How to assess the aortic valve with echocardiography

How to assess the aortic valve with echocardiography

 

Aortic valve disease can have a range of aetiologies, including:

• Congenital:

–  Unicuspid, quadricuspid or bicuspid aortic valve. The first two are usually discovered in infancy, but a bicuspid valve may remain asymptomatic for many decades. Whilst relatively common in humans, bicuspid aortic valves are rare (but not unheard of) in canines. In humans, a severe aortic stenosis in a patient under the age of 50 is almost always due to a bicuspid aortic valve.

–  Prolapse of an aortic valve cusp into a ventricular septal defect (VSD), most commonly in subaortic perimembranous defects.

 

Many congenital aortic valve abnormalities are associated with other aortic abnormalities, such as:

–        Dilatation of the aortic root. This can be a post-stenotic dilation, commonly found in patients with bicuspid aortic valves, as a result of both intrinsic weakness of the aortic wall and due to impingement of an eccentric jet onto the wall; or, a dilatation as found in connective tissue diseases, such as Marfan’s. Such patients are at increased risk of aortic aneurysm or dissection.

–  Aortic coarctation, defined as a narrowing of the aortic arch (Li et al., 2007).

–  Supravalvular aortic stenosis caused by a narrowing of the ascending aorta, as in familial hypercholesterolemia or the hourglass-shaped constriction at the sinotubuar junction as seen in William’s syndrome.

–  Subvalvular aortic stenosis, such as a subaortic membrane or muscular subaortic stenosis.

 

• Rheumatic:

–        Uncommon now in the United Kingdom, Europe and the USA. Almost always in conjunction with rheumatic mitral valve disease. May cause varying degrees of stenosis and regurgitation. Findings are echogenic, scarred leaflet tips, progressing to commissural fusion, with characteristic doming in systole as seen from the parasternal long axis view (PLAX).

 

• Calcific:

–  Commonly termed “degenerative,” it is now believed by many to actually be an active process linked with atherosclerosis, due to the strong correlation between severity of coronary artery disease and aortic valve calcification (Freeman & Otto, 2005). Aortic sclerosis may be a milder form of the same disease. In contrast to rheumatic valve disease which starts at the cusp tips, calcific disease begins at the base of the cusps. Cusps appear highly echogenic and thickened, and in severe aortic stenosis, it may be difficult to discern any movement at all.

 

• Inflammatory disorders and endocarditis:

– Endocarditis more commonly results in regurgitation through leaflet perforation, but can occasionally also cause a degree of obstruction if the vegetation is directly attached to the aortic cusps themselves. Patients with pre-existing valve abnormalities, such as a bicuspid valve, are particularly prone to endocarditis.

–  Inflammatory disorders such as systemic lupus are associated with Libman-Sacks endocarditis, which is again most frequently associated with regurgitation.

This broad range of causes – some of which may coexist and may present in different ways both between patients and in the same patient over time – makes a thorough echocardiographic examination vitally important. For example, a heavily calcified aortic valve may also be bicuspid (whether or not this is actually discernible via transthoracic echo), and a search for associated congenital abnormalities is important. For example, with a patient undergoing aortic valve replacement, replacement of the ascending aorta is also indicated if dilation is at or exceeds 55mm.Sticking with the example of a bicuspid valve, it may initially present as a regurgitant lesion, but stenosis may become the dominant lesion over time.

 

 

How to assess with echocardiography

 

In assessing a patient with aortic valve disease, it is important to:

• Assess the valve itself
• Check for any associated abnormalities
• Quantify the severity of the stenosis or regurgitation, if greater than mild.
• Assess the systolic and diastolic function of the left ventricle.
• Assess pulmonary pressures.

 

Assessing the valve

Every thorough echocardiographic examination begins with the parasternal short-axis (PLAX) view. From this view, an immediate appreciation of left ventricular function and the aortic valve itself is gained. In rheumatic and congenital bicuspid valves, the characteristic systolic doming can be appreciated.

 

The short axis view allows the number of cusps to be visualised in all but the most calcified of valves. It is important to count the cusps in systole, as when the valve is closed during diastole, a bicuspid valve with a raphe can easily be mistaken for a normal tricuspid valve.

 

Checking for associated abnormalities

In rheumatic aortic valve disease, it is important to check all of the other valves, including the tricuspid and pulmonic valves. With a bicuspid aortic valve, or even a severely calcified valve in which the number of cusps may not be known, the aortic root and ascending aorta must be evaluated and measured using high parasternal and suprasternal views. The aorta should be measured at the aortic sinuses, sinotubular junction, and ascending aorta.

Colour flow Doppler is helpful in order to get an immediate appreciation of possible coarctation from the suprasternal approach. Continuous wave (CW) Doppler is important in grading the severity of any stenosis, showing a high systolic velocity which may continue throughout diastole (‘diastolic tail’), indicative of severe coarctation.

