11.8.4 Echocardiography of aortic stenosis

As the severity of symptoms is not directly related to the severity of stenosis, the values obtained from the various cardiological tests must always be interpreted in their clinical context. Transthoracic or transesophageal echocardiography is the technique of choice, as it allows non-invasive measurement of aortic valve area and gradient, assessment of ventricular function, and investigation of associated valvular disease. If there is no need to examine the coronary arteries, catheterisation is not performed: echocardiographic data are sufficient in 85% of cases [25]. However, coronary angiography is still indicated in cases of ischaemic symptoms and in men over 45 years of age or postmenopausal women undergoing aortic valve replacement (AVR) on ECC.      

 When in doubt, two other tests can be used to complement echocardiographic data.
  • The advantage of multi-slice CT is that it highlights calcified areas and calculates an index of the degree of calcification, making it possible to quantify the calcium burden on the aortic valve in degenerative stenosis. Valve calcium burden (calcium score ≥ 1,600) is an independent predictor of perioperative mortality (HR 1.71) [7]. Its excellent spatial resolution makes it ideal for the measurements required for percutaneous valve implantation (TAVI). Angio-CT visualises the coronary arteries with sufficient accuracy to exclude ischaemic disease, but coronary angiography is still required in the case of a positive image.
  • MRI is invaluable for assessing tissue structure, particularly the presence of fibrosis within myocardial hypertrophy (late gadolinium enhancement), which may explain poor ventricular performance despite preserved ejection fraction [3]. However, it cannot assess calcification and its spatial resolution is inferior to that of CT.
 By catheterisation, the aortic valve area is calculated using a simplified Gorlin formula [13]:
 
SVAo (cm2) = K · CO / √ ΔPm
 
where: CO = cardiac output (L/min)
ΔPm = mean pressure gradient (mmHg)
K = constant
 
This relationship shows that the pressure gradient varies with the square of the cardiac output. This means that the gradient is a function of LV systolic performance (pressure generated and rate of contraction) and stroke volume, and must always be interpreted in relation to the latter. When function is preserved, severe aortic stenosis produces a mean transvalvular gradient greater than 40 mmHg, but as ventricular function declines, the gradient decreases regardless of the degree of valve stenosis. Similarly, hypovolaemia reduces the gradient across the stenosis because the stroke volume is lower. Conversely, hypervolaemia or adrenergic hyperstimulation increases the gradient, which tends to overestimate the extent of the stenosis. A hemodynamic state close to equilibrium is therefore essential to obtain reliable data. This is particularly important in the operating room, where blood volume, blood pressure and cardiac output are constantly changing. As we are often faced with inconsistencies between the various measurements, it is essential to base the diagnosis not on a single element but on a synthesis of the various results: 2D/3D imaging, Doppler flow, pressure gradients, equation of continuity, LV function and dimensions, degree of calcification, age of the patient, symptoms and clinical context. The criteria for quantification of aortic stenosis are summarised in Table 11.12.
 
Tab11 12

2D/3D Exam

2D/3D TEE directly visualises the valve in its short axis ("front" view at 40°) and in its long axis ("side" view at 120°). A number of observations can be made.

  • Number of cusps; normally tricuspid, the aortic valve is bicuspid in 1-2% of the population; in almost three quarters of cases the right and left cusps are fused by a raphe, and opening occurs between this large anterior valve and the posterior non-coronary cusp (see Aortic bicuspidity) [32].
  • Size of the valve and the aortic ring; the latter is a virtual structure corresponding to the implantation base of the cusps (see Figure 11.8) [36].
  • Outflow tract diameter; several different measurements are essential for sizing a prosthesis and performing a prosthetic or transcatheter (TAVI) implantation (see Figure 11.11).
    • Left ventricular outflow tract (LVOT), measured just below the valve between the septum and the base of the anterior mitral leaflet;
    • Aortic ring diameter;
    • Diameter of the sinuses of Valsalva;
    • Distance between the free edges of the cusps;
    • Diameter of the sinotubular junction.
  • Degree of opening in systole; the size of the orifice gives an idea of the degree of stenosis (mild, moderate or severe). Quantification by planimetry has the advantage of being a measure independent of haemodynamics, but is questionable (see below).
Calcifications; the location and size of the calcium clusters are specific to different pathologies (see Figure 11.101).
  • Degenerative calcific disease: in the body and at the base of the leaflets;
  • Rheumatic fever: at the commissures (commissural fusion);
  • Bicuspidity: predominant in the raphe.

Video: long-axis view of a tight aortic valve stenosis; the cusps practically stand still; the calcifications of the aortic root form shadow cones.


