoid Arthritis
Aortic Abnormalities/Dilation
Aortic Root Dissection
Connective Tissue Disorders (Marfan, Ehlers-Danlos)
Hypertension
Annuloaortic ectasia
Ankylosing Spondylitis
OsteogenesisImperfecta
Syphilitic Aortitis
The most common cause of isolated AR is now aortic root dilation. 1,3,4 This is vastly different than
before 1980 when the majority of AR was post-inflammatory, generally related to the effects from
rheumatic fever.2 In a single center review of 268 adults referred for aortic valve replacement for
isolated AR United States for aortic valve replacement between 1993 and 2005, 46% of the patients’ AR
resulted from a problem with the leaflets.3 The most common was a congenital bicuspid valve
(unaffected by endocarditis), followed by endocarditis, 33% of whom had a bicuspid valve. Thus for
those with valvular conditions causing AR, 61% had a bicuspid valve.
In this study, the majority of known causes of isolated AR was the consequence of a condition affecting
the ascending aorta: dissection was the most common, followed by Marfan’s syndrome and aortitis.
Interestingly in a third of all of the cases, the cause of the AR was not determined. Those with an
undetermined etiology were the oldest group and the majority (91%) had hypertension, suggesting that
altered elasticity and/or geometry of the aortic root may have been the cause of valve incompetence.
Systemic hypertension is thought to play a role in aortic dilation through wall stress as well as
contributing to cystic medial necrosis in the elderly.17 There is also evidence that many patients with a
bicuspid aortic valve have disorders of the connective tissue which can result in aortic dilation. The
aortic expansion rate is higher in patients with bicuspid valves than in patients with tricuspid valves. 5
Most commonly, however, aortic insufficiency occurs in conjunction with aortic stenosis and is
secondary to degenerative (senile) calcification. In one study of 236 surgically excised valves at the Mayo
clinic, 46% of the combined insufficiency and stenosis was secondary to degenerative calcification.
Bicuspid and post-inflammatory etiologies (17% each), post-therapeutic (13%), and indeterminate (8%)
etiologies made up the rest.
Chronic V. Acute Aortic Regurgitation
In general, about 20% of AR is acute, the remainder is chronic. Acute AR is almost entirely due to
endocarditis or acute aortic dissection. Different physiologic parameters are present in acute v. chronic
AR due to the lack of adaptation of LV compliance.6,7
Chronic
Bicuspid Valve, Hypertension
Dilated
Normal
Wide
Flat
Etiology
LV size
LVEDP
Pulse Pressure
CW Doppler Slope
Acute
Endocarditis, Aortic Dissection
Normal
Elevated
Narrow
Steep
Evaluation
The evaluation of aortic insufficiency is accomplished by 4 echocardiographic methods:
2 D inspection
Color Flow Doppler
CW
PW Doppler
2D Imaging
2 D inspection is used to evaluate the etiology of the regurgitation.
AR may be due to either abnormalities of either the leaflets or the
aortic root. Using the SAX and LAX views, the aortic valve leaflets
are inspected for poor coaptation and other abnormalities and the
root is examined for changes that would alter the geometry
of the structures supporting the leaflets.
Leaflet prolapse, perforations, bicuspid valves and annular dilation
SAX of AV in end diastole. Leaflets are unable
to coaptcompletly due to healing vegetation
are all diagnosed from 2D imaging. Leaflet prolapse is identified
on the RCC
when any portion of the leaflet extends past the annular plane into the
LVOT. Regurgitation from endocarditis can be caused by either leaflet perforation
or from vegetation(s) causing improper leaflet closure.
LAX view of aorta showing a measurement of the annulus, and
effacement of the sinotubular junction (arrow) in a patient with
Marfan Syndrome
Annular dilation, by preventing complete leaflet coaptation, also
causes aortic regurgitation and may be secondary to
hypertension, connective tissue disorders (Marfan syndrome),
or cystic medial necrosis. Marfan syndrome is characterized by
effacement of the sinotubular junction with dilation of the
annulus as well as the sinuses of Valsalva. In contrast, cystic
medial necrosis usually has an identifiable STJ. Less common
causes of aortic annulus dilation are syphilitic aortitis and
osteogenesis imperfecta.5
The disease processes that cause aortic stenosis (bicuspid valve,
rheumatic and calcific disease) also may result in aortic insufficiency.
This is due to changes in the flexibility and/or shape of the valve
resulting in poor coaptation of the leaflets.
Associated 2D findings
Chronic left ventricular volume overload from aortic regurgitation
results in progressive dilation of the ventricle. The LV shape becomes
more spherical. Systolic function is initially able to be maintained,
ME 4 ch – dilated, spherical LV
however over time LV performance declines and the changes can be
irreversible. In contrast, acute AI does not result in LV dilation, however without the compensatory
dilation, more symptoms may be appreciated. 7
Indirect 2D and M-Mode findings
If the regurgitant jet impinges on the anterior leaflet of the mitral valve,
it can cause impaired mitral leaflet opening. This results in an increased
distance between the maximal anterior motion of the mitral valve in
early diastole (the E point) and the most posterior motion of the
interventricular septum. This is referred to as increased E point septal
separation (normal is < 6 mm). Increased E point separation is also seen
in LV dysfunction.