 

Quantifying severity

A Doppler assessment of flow through the aortic valve should be a fundamental part of any echo exam. If velocities greater than 2.5m/s are recorded with CW, and/or a regurgitant jet is noted on colour flow Doppler (given that, unlike the other valves where trivial degrees of physiologic regurgitation is extremely prevalent and considered a normal variant, aortic regurgitation is not considered a common finding in ‘normal’ individuals), accurate quantification and grading of severity is essential.

 

Quantifying severity: stenosis

The most important measurements for aortic stenosis are the maximum stenotic jet velocity, the mean transaortic pressure gradient, and the aortic valve area.

 

• Maximum jet velocity: the initial examination is performed from an apical view (normally the five chamber), but given that the recorded jet velocity depends not only upon the velocity of the blood but also the angle of insonation, this may not be the site where the maximal velocity can be recorded.

The Doppler equation is as follows:  fD = 2fTvcosθ / c   ,   therefore v = fDc / 2fTcosθ

Where fD = Doppler shifted frequency, fT = transmitted frequency, v = velocity of moving blood, c = speed of sound (assumed to be 1540m/s), and cosθ = the cosine of the angle of insonation.

From this equation, it should be clear that any deviation in the angle of insonation away from parallel (i.e. away from 0 or 180 degrees), which would give a cosine less than 1, will result in an underestimation of the velocity of the jet.

Careful angulation, and measurements from a variety of views (including suprasternal and right sternal edge), is vitally important when an intermediate value is found, i.e. between 3m/s and 4m/s. A dedicated CW (‘blind’) probe should also be used, given that its smaller footprint allows for unique angles of insonation, and it has a higher signal-to-noise ratio.

 

• Mean gradient: The mean pressure drop across the valve is again calculated from the CW Doppler trace, using the Bernoulli equation. Written in full, this equation is:

However, both viscous friction and flow acceleration can be ignored, as the effects of these are assumed to be negligible within the cardiac system (Armstrong & Ryan, 2010). Where the proximal velocity (V1) is less than 1m/s, this can also be ignored, as squaring this number will make it even smaller.

The maximum gradient can be calculated from the maximum velocity (simply using 4V², as above), but the mean is more helpful to report as it can be directly compared with the mean gradient obtained in the cardiac catherisation laboratory. The maximum gradient cannot be directly compared, because the max. gradient by echo represents the maximum physiologic gradient (the pressure difference between the aorta and the left ventricle at a real point in time), whereas the max. gradient by catheterisation is the non-physiologic measure of the peak-to-peak gradient (peak aortic gradient minus peak left ventricular gradient – which do not actually occur simultaneously).

The mean gradient is calculated by the ultrasound system from the user tracing the spectral Doppler envelope, after which the system can average each individual instantaneous gradient over the systolic ejection period.

 

 

• Aortic valve area

The aortic valve area can be calculated from two main methods.

1. Planimetry: From the short axis view, the anatomic orifice area can be traced using planimetry, in order to grade the severity of stenosis. This may be difficult in heavily calcified valves, where excessive reverberation and shadowing obscures the true orifice. Turning gains down and zooming in over the valve may help. A rheumatic valve, with its classic triangular orifice area, may be easier to planimeter.

2. Continuity equation: The continuity equation is based on the principle of the conservation of flow. This states that the stroke volume proximal to the valve, and the stroke volume through the valve, will be equal.

 

Flow (Q) = Cross Sectional Area (CSA) x  Time Velocity Integral (TVI)

Therefore, CSA (aortic) x TVI (aortic) = CSA (LVOT) x TVI (LVOT)

From this it can be seen that CSA (aortic) = CSA (LVOT) x TVI (LVOT) / TVI (aortic)

Hence, in order to find the cross-sectional area of the aortic orifice, we must find the three other pieces of the puzzle.

 

To calculate the cross-sectional area of the LVOT (left ventricular outflow tract), we assume a circular geometry. In the PLAX view, with our image optimised (zoom, focal point, optimal gains and transducer frequency), the diameter of the LVOT is measured. As this uses the axial resolution of the ultrasound scanner, it has the potential to be highly accurate; the main issue here is intra and interobserver variability and the fact that any errors will be squared.

 

The diameter (or from it, the derived radius) can then be used to calculate the cross-sectional area using the fact that that the area of a circle is πr² , which we assume to be true for the LVOT (although this may not in fact be the case, numerous studies have validated this measurement against ‘gold standards’).

 

The TVI is obtained by tracing the spectral Doppler envelope. The TVI of the LVOT is obtained in the 4 chamber view using pulsed wave Doppler due to its range resolution. The sample gate is placed at the same point at which the LVOT diameter is measured, i.e. around 1cm away from the aortic leaflets, so that the aortic closing (but not opening) click may be seen. Failure to sample at the same point at which the diameter was measured will lead to errors in the AVA calculation. It is important to reduce gains so that the centre of the spectral trace is black, and the edge of the envelope can be easily traced.