Video: short-axis view of a tight aortic valve stenosis; the right and non-coronary cusps are blocked by calcium deposits; only the left cusp allows a small opening in systole.
  • Size of the ascending aorta; dilatation is often associated with biscuspidation.
  • Presence of a septal spur at the root of the LVOT, which may be surgically resected to limit the risk of dynamic subaortic obstruction after AVR. The thickness of the septum is measured at the level of the spur and at the level of the adjacent septum to allow the surgeon to estimate the depth of resection possible without risk of iatrogenic VSD (see Figure 13.14).

Fig13 14en

 Figure 13.14: Intra-operative transesophageal echocardiography should determine the thickness of the septum at two points before ECC: at the level of the spur where it is thickest (A, in blue) and in the subaortic zone where it is thinnest (B, in green). This second measurement is essential for the surgeon to avoid too deep a resection with the risk of iatrogenic VSD; it is also important to indicate the distance between the aortic annulus and the maximum bulge [According to: Swistel DG & Balaram SK. Surgical myectomy for hypertrophic cardiomyopathy in the 21st century, the evolution of the "RPR" repair: resection, plication and release. Progr Cardiovasc Dis 2012; 54:498-502] .

The 2D examination is not complete without an assessment of the size of the LA and LV, the extent of concentric hypertrophy (posterior wall thickness > 1.2 cm) and ventricular function.

 Velocity across the aortic valve

Flow across the stenosis is measured by transgastric Doppler, which is the only way to align with the aortic valve on TEE: deep transgastric view at 0° and long-axis transgastric view at 120° (Figures 11.112 and 11.113) [33]. For the value to be correct, the axis of the Doppler interrogation must be identical to that of the aortic flow where it is fastest, i.e. just downstream of the stenosis (vena contracta, see Valve echocardiography). This can be difficult with the transgastric approach because the transducer positions are limited by the mechanics of the probe and because the Doppler beam has to pass through the valve to sample the flow at its outlet in the root of the aorta [15]. However, the valve is highly deformed and its axis can be misaligned. If the alignment is correct, the coloured flow shows a zone of concentric acceleration (PISA) upstream of the valve, a constricted flow through the orifice, a vena contracta just downstream and a swirling zone in the ascending aorta (Figure 11.114). The more the Doppler axis is out of phase with the flow, the lower the measured velocity and the more the gradient will be underestimated.


Video: 120° long-axis transgastric view of a tight aortic stenosis; there is a zone of concentric acceleration on the ventricular side (PISA); presence of a minimal insufficiency. The direction of flow is well within the ultrasound axis and allows Vmax to be recorded accurately.

Fig11 112 en

 Figure 11.112: Aortic flow on TEE. A: Positioning of the Doppler axis in the 120° long-axis transgastric view. B: Positioning in the 0° deep transgastric view [6].

Fig11 113 en

 Figure 11.113: Aortic flow. A: Spectral aspect of pulsed Doppler flow in the Chasse chamber, 3-5 mm upstream of the aortic valve (Vmax 140 cm/s); the sensor must be in the middle of the flow. B: Spectral aspect of continuous Doppler in a tight aortic stenosis; the Vmax (5 m/s) represents the velocity through the valve (yellow arrow); the superimposed image (double contour) at approximately 0.8 m/s is the velocity through the LVOT (green arrow).

The flow of aortic stenosis can sometimes be confused with that of mitral regurgitation, as both are high-velocity systolic flows away from the apex. The difference is that the MI flow is rounded, begins during the isovolumetric contraction phase and ends during the isovolumetric relaxation phase, whereas the aortic flow is more triangular and its duration is reduced to the ejection phase (see Figure 11.77C).
 
The maximum velocity (Vmax) of the jet is the highest value obtained during the examination, without angular correction and regardless of the view used. It is advisable to take the average of at least 3 consecutive measurements, avoiding post-extrasystolic cardiac cycles. In severe stenosis, Vmax is ≥ 4 m/s [4]. On the spectral image of continuous Doppler flow, the trace of severe stenosis is dense, well defined and rounded in shape (peak mesosystolic velocity) (see Figure 11.114B above). Two superimposed traces can often be seen: that of the flow through the valve (maximum velocity) and that of the flow in the outflow tract, which appears as a denser trace at the base of the image (Vmax approximately 1 m/s). In mild or moderate aortic stenosis with good ventricular function, the spectral flow image is triangular with a protosystolic peak; the flow acceleration time is < 80 msec. In narrow aortic stenosis, the image is rounded with a mesosystolic peak and an acceleration time > 100 msec. In dynamic LVOT stenosis, the shape of the tracing is pathognomonic: notch in the ascending slope with mesosystolic narrowing and sharp telesystolic peak; this particular appearance is due to subocclusion of the LVOT by the anterior mitral leaflet (SAM) during the first third of systole, followed by acceleration of Vmax (> 2.5 m/s) and a decrease in stroke volume (narrow curve) (Figure 11.115).
 
Fig11 114 en 
 
 Figure 11.114: Flow in narrow aortic stenosis. A: The coloured flow shows a PISA upstream of the valve, a constricted flow through the orifice, a vena contracta just downstream and a swirling zone in the ascending aorta. The Doppler axis (US, ultrasound) coming from the LV must be aligned within the stenosis channel to capture Vmax at the vena contracta; this is not always possible. B: Image of the spectral flow; the Vmax (5.1 m/s) is used to calculate the maximum gradient (103.6 mmHg); the integral of the velocities (VTI 129.5 cm), calculated by drawing the envelope of the flow, is used to calculate the mean gradient (63.7 mmHg). The two superimposed curves at the base of the trace represent the velocity in the outflow tract (domed appearance) and the velocity in the ventricular cavity (telesystolic acceleration). 
 
Fig11 115 en
 
 Figure 11.115: Aortic flow using spectral Doppler. A: Flow pattern in mild aortic stenosis with good ventricular function. The image is triangular with a protosystolic peak; the flow acceleration time is < 80 msec. B: Flow silhouette in a narrow aortic stenosis. The image is rounded with a mesosystolic peak and an acceleration time > 100 msec. C: Flow image in dynamic LVOT stenosis; the shape of the tracing is pathognomonic: notch in the ascending slope (arrow) with mesosystolic narrowing and sharp telesystolic peak.
 
 The velocity integral (VTI) is the first derivative of velocity with respect to time; it is the distance (D in cm) travelled during systole by a sample of blood corresponding to a perfect cylinder of cross-sectional area S and length D. In a tight stenosis, it is ≥ 100 cm. Multiplying this by the cross-sectional area of the cylinder (cm2) gives the volume of the sample (cm3), in this case the stroke volume (SV). VTI represents the workload of the LV throughout systole and is therefore a better index than Vmax [31].
 
 Pressure gradients
 
Echocardiography can also be used to measure the pressure gradient non-invasively by simplifying Bernoulli's equation:
 ΔP= 4 (V2 - V1)2
where V2 = VmaxVAo and V1 = VmaxLVOT
If V1 < 1.5 m/s, V1 can be neglected and the equation becomes
ΔP = 4 (Vmax)2
 
The normal velocity (Vmax) across the aortic valve is 1.0 - 1.5 m/s; the physiological gradient is less than 7 mmHg. The maximum gradient is a dynamic concept dependent on driving pressure and stroke volume. It varies with the square of velocity (Bernoulli equation) or cardiac output (Gorlin formula). In stenosis, it is increased not only by the increase in intraventricular pressure (sympathetic stimulation), but also by the increase in stroke volume (transfusions) and the decrease in downstream pressure [10]; the latter may result from a decrease in systemic resistance (vasoplegia, septic shock) or a decrease in ascending aortic pressure due to intra-aortic balloon pump (IABP).It is not uncommon for LVOT Vmax to exceed 1.5 m/s, especially after aortic valve replacement in severe LVH. Under these conditions, it is essential to use the full Bernoulli equation ΔP= 4 (V2-V1)2, otherwise the Vmax and gradient of the prosthesis will be grossly overestimated. The mean gradient is the average of the instantaneous gradients during systole and is therefore less dependent on haemodynamic conditions than the maximum gradient. In a tight stenosis it is ≥ 40 mmHg [4].
 
Apart from losses due to friction and vortices, the product of kinetic energy (Ec) and pressure energy (Ep) remains constant in the flow of a fluid. When passing through a stenosis, the velocity increases (increase in Ec) and the pressure decreases (decrease in Ep); this is the situation in the vena contacta. After the stenosis, the aorta is wide, the velocity decreases and the pressure increases again: this is the phenomenon of pressure recovery or reconversion from Ec to Ep distal to the vena contracta (Figure 11.116). This transformation can represent a 20% reduction in the true pressure gradient across the stenosis [5]; it affects direct pressure measurement by puncture of the ascending aorta when the surgeon wishes to confirm the transvalvular gradient. Pressure recovery is proportional to the ratio between the area of the stenosis (SVAo ) and the area