Eccentric AR jet directed toward the anterior
mitral valve leaflet
A discrete area of curvature of the anterior mitral valve leaflet into the
left atrium secondary to the pressure from the regurgitant jet may also
be seen. This is termed “reversed doming” since the direction of
curvature is opposite to that seen in rheumatic mitral stenosis. A raised
fibrotic lesion on either the anterior leaflet or the septum may develop
in chronic AI, due to the flow abnormalities. This can be visualized as a
brighter area on 2D imaging. In addition, high frequency fluttering of
the anterior mitral valve leaflet may also be seen on M mode but rarely
appreciated on 2D imaging due to the difference in sampling rate. This is
the equivalent of the Austin-Flint murmur. 8
.
Reverse doming of the AML resulting from an
eccentric AR jet
Indirect Signs of Aortic Regurgitation
Increased E point-septal separation (> 6mm)
High Frequency fluttering of AMVL
“Reverse doming” of the AMVL
Jet lesion on septum or AMVL
Color Flow Doppler
M-mode of the mitral valve, demonstrating
high-frequency diastolic fluttering of the
anterior mitral leaflet due to severe AR
COLOR FLOW DOPPLER
CFD can be applied in both the AV SAX and the AV LAX view
to evaluate the aortic valve. If color Doppler cannot be applied
to the LVOT from the ME AV LAX view because of annular
calcification or shadowing of the LVOT from a prosthetic
mitral or aortic valve, a deep TG LAX or TG LAX view is used.
Standard technique is to use a Nyquist limit of 50–60 cm/s,
and a color gain that just eliminates random color speckle
from non-moving regions. Typically, a central jet implies
dilation of the annulus and an eccentric jet indicates a leaflet
abnormality. The regurgitant jet flow has three
components that can be visualized in the AV LAX view: the
flow convergence in the aorta, the vena contracta through
the regurgitant orifice and the jet direction and size in the
LVOT.
Vena Contracta
Flow Convergence
LVOT jet
JET WIDTH/LVOT RATIO
The width of the jet in the LVOT and its ratio to the diameter of the
LVOT is one indication of AR severity. The jet should be measured just
below the valve and within 1 cm of the valve. A central jet that takes up
greater than 65% (or 2/3) of the LVOT is graded as severe.9, 10, 11
Jet width
LVOT width
10
Jet Width to LV ratio
Central Jet*
Mild
Moderate
Severe
< 25% LVOT
25-65% LVOT
> 65% LVOT
*At Nyquist limit of 50-60 cm/s
There are important limitations to CF imaging of the regurgitant jet. If the jet is not uniform or have
parallel borders in the LV outflow, it can be difficult to know where to measure it. Eccentric jets often
appear narrow and their severity can be underestimated. Conversely, central jets tend to expand fully in
the LVOT and may be overestimated. In addition, diffuse jets that arise from the entire coaptation line
are difficult to measure. This type of jet can be suspected and identified from the SAX view. In addition,
the size of the jet will depend on hemodynamic conditions. 18, 19
Of note, the length of the jet into the LVOT is not a reliable method for determining severity. 9
VENA CONTRACTA
LA
Vena Contracta
AO
LV
RV
The Vena Contracta is defined as the smallest portion of the jet
at the level of the aortic valve, immediately below the flow
convergence region. It is different from the jet width (measured
in the LVOT, BELOW the aortic valve). The VC will be
significantly smaller than that of the jet width because the jet expands immediately after the VC. The VC
is an estimation of the Regurgitant Orifice Area. The size of the vena contracta is independent of flow
rate and driving pressure for a fixed orifice and has been shown to correlate well with angiographic
findings as well as accuracy with eccentric jets. It is much less load and SVR dependent than
measurement of CFD jet width. A VC of 0.6 is consistent with severe AI. 10, 11, 12
Vena Contracta*
Mild
Moderate
< 0.3 mm
0.3-0.6 mm
*At Nyquist limit of 50-60 cm/s
Severe
> 0.6 mm
10
Continuous Wave Doppler
Jet Intensity and Duration
AR flow
Aortic systolic flow
CW tracing in the deep TG view displaying an aortic
regurgitant density nearly equal to that of the aortic
forward flow, which can indicate moderate to severe AI
The spectral recording of AI begins at aortic valve closure with a rapid
increase in velocity to a maximum of 3-5 m/s, followed by a gradual
decline in velocity during diastole. An easy screening evaluation of the
AI severity is to compare the intensity of the regurgitant signal to that of
the antegrade signal. The density of the signal reflects the volume of
regurgitation, therefore intensity of the regurgitant signal that matches
or is close to the intensity of the antegrade signal can indicate moderate
to severe AI. A faint spectral display is compatible with trace or mild AR.