 

Finally, the TVI of the aortic jet must be calculated. This may be obtained from the same location as the LVOT TVI, using continuous wave Doppler, but it may also be derived from other sites – wherever the maximal jet velocity can be found – as discussed above. The spectral Doppler envelope is again traced and TVI calculated by the ultrasound machine.

 

The advances of the continuity equation are that it gives the effective orifice area, rather than anatomic (which may underestimate the severity of the stenosis), and it can be used for even the most calcified of valves. The disadvantages is that it involves a number of measurements and therefore the potential for error is high, particularly in LVOT diameter and a possible failure to find the optimal angle of insonation.

 

AVA is almost unaffected by variations in flow, except for the very highest and very lowest of output states. These can be recognised by a maximum velocity and mean gradient that is a lot lower than one would expect, given the degree of stenosis expected from 2D imaging, and that is likely to be somewhat discordant with the AVA calculation. A proposed modification is to calculate valve resistance, but this has not enjoyed widespread clinical acceptance.

 

• Velocity ratio

It is important to briefly mention the velocity ratio. This calculation is popular with many clinicians, as it eliminates the CSA calculation, and also provides an intrinsic indexing for body size. By dividing the LVOT VTI or the maximum velocity over the aortic valve VTI or maximum velocity, a ratio is obtained. If this is close to 1, there is little or no obstruction, whereas a value of 0.25 represents severe stenosis. This calculation is also very helpful in low flow states or with ventricles which cannot generate a high pressure gradient (for example, concomitant severe mitral regurgitation, or the decompensation phase of aortic stenois).

 

 

Quantifying severity: regurgitation

Aortic regurgitation can be quantified as a regurgitant volume or regurgitant fraction. It can also be assessed qualitatively.

The most popular qualitative method is that of colour flow Doppler. A visual assessment of the jet area relatively to the LVOT can give some indication as to the severity of regurgitation; however, this is heavily influenced by the eccentricity of the jet (jets which impinge onto the septum or anterior mitral valve leaflet may be underestimated in size), the driving force (pressure gradient) of the jet, and machine settings such as colour gain and pulse repetition frequency.

Another semi-quantitative method is to look at the density of the CW spectral signal, particularly when compared with the antegrade signal.

A final semi-quantitative method is to look for diastolic flow reversal in the descending aorta, using PW or CW Doppler. The duration and velocity of this reversal will increase with increasing severity of aortic regurgitation (AR). Whilst this is not specific to AR, and does occur with decreased aortic compliance with age, a holodiastolic flow reversal indicates at least a moderate severity of AR. Flow reversal seen in the descending thoracic aorta from the subcostal approach indicates severe regurgitation.

 

Regurgitation can be quantified using two main methods. The least likely of these to be used is the proximal isovelocity surface area (PISA) method. This is based on the concept that flow accelerates towards an orifice in concentric velocity shells. Using colour Doppler, these shells or surface areas can be visualised. By lowering the baseline and thus the Nyquist limit to promote aliasing, the hemisphere expands, making the radius measureable. By zooming over this area, the radius can be measured, and flow calculated from 2πr²  multiplied by the aliasing velocity (read off the scale). By dividing this by the maximum regurgitant velocity obtained from CW, the effective regurgitant orifice area (EROA) can be calculated as:

 

EROA =  2πr²  multiplied x  Valiasing / V regurgitant jet max

 

This is very difficult to perform with transthoracic echocardiography (TTE) due to the unfavourable angle of incidence from the PLAX view, and the fact that this cannot be viably performed from the apical views due to poor lateral resolution at depth.

 

Colour flow Doppler can also be used to measure the vena contracta width, but again, this is rarely performed for aortic regurgitation because the vena contracta is normally so small (when compared with mitral regurgitation, for example), that the smallest of measurement errors could have a very large clinical impact. Still, a vena contracta width of more than 0.6cm would indicate severe AR.

 

The more commonly used method to quantify aortic regurgitation is by a comparison of stroke volumes between the aortic annulus and another competent valve – preferably the mitral valve, but if this suffers from significant disease, then the pulmonic valve has to be used (this is not preferred as achieving good endocardial definition for measurement of this site can be difficult). This cannot be performed as a measure for AR in the presence of an intracardiac shunt.

 

Stroke Volume (SV) = CSA x VTI (as above)

By comparing the stroke volume leaving the left ventricle through the LVOT with the stroke volume entering the left ventricle through the mitral valve, the regurgitant volume can be found, where regurgitant volume (ml) = SV LVOT – SV mitral.

This can also be expressed as the regurgitant fraction (%) = (SV LVOT – SV mitral / SV LVOT) * 100

The EROA can also be calculated from:   EROA = RV / VTI of the AR jet (from CW)

 

 

Once the severity of the aortic regurgitation and/or stenosis has been established, it is important to assess the function of the left ventricle, and any associated impact of potential pressure loading of the pulmonary veins and ultimately the pulmonary artery. Methods for assessing systolic and diastolic function, as well as estimating RVSP and PASP, will be discussed later.