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AORTIC VALVE: Aortic valve case studies Daryl Oakes, MD Clinical Assistant Professor of Anesthesia Stanford University Medical Center LEARNING OBJECTIVES: At the conclusion of the lecture, the participants will be able to discuss the echocardiographic evaluation of aortic valve disease and associated systemic manifestations and their impact on surgical decision‐making. TOPICS COVERED: 1. Anatomy of the aortic valve and annulus 2. Bicuspid Aortic Valve disease 3. Aortic Stenosis: a. The Basics b. Subvalvular AS: Fixed and Dynamic obstruction c. Low‐flow low‐gradient AS d. Prosthetic valve with high gradients 4. Aortic Insufficiency: a. The Basics b. Aortic Dissection c. Endocarditis INTRODUCTION: ANATOMY The aortic valve complex is made up the aortic valvular annulus, the aortic valve leaftlets, and the aortic root. The aortic annulus has a crown‐like structure that attaches proximally and anteriorly to the muscular and membranous ventricular septum and extends distally into the aortic sinuses and to the medial layer of the aorta.1 The aortic valve is trileaflet with each leaflet suspended to the sinotubular junction at commissures, ridges in the aortic wall at these points of leaflet attachment. Below each commissure is a triangular space, the interleaflet triangle, which is an extension of the ventricular outflow tract. The triangle between the right and the noncoronary leaflet is closely associated with the bundle of His which passes through the fibrous central skeleton to the inferior portion of the membranous ventricular septum. This relationship can explain conduction system injury occasionally seen during aortic valve surgery and endocarditis. The free edge of each cusp, the lunula, is slightly thickened and forms the 2
Mackie BD. MedscapeReference. June 27, 2011.
coaptation surface. There is a nodular thickening of the central portion of edge leaflet call the Node of Arantius. Valvular closure occurs when the pressure within the cusps is higher than the ventricular pressure and the hammock‐like pockets of the cusps are forced backward toward the ventricle. CASE 1: Bicuspid Aortic Valve Disease The most common variant is the bicuspid or bicommissural aortic valve (BAV); approximately 0.5‐2% of the population has this variant. The variation has a male predominance 3:1. Although occasionally the valve forms with 2 equal cusps “pure” BAV, more commonly there are three apparent cusp elements with a raphe fusing of one or more cusps to produce a valve with two or occasionally one cusp. Extremely rarely, quadricupid valves have been described.
Sievers and colleagues developed a classification of aortic valve morphologies based on single center retrospective analysis between 1999‐2003 of 1206 patients undergoing AV surgery.3 The figure below provides a schema for describing different valve morphologies. Seivers et al. J Thorac Cardiovasc
Surg 2007;133:1226-33.
The bold line represents a raphe, The bold line represents a raphe, the conjoined segment of two under developed cusps which extends into the commissure.
Seivers and colleagues then analyzed 304 of 409 patients who were noted to have bicuspid aortic valves (with bicuspid or unicuspid morphology) and described the types and frequency of valve configurations found.3
Siever’s categorized bicuspid aortic valves into: Type 0 (No raphe, 2 equal leaflets) Type 1 (1 raphe, 2 asymmetric leaflets) Type 2 (2 raphe, 1 leaflet, “unicuspid”) Fusion of the left and right cusps was the most common Type 1 configuration and fusion of the left and noncoronary cusps the least common. The bicuspid valves were more commonly stenotic than insufficient (approximately 3:2). R-right coronary cusp, L-left coronary cusp, N-noncoronary cusp, I-insufficient, S-stenotic, Bbalanced, No-normal function. (Seivers et al. J Thorac Cardiovasc Surg 2007;133:1226-33.)
Bicuspid aortic valves (BAV) are associated with a number of other cardiac anomalites: 6% pts with BAV will have coarctation (and conversely, 50‐75% of patients with coarctation will have BAV)4; Left‐Right fusion is more frequently associated with coarctation than other configurations. Right‐non fusion is more commonly associated with cusp pathology. Other less common associated anomalies include VSD, ASD, Hypoplastic left heart syndrome, patent ductus arteriosis, bicuspid pulmomary valve, Ebstein’s anomaly. In a number of syndromes, BAV is paired with various left‐sided lesions: Shone’s syndrome (multiple left sided obstructive lesions) Williams Syndrome (supra‐
aortic stenosis), Turner’s Syndrome (aortic coarctation).5 Additionally BAV is associated with an increased risk of aortic disease related to abnormalities in the aortic media leading to cystic medial necrosis. A deficiency in fibrilin‐1 contributes to smooth muscle detachment from elastin and collagen and increases in matrix metalloproteinases, leading to matrix breakdown and cell death.
Genetic factors such as these as well as flow dynamics appear to lead to significantly increased rates of aortic dilation, aneurysm, and dissection. Right‐Left fusion is associated with early aortic root dilation, Right‐Non fusion is associated with aortic arch dilation.6 Frazel et al has described 4 “clusters” of morphologies characterizing the aortic dilation associated with BAV: 1‐ root only enlargement, 2‐
ascending aorta only enlargement, 3‐ascending and proximal aortic arch enlargement, 4, root, ascending and proximal aortic arch enlargement.7
Fazel, S. et al. JTCVS 135:901, 2008.
AORTIC STENOSIS: The Basics: Echocardiographic assessment of aortic stenosis begins with a 2‐D examination of the valve morphology, including number, motion, relative size of valvular cusps, presence of calcifications, and the structure of the left ventricular outflow tract (LVOT), aortic root, and proximal ascending aorta. Although the stenotic orifice may be visualized with 2‐D echocardiography, Doppler modalities are primarily used to characterize the degree of stenosis. Table A below summarizes the recommended methods of assessing aortic stenosis and we will review them briefly here.8 1. Aortic Stenosis Jet Velocity: AS jet velocity is directly measured by Doppler in the deep TG or TG LAX view, where the Doppler beam is approximately parallel to the flow through the aortic valve orifice. The maximum velocity is achieved just past the orifice of the valve at the point of maximal flow convergence (the vena contracta). Although the maximum velocity is flow dependent and requires good alignment of the Doppler beam with the direction of flow, it is the strongest clinical predictor of outcome. 2. Mean Transvalvular Gradient: The mean gradient across the valve orifice can be calculated using the Bernoulli equation, which simplifies in the clinical setting to PG= 4v2. This assumes that the proximal velocity in the LVOT is <1.0cm/s. If LVOT velocity is >1.5cm/s or the aortic velocity is <3.0cm/s, the proximal velocity must be accounted for: PG= 4 (vmax2 – vproximal2). Although the mean velocity is the most comparable 9
http://www.echoincontext.com/doppler01/doppler01_15.asp
Table A. Echocardiographic Assessment of Aortic Stenosis: Summary of ASE Recommended Techniques Measurement
Formula
Concept
Advantages
Limitations
Units
Cutoffs
AS Jet Velocity
Direct CW Doppler
measurement
Velocity increases as effective
orifice area decreases
A direct measurement
Requires adequate alignment
of Doppler beam with flow;
flow dependent
m/s
Mild: 2.6-3.0
Moderate: 3-4
Severe: >4
Calculated from the velocity
using the Bernoulli equation
(instantaneous gradient=4v2)
Averaged from all the
gradients derived from the
velocity curve
Limited by accuracy of
velocity curve; flow
dependent
mmHg
Mild: <20 (<30)
Moderate: 20-40 (30-50)
Severe: >40 (>50)
Measures effective orifice area
which is more clinically
predictive; relatively flow
independent
LVOT diameter is squared,
increasing any measuring
errors; requires multiple
measurements (VTILVOT,
VTIAV)
cm2
Mild: >1.5
Moderate: 1.0-1.5
Severe: <1.0
Mean gradient
v2/N
AVA calculated
from Continuity
Equation
AVA= (CSALVOT x
VTILVOT)/VTIAV
Conservation of Mass, SV
ejected from LV is same in
LVOT as SV that flows through
the valve
Simplified
Continuity
Equation
AVA= (CSALVOT x
vLVOT)/vAV
Ratio of LVOT velocity and AV
velocity is similar to ratios of
VTIs in native AS
Simpler than using VTI;
relatively flow independent
Less accurate when velocity
curve is atypical
cm2
Mild:
Moderate:
Severe: <1.0
Velocity Ratio
VR= VLVOT/VAV
Effective AVA as a proportion
of LVOT area
No need for LVOT
measurement
Limited longitudinal data.
LVOT size variability not
accounted for
None
Mild: >0.50
Moderate: 0.25-0.50
Severe: <0.25
Planimetry of
Anatomic Valve
Area
2D, 3D imaging
Anatomic CSA measured in
SAX view of valve using 2D or
3D imaging
Provides data even when
Doppler measurements not
possible
Accuracy limited in setting of
severe calcification, difficult
to determine minimum orifice
cm2
Mild:
Moderate:
Severe: <1.0
Adapted from ASA Guidelines and Standards: Echographic Assessment of Valve Stenosis: EAE/ASE Recommendations for Clinical Practice, 2008.
Baumgartner H., et al. J Am Soc Echocardiogr. 2009 Jan;22(1):1-23. to other clinical measurements, in the setting of elevated proximal velocity or low flow it is impractical to recalculate the P for each velocity including the proximal velocity so the peak gradient is utilized. Transvalvular gradients are also flow dependent and are limited by the reliability of the velocity measurements. 3. Aortic Valve Area by Continuity Equation: The priniciple of conservation of mass, assumes that total flow volume through the valve is equal to total flow volume just proximal to the valve. The stroke volume (SV) ejected from the left ventricle can be calculated by multiplying the cross sectional area of the LVOT by the integrated velocity‐time of flow through the LVOT. Since the SV through the stenotic orifice must be equal to the SV in the LVOT, the cross sectional area of the effective valve orifice can be derived by dividing the flow volume through the LVOT by the VTI through the valve: AVA = CSALVOT x VTI LVOT/VTIAV. Baumgartner H., et al. J Am Soc Echocardiogr. 2009
Jan;22(1):1-23 The AVA calculated with the continuity equation is largely flow independent. As we will discuss a little later, very low flows may interfere with the accuracy of the measurements. The technique is limited by the need for multiple measurements. Although Maslow et al10 has described the “double envelope technique” which allows for obtaining the VTILVOT and VTIAV using the CW velocity curve for a single beat, many authors suggest using a separate PW velocity curve for the LVOT. Averaging velocity curves from at least three beats for sinus rhythm and more than five beats for irregular rhythms has been suggested to account for beat‐to‐
beat variability. Error may be introduced by variability in the measurement of LVOT diameter. Since the LVOT diameter is Velocity curve of stenotic orifice Velocity curve of LVOT 2
squared, CSALVOT=( ½ dLVOT) , small Adapted from Maslow AD, et al. Anesth Analg. 2000 Sep;91(3):509­16. differences will be augmented potentially altering the calculated area. Double Envelope Technique 4. Additional techniques: Techniques such as the simplified continuity equation, the velocity ratio (“the dimensionless index”), and planimetry are also utilized, but the data supporting their use is more limited. Simplified Continuity Equation: The simplified continuity equation for AVA uses peak velocities in the LVOT and across the valve to estimate effective orifice area, AVA = CSALVOT x VmaxLVOT/VmaxAV. Using peak velocity is simpler, but critics believe this method is less reliable than VTI. As with the AVA derived from the continuity equation using VTI, LVOT measurement introduces a source of potential error. Velocity Ratio: The velocity ratio (VR) or “dimensionless index” compares the maximum velocity in the LVOT to the maximum velocity through the valve orifice, VR = VmaxLVOT/VmaxAV. This method eliminates any error caused by the LVOT measurement. The ratio is close to 1 for normal valves and decreases to <0.25 for severe stenosis. Planimetry: This technique involves visualization of the valve orifice in SAX with 2D echo and directly outlining the anatomical orifice to obtain an area. This method is complicated by the difficulty visualizing the orifice boundaries due to calcifications or, in the setting of prosthetic valves, reflections from the valve housing. Also, given that the area may be larger or small in different planes, it may be difficult to ensure the planimetry measurement is made in the plane with the smallest orifice. Although this method can give an estimate of the orifice area when Doppler modalities are not possible, it measures the anatomic not the effective orifice, the later being the area most associated with clinical outcome. 5. Nonclinical Measurements: Measurements such as LV% stroke work loss, recovered pressure gradient, energy loss index, valvulo‐arterial impedance, aortic valve resistance, and projected valve area at normal flow rate can provide complementary information, but these measurements are complex and cumbersome and generally not considered practical in the clinical setting. CASE 2: Fixed Subvalvular Aortic Stenosis Subvalvular stenosis can be fixed or dynamic. Fixed stenosis is most frequently (90%) caused by a discrete membraneous ridge on the ventricular septum that partially or completely encircles the LVOT. Fixed stenosis may also be due to obstruction due to a thick fibromuscular ridge, a “tunnel‐like” narrowing of the LVOT (also associated
with aortic valvular hypoplasia), abnormal mitral valvular attachments, or accessory endocardial Discrete Subaortic Membrane cushion tissue. The discrete membrane lesion is generally acquired, apparently related to progressive fibrosis of the membranous septum from turbulence in the LVOT. Abnormalities in the relationship between the mitral valve, the aortic valve and the LVOT have been noted in patients developing discrete subaortic stenosis. A familial pattern has also been described, suggesting a genetic susceptibility. Discrete subvalvular stenosis occurs in approximately 6% adults with congenital heart disease with a 2:1 male predominance.11 Additional cardiac malformation are seen in 50‐
13
Garg R, et al. Ann Card Anaesth, 2009 May-Aug;12(2):17
65% of patients12 including patent ductus arteriosis, ventricular septal defect, aortic coarctation, pulmonic stenosis. Surgical resection can be complicated include MV injury, AR, VSD, bundle branch block, and complete HB. Recurrence of the membrane is more likely if the membrane is <6mm from AV, if membrane must be peeled off the mitral valve or aortic valve, and if the peak LVOT gradient is >60mmHg. A discrete membrane may be visualized on 2D and 3D echo examination of the LVOT, but occasionally the membrane is very thin and not clearly apparent. The membrane may be a thick fibromuscular band or have attachments to the mitral or aortic valve distorting the anatomy and valvular function. Elevated intracavitary velocities can be observed on PW, CW, and Color Doppler through the LVOT. The CW velocity curve in LVOTO will be smooth and rounded and peak later in systole as the degree of stenosis increases. High velocity flows and turbulence in the outflow tract, particularly in the setting of peak LVOT Doppler gradients >50mmHg, are associated with secondary damage to AV. Aortic regurgitation from thickening and sclerosis of leaflets is common. The grading of AR may be complicated by LVOT turbulence and the increased flows associated with moderate and severe AR can result in even higher LVOT gradients. In the setting of concomitant aortic valvular stenosis, the elevated proximal velocity in the LVOT must be taken into consideration. If LVOT velocity is >1.5m/s, the Bernoulli equation is P=4(VAV2‐VLVOT2). CASE 3: Dynamic Subvalvular Stenosis – Hypertrophic Cardiomyopathy Dynamic subvalvular stenosis is observed in the setting of hypertrophic cardiomyopathy (HCM) and is frequently associated with systolic anterior motion of the MV (SAM). HCM has multiple variants and obstruction can occur apically and in the mid portions of the chamber as well as in the LVOT. Most common is asymmetric septal hypertrophy, involving significant thickening and prominence of the ventricular septum just below the aortic valve. Dynamic LVOTO may be unmasked after replacement of a stenotic aortic valve in a patient with significant concentric hypertrophy due to more complete emptying of the ventricle during systole and entrainment of the anterior mitral valve leaflet or chordal elements into the LVOT (SAM).14 A characteristic “inch worm” appearance of the anterior MV leaflet tip is evident on 2D echo often accompanied by varying degrees of mitral valvular regurgitation from incomplete MV closure. SAM also develops independent of HCM in patients with 16
myxomatous, redundant valve tissue or may develop after valve Elliot
PM
et
al.
UpToDate
Jan
2012
repair in patients with long residual posterior leaflets.15 Maslow and colleagues noted that coaptation of the leaflets nearer to the LVOT after repair was more likely to result in SAM. Higher risk of SAM was noted in patients with long posterior leaflets, particularly with anterior leaflet to posterior leaflet ratios (AL/PL) < 1.3, and septum to coaptation distances (C‐sept) < 2.5 cm.15 17
Ommen SR, et al. Heart 2008;94:1276-128.
18
Willert J et al. Anesth Analg 2006;102:1361–2.
Similar to fixed LVOT obstruction, turbulence in the LVOT is visualized on color Doppler, and increased LVOT velocities and an intracavitary gradient are present. The CW velocity curve is late‐peaking with a concave pattern prior to the peak giving it a characteristic “dagger‐like” appearance (see image).19 The aortic valve disease can coexist with dynamic LVOTO so careful assessment of AV anatomy and motion is important. As with fixed subvalvular stenosis, pressure gradient calculation must take into account increased the increased proximal velocity and careful assessment for significant degrees of AR is necessary particularly when very high LVOT gradients are noted. http://rwjms1.umdnj.edu/shindler/ihss.html
Although septal ablative therapy is also available, myotomy with myectomy has been the predominant surgical approach to dynamic LVOTO associated with HCM. Resection of a segment of septal tissue can increase the diameter of the LVOT and greatly decrease LVOT velocities. Complications of myotomy with myectomy include inadvertent VSD with perforation of the membranous septum, conduction system injury, injury to the mitral or aortic valves. Careful TEE measurement prior to the procedure and evaluation after the procedure can help guide surgical intervention and possibly help avoid complications (citation).20 CASE 4: Low‐flow, Low gradient Aortic Stenosis Assessment of aortic stenosis can be difficult in patients with low cardiac output, such as patients with poor LV function, severe MR or severe MS. Low‐flow, low‐gradient AS is defined as effective orifice area <1.0cm2, mean gradient <30‐40mmHg, LVEF <40%. Although the continuity equation for the estimation of effective orifice area is largely flow independent, low flow states can result in valve areas that over‐estimate the true degree of valve stenosis. Pseudostenosis occurs when the transvalvular flow is inadequate to fully open the valve leaflets. In this setting a moderately stenotic valve can appear severely stenotic. A dobutamine stress challenge can help distinguish between a truly stenotic valve and pseudostenosis. If inotropic stimulation results in increased transvalvular velocities, increased pressure gradients and an increase in the estimated valve area, the valve stenosis is related to low cardiac output and likely will not respond to surgical intervention. If the valve area remains stable despite increased transvalvular velocities and pressure gradients, the valve is truly stenotic and surgical replacement would provide hemodynamic benefit. No increase in either valve area or flow velocities and pressure gradients, however, suggests that there is no contractile reserve and this subgroup of patients has very poor surgical outcomes. Being able to distinguish between these subpopulations can be critical in clinical decision‐making. Table B. Assessment of Low-Flow, Low-Gradient Aortic Stenosis
With Dobutamine Stress
Significance
Pseudostenosis
Increased AVA >1.0cm2
No true stenosis
Severe stenosis
AVA< 1.0cm2, AS jet velocity
>4.0m/s, Mean PG >40mmHg
True stenosis, surgical intervention
benefitial
SV and EF increase <20%
High surgical mortality and poor
long-term outcome even in setting of
true stenosis
No contractile reserve
Adapted from ASA Guidelines and Standards: Echographic Assessment of Valve Stenosis: EAE/ASE Recommendations for Clinical Practice, 2008.
Baumgartner H., et al. J Am Soc Echocardiogr. 2009 Jan;22(1):1-23
Low gradient, low flow AS may also be seen in the context of normal LV function. Severe concentric hypertrophy with markedly reduced chamber size, limits stroke volume and can result in low cardiac output and thus lower flow velocities and pressure gradients than expected for a given degree of stenosis. Effective orifice area (EOA) by continuity equation, however, is considered accurate in this situation.8 Given that this scenario often occurs in smaller, elderly women there may be a need to index for body size. (Significant AS is associated with an indexed AVA < 0.6 cm2/m2) Similarly low cardiac out put states such as severe HTN, severe MR or severe MS in the setting of AS can result in low flow velocities and low gradients even in the presence of real and significant aortic valve stenosis. Again, estimates of AVA area by continuity equation are generally reliable. Some care, however, must be taken in the setting of severe MR that the AS velocity curve is not confused with the MR velocity curve which is slightly longer in duration. CASE 5: Elevated valve gradient after prosthetic valve placement. After aortic valve replacement, transvalvular gradients are frequently elevated given the hyperdynamic state of the heart after bypass, as well as increased heart rates frequently associated with inotropic use after bypass. When high pressure gradients are seen immediately after AVR, the differential includes prosthetic valve dysfunction, presence of subvalvular or supravalvular obstruction, patient‐prosthetic mismatch (PPM), pressure recovery phenomenon, and measurement error.21 Abnormal prosthetic valve function such as inadequate leaflet openning or inappropriate seating in the annulus can causes significant slow obstruction. As mentioned earlier, the relief of valvular obstruction with AVR can occasionally unmask subvalvular stenosis and, rarely, supravalvular stenosis. PPM occurs when the valve prosthesis size is too small for the hemodynamic needs of the patient and associated with poor long‐term and short‐term outcomes.21 EOA indexed for body surface area is the only factor that has been shown to be consistently predictive of increased gradients and worsened clinical outcomes. PPM is considered insignificant if indexed EOA is >0.85 cm2/m2, moderate PPM if indexed EOA is 0.85‐0.65 cm2/m2, and severe PPM if indexed EOA is <0.65 cm2/m2. Interestingly, obesity does not seem to increase PPM despite higher BSAs, possibly due to the fact that cardiac output requirements in obese patients tend to be lower than non‐obese patients with the same BSA.22 Even when no true flow obstruction exists, the phenomena of pressure recovery can produce apparent increased Doppler‐derived gradients across valves. The effect is much more pronounced with prosthetic valves, but can be seen in certain circumstances with native valves. Normally, the flow stream prior to the valve has a relatively low velocity and high pressure. As the flow converges on the valve orifice, the velocity increases and the pressure drops until it reaches maximum velocity and minimum pressure just beyond the actual valve orifice in the “vena contracta.” Depending on the geometry of the valve orifice and the aorta beyond the orifice some portion of this kinetic energy (from the increased velocity) is converted into potential energy resulting in “pressure recovery”. Orifices that have a flatter profile such as prosthetic valves produce a greater degree of flow Bach DS. JACC Cardiovasc Imaging. 2010 Mar;3(3):296-304.
convergence and a smaller effective orifice and thus higher velocities and greater pressure gradients. Smaller aortic diameters (ie. <30mm) will enhance the magnitude of this effect as there is less re‐expansion of the flow stream and less kinetic energy is lost as turbulence and heat and more “recovered” as pressure. As a result maximal Doppler velocities and gradients derived from these velocities will be greater than the gradients obtained at catheterization. Valves with multiple different sized orifices such as mechanical bileaflet prosthetic valves can exhibit a significant degree of pressure recovery. The velocity of flow the smaller central orifice of a bileaflet prosthetic valve will be higher than the lateral orifices resulting in a greater pressure drop in the vena contracta of the central orifice. Just beyond the valve, the pressure will rise again due to the re‐expansion of the flow stream and decrease in velocity and “recovered” potential energy. Pressure gradients derived from the peak velocity through this central orifice will be higher than those measured in the lateral orifices and more significantly exaggerate the true physiologic gradient. This effect has largely been incorporated in the normal Doppler gradients recorded for these valves, but may become significant for very small valve sizes (ie. 19mm or smaller). Zoghbi et al. J Am Soc Echocardiogr. 2009 Sep;22(9):975-1014.
The effect of pressure recovery on the Doppler gradient can be calculated by the following equation: Pressure recovery (mmHg) = PGmax x 2 x (EOA x AoA) x (1 ‐ [EOA/AoA]) where PGmax represents the Doppler‐derived gradient. PGnet (the pressure gradient after pressure recovery) then be estimated by: PGnet = PGmax ‐ {PGmax x 2 x (EOA x AoA) x (1 ‐ [EOA/AoA])}. AORTIC INSUFFICIENCY The Basics: Assessment of aortic insufficiency (AI) requires an integrated approach utilizing and comparing multiple pieces of data from different modalities of analysis. It is important to avoid complete reliance on any one parameter, but rather evaluate the different measurements in aggregate weighing each piece of data by how reliable it is in that particular clinical setting. A summary of echocardiographic parameters for evaluating AI can be found in the Table C and D below and we will review them briefly here.23 Initial echocardiographic evaluation begins with a general assessment of the heart and valve complex with 2D echo evaluation including characterization of the presence, absence, and degree of chamber enlargement, leaflet abnormalities, aorta or aortic root pathology (aneurysm, dissection). Color Doppler allows for analysis of the regurgitant jet at the point of flow convergence in the aorta before the regurgitant orifice, at the vena contracta, and in the LV where it can characterize the spatial orientation and size of regurgitant jet. To avoid exaggerating or underestimating the size of the flow patterns, careful attention to color Doppler settings is important, ie. a Nyquist limit of 50‐60 cm/s and a color gain setting that just eliminates color in non‐moving areas. 1. Proximal Jet Width and Area and Ratio of LVOT: Clinically, the visual appearance of the jet in the LVOT is the most heavily relied upon criteria for assessing aortic regurgitation. Proximal jet width and area (measured within 1 cm of valve) and ratio of jet width to LVOT width are measured best in ME LAX when AV is in near field. The CSA of the proximal jet as a ratio of the LVOT area provides an additional dimension to the measurement and is visualized in the ME AV SAX. These measurements, however, may be complicated by variable jet geometry (central jets that expand rapidly in the LVOT, non‐circular jets, eccentric jets). 2. Vena Contracta Width: Color Doppler can be used to measure the diameter of the regurgitation jet at the point of maximum flow convergence, the vena contracta. This diameter is reflective of the effective regurgitant orifice diameter and is one of the most resilient measurements for assessing the degree of aortic regurgitation. Given the small size the of vena contract, small variations in measurements can result in a relative large percent error. Additionally this measurement is not helpful in complex jets with multiple orifices. 3. Aortic Flow Reversal: Pulse Wave Doppler measurements include measurement of degree of aortic flow reversal in the thoracic aorta. Severe aortic regurgitation is associated with holodiastolic flow reversal in the distal thoracic and abdominal aorta. Varying degrees of partial diastolic flow reversal is seen in mild and moderate regurgitation. Echocardiographic Methods for Evaluation of Aortic Insufficiency Parameter
Method
Concept
Advantages
Limitations
Grading
Enlargement may be
secondary to other causes;
may be normal in acute,
significant AR
(Normal = LV minor-axis <
2.8 cm/m2; LVEDV < 82
ml/m2)
Mild: Normal
Moderate: Normal or
dilated
Severe: Moderate-Severe
dilation (except in acute AR,
or dilation due to other
etiologies)
Severe: Abnormal, flail,
and/or wide coaptation
defect
ANATOMIC
2D
Dilation of LV is a response
to chronic volume overload
Sensitive for chronic
significant AR and
predictive of
outcomes; normal
size excludes chronic
significant AR
2D
Leaflets may have evidence
of thickening or sclerosis,
vegetations or
performations, or
intrinsically normal but
associated with aortic root
dilation
Simple, usually
abnormal in severe
AR
Poor accuracy, may over
or underestimate defect
Color
Increased regurgitant flow
will appear as a larger color
doppler signal in the LVOT
Simple, very
sensitive and quick
screen for AR
Qualitative; Inaccurate
with noncircular jets; jets
can expand rapidly and
unpredictably
Jet width/LVOT
width, (%)
Color
The size of the regurgitation
jet with respect to LVOT
Simple
Inaccurate with
noncircular or eccentric
jets; Assumes LVOT size
is normal
CSA Jet/CSA LVOT,
(%)
Color
The cross sectional area of
the jet in relation to the cross
sectional area of the LVOT
Simple, sensitive and
quick screen for AR
Inaccurate with eccentric
or rapidly expanding jets;
assumes LVOT size
normal.
Vena Contracta
width, (cm)
Color
The point of maximal flow
convergence (VC) allows for
estimation of the effective
orifice size
Simple, quantitative,
highly feasible to
measure, more
reliable than jet width
and area in the LVOT
Inaccurate for multiple,
complex jets; potential for
large % errors given small
values
Mild: <0.3 cm
Moderate: 0.3-0.6 cm
Severe: >0.6 cm
(Nyquist Limit 50-60cm/s)
Jet density
CW
The more flow, the denser
the Doppler signal
Simple
Qualitative;
complementary data only
Mild: Incomplete or faint
Moderate: Dense
Severe: Dense
Left Ventricular size
Aortic Leaflets
DOPPLER
Jet width in LVOT
Jet deceleration rate
(Pressure Half Time),
(ms)
Diastolic flow reversal
in descending aorta
PISA method
CW
The rate of equalization
between the aortic diastolic
pressure and the LVDP
Simple
PW
Hemodynamically
significant regurgitation will
result in direction of flow in
diastole due to retrograde
flow into the LV
Simple
Color
Blood converging on
regurgitant orifice forms
hemispheric shells of
increasing velocity and
decreasing surface area.
Quantitative,
provides both EROA
and RV
Not specific, can be
influenced by other
factors such as changes in
compliance of LV or
vasculature and
hemodynamics
Not specific, can be
influenced by other
factors such as changes in
LV or vascular
compliance; Brief initial
flow reversal can be
normal
Feasibility limited by far
field imaging,
calcifications, multiple
jets, eccentric jets;
inaccurate in setting of
aortic aneurysm; limited
experience
Mild: Small, if central
Moderate: Intermediate
Severe: Large, if central;
variable, if eccentric
Mild: <25%
Moderate 25-45%
Moderately Severe: 4664%
Severe: > 65%
Mild: <5%
Moderate: 5-20%
Moderately Severe: 2159%
Severe: > 60%
Mild: Slow, > 500 ms
Moderate: Medium, 500200 ms
Severe: Steep, <200 ms
Mild: No/Brief diastolic
reversal
Moderate: Intermediate
Severe: Prominent
holodiastolic
flow reversal
Measurements with Specificity for Severity of AR Supportive signs for AR Quantitative Parameters Adapted from Zoghbi WA et al. J Am Soc Echocardiogr. 2003 Jul;16(7):777‐802. . Echocardiographic Methods of Evaluation of Aortic Regurgitation Parameter
FLOW
QUANTITATION:
Regurgitant Volume
(RV), (ml/beat)
Method
2D, PW
Regurgitant
Fraction (RF), (%)
2D, PW
Effective
Regurgitant Orifice
Area (EROA), (cm2)
2D
PW
CW
Concept
If no shunts, RV is the
difference between flow
through regurgitant valve
and a normal valve
RV= SVregurgValv-SVnormValv
RF=SVregurgValv-SVnormValv
SVregurgValv
(SV=CSAvalve x VTIvalve)
EROA= RV/ VTIregurgValv
Advantages
Limitations
Grading
Quantitative; valid
with complex,
multiple jet lesions;
provides EROA and
RV
Requires doppler-able
competent valve;
multiple measurments;
error in valve diameter
squared for AV and PV;
Shunts
Mild: < 30 ml/beat
Moderate: 30-44 ml/beat
Moderate Severe: 45-59
ml/beat
Severe: > 60 ml/beat
Requires doppler-able
competent valve;
multiple measurements
Uses multiple
measurements; time
consuming
Mild: <30%
Moderate: 30-39%
Moderate Severe: 40-49%
Severe: > 50%
Mild: <0.10cm2
Moderate: 0.10-0.19cm2
Moderate Severe: 0.200.29cm2
Severe: > 0.30cm2
Quantitative Parameters Adapted from Zoghbi WA et al. J Am Soc Echocardiogr. 2003 Jul;16(7):777‐802. 4. Deceleration Rate of Aortic Regurgitation Jet (Pressure Half Time): The CW doppler curve of the aortic regurgitation jet can be used to assess the deceleration rate and pressure half time. These measure the rate of equalization of pressures between the aorta and the left ventricle during diastole. The more severe the regurgitation, the larger the regurgitant volume filling the left ventricle, and the faster the left ventricular diastolic pressure will rise and slow the velocity of the regurgitation jet. This can be visualized by a steep deceleration slope of the regurgitation velocity curve. The peak velocity and the deceleration slope of the regurgitant jet can be used to determine the pressure half time (PHT). Although these measurements can be helpful, changes such as LV ischemia can increase rate of pressure equalization (increase slope, shorten PHT) and LV dilation can decrease the rate (decrease slope, lengthen PHT) independent of the degree severity of AI. Other factors that affect rate of pressure equalization, such as vasodilation or HTN can also alter the measurements and should be taken into consideration. 5. PISA of AR jet PISA of the convergence of flow on the regurgitant orifice has been described for aortic insufficiency, but this measurement is limited by far field window (deep TG) needed for adequate alignment of the Doppler with the direction of flow. 6. Regurgitant Flow Volume/Fraction/EROA: Pulse wave Doppler measurements can determine regurgitant flow volume and regurgitant fraction using the VTI of the velocity curves through the regurgitant valve and a competent valve. The RV can be used to determine the effective regurgitant orifice area of the regurgitant valve. Regurgitant Volume = Stroke Volumeregurg valve – Stroke Volumenormal valve Regurgitant Fraction = Stroke Volumeregurg valve – Stroke Volumenormal valve Stroke Volumeregurg valve Effective Regurgitant Orifice Area = RV / CW VTIregurg valve Case 6: Aortic Regurgitation in Aortic Dissection Identifying not only the presence of valvular insufficiency, but also the cause in the setting of acute ascending aortic dissection (Stanford Type A dissection) can be critical to surgical decision‐making. Movsowitz et al24 described the types of valve abnormalities associated with aortic insufficiency in the setting of dissection include:  poor coaption of normal leaflets due to sinotubular junction dilation  disruption of the leaflet attachments due to dissection flap into the aortic root  prolapse of the dissection flap between the leaflets  leaflet abnormalities independent of the dissection: 1. bicuspid valve with leaflet prolapse 2. degenerative leaflet thickening with poor leaflet coaptation The standard aortic repair involves a supracommissural replacement of the dissected aorta and the any dissected areas of Movsowitz et al. JACC 2000.
the aortic root are readapted with glue or felt. Separate valve replacement is performed for severe valvular dysfunction independent of the dissection such as degenerative thickening or leaflet prolapse due to bicuspid valve disease. However, if there Causes AR in Type A was aortic valvular insufficiency due to dilation of the sinotubular junction, this will be resolved with the reconstruction of the sinotubular junction by the ascending aortic tube graft. In the setting of the aortic root dilation, root replacement with a composite valve graft is frequently preformed. Alternatively, for Type A dissection in the setting of aortic root abnormalities, some surgeons advocate valve‐sparing aortic root replacement (eg. Tirone‐David Procedure) for patients with intrinsically normal leaflets and suspected aortic tissue defects.25 If the aortic valve is diseased and the aortic root is normal, an AVR with an ascending aortic replacement from the sinotubular junction distally is generally performed. CASE 6: Aortic Valve Endocarditis Transesophageal echocardiography has a high sensitivity for identifying intracardiac lesions associated with endocarditis.26 In fact, TEE findings of an oscillating cardiac mass on valvular or supporting structures or implanted materials, evidence of abscess, new partial dehiscence of a prosthetic valve, or new valvular regurgitation are all major criteria in the Duke criteria for endocarditis.27 Vegetations attached to the valve or endocardial structures are present in approximately 80% patients with endocarditis.28 Higher rates of complications have been associated with echographic features such as large vegetation size, prolapsing of vegetation into downstream chamber and involvement of extravalvular structures.28 However, intracardiac masses not associated with infection can also look like vegetations, including papillary fibroma, Lambdl’s excrescences, strands, sutures on a prosthetic valve, redundant chordae or false cords in the LV, the Chiari network in the RA, or prominent chordal insertions on leaflet tips. Features that distinguish between vegetations from other noninfectious masses include gray scale similar to myocardium, location on upstream side of the valve, lobulated or amorphous shape, and chaotic motion that is independent of leaflet motion.29 Echographic Characteristic
Endocarditis
Not Associated with Endocarditis
Texture
Gray scale and reflectance
similar to myocardium (rather
than leaflet)
Reflectance of calcium or
pericardium, white appearing
Location
Upstream side of valve, in path
of jet, prosthetic material
Downstream side of valve; outflow
tract attachment
Shape
Lobulated, Amorphous
Stringy or hair-like strands with thin
attachments
Other
Motion that is chaotic or
orbiting, and independent of
leaflet motion
Lack of turbulent flow or valvular
regurgitation
30
Adapted from Schiller NB et al. UpToDate. June 2008.
New valvular regurgitation has been reported to occur in as many as 63% of patients.29 Assessment of valvular function in the setting of endocarditis can be complex. Hemodynamic instability and high heart rates in patients with acute decompensation from valvular disruption and sepsis can make imaging challenging. Even in stable patients, multiple, often eccentric regurgitant jets due to native valvular perforation and can make quantification of severity of the lesion difficult. Annular abscess complicates 10‐40% of endocarditis in native valves and is more common in endocarditis of the aortic valve. The native aortic valve more susceptible to annular involvement than mitral valve (41% vs 6% in one study).29 In prosthetic valve endocarditis, peri‐annular involvement is not infrequent and results in valve dehiscence and paravalvular leak.29 Annular abscess is also associated with conduction system disease particularly when the annulus between the right and non‐coronary cusps is involved. In the setting of endocarditis with peri‐
annular abscess, fistulization occurs in 6‐9% of cases.31 Unusual flow patterns should be examined for possible presence of an aortico‐cardiac fistula. Fistulization with the left atrium, right atrium, right ventricle, circumflex artery, pericardium, ventricular septal defects have all been described. The high morbidity and mortality associated with endocarditis make careful echocardiographic evaluation critical and can be valuable in surgical planning. References
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