The intensity is also related to the direction of the jet relative to the
ultrasound beam and therefore can sometimes be misleading. This
should be considered a qualitative measure and recognized as not as
accurate as others. 13, 14
To obtain the CW profile, the deep transgastic LAX or the transgastic
LAX view can be used. Color Doppler can localize the jet and assure
proper placement of the Doppler curser.
Additionally, in moderate or severe regurgitation, the signal can easily be recorded throughout diastole,
whereas mild AR may not appear holodiastolic, with a recordable signal only at the beginning or end of
diastole.
SLOPE
Slope of AI jet obtained in TG LAX
view. > 3 m/sec = severe
The shape of the CW Doppler spectral profile depends on the timevarying instantaneous pressure gradient across the valve in diastole. The
slope of the wave profile therefore can reflect the severity of the
regurgitation since a larger regurgitant orifice allows for more rapid
equilibration of pressures between the aorta and the LV. As a result, in
severe AI, the slope of the spectral profile will be steeper. A regurgitant
velocity slope greater than 3 m/sec is consistent with severe AI. 13, 14
Pressure Half Time
Pressure Half Time is the time required for the peak
pressure to reach one half of its maximum value and is
used as another measurement of the rate of pressure
equilibration. With the steeper slope that is seen in
severe AI, the PHT is shorter. A PHT of 500 ms is
consistent with mild AI whereas a PHT of 200 ms is
considered severe AR. 13,14
Peak Pressure
½ Peak Pressure
PHT = Time required
to reach ½ peak
pressure
10
Mild
<2
>500
Slope m/s
PHT ms
Moderate
2-3
500-200
Severe
>3
< 200
It should be noted that in acute AR, even if only moderate, a significant increase in end diastolic
pressure can be seen due to the lack of LV compliance. The LV has not yet adapted, as it has in chronic
AR, therefore the slope may be quite steep. Similarly, any other factors that affect LV diastolic pressure
(ischemia, systolic dysfunction) or aortic pressure (sepsis, patent ductus, vasodilators) will result in more
rapid equilibration of pressures and a steeper slope (and an inaccurate/increased grading of the AR).
Another limitation of this method is seen in eccentric jets. Precise placement of the CW Doppler may be
difficult with these jets and can be unreliable.
Pulsed-Wave Doppler
Flow Calculations
Regurgitant fractions and orifice areas can be calculated using the continuity equation. 11, 15
The Aortic Regurgitant Volume is the difference between the forward stroke volume across the LVOT
and the stroke volume across the mitral or pulmonic Valve (provided there is no significant MR or
intracardiac shunt).
Aortic Regurgitant Volume= AV Systolic Forward Volume- PV Volume (or MV volume)
Volume = CSA x VTI
PV flow = PV area x PV VTI
Severe > 60 cc/beat
MV flow = MV area x MV VTI
To determine stroke volume across the PV, measure the PA diameter and determine the area by
2π(d/2)2. Obtain the TVI by placing CW through the PV (at the ME ascending aorta SAX view). Similarly,
measure the diameter of the LVOT and determine the area by 2π(d/2)2. Multiply this by the AV VTI
obtained in the deep transgastric view of the LV.
Once Aortic Regurgitant Volume is determined, Regurgitant Fraction and Effective Regurgitant Orifice
Area (ERO) can also be calculated:
Regurgitant Fraction = Aortic Regurgitant Volumex 100 %
LVOT Stroke Volume
Severe > 50%
Effective Regurgitant Orifice Area (ERO) = Aortic Regurgitant Volume
Aortic Regurgitant TVI
Severe > .30 cm2
10
Regurgitant Volume cc/min
Regurgitant Fraction %
EROA cm2
Mild
< 30
< 30
< 0.1
Moderate
30-59
30-49
0.1-0.29
Aortic Diastolic Flow Reversal
Regurgitant flow reversal in the descending aorta that lasts
throughout the diastolic period is often a sign of significant AR.
Brief diastolic flow reversal is normal, however with increasing
severity of aortic regurgitation both the duration and the velocity
of the flow increase. Holodiastolic flow reversal is usually indicative
of at least moderate AR. One limitation to this measure is that
the reduced aortic compliance seen with advancing age may
also result in reversal of the diastolic flow.
Severe
60 cc/min
>50
> 0.3
Caudad
Cephalad
Desc LAX view of
the aorta
Pulsed Doppler obtained in the
thoracoabdominal aorta showing flow
reversal throughout diastole
From: ACC/AHA 2006 Practice Guidelines for the Management of Patients With Valvular Heart Disease: Executive Summary
10JACC Vol. 48, No. 3, 2006 Bonow et al. 605 August 1, 2006:598–675ACC/AHA PRACTICE GUIDELINES—EXECUTIVE SUMMARY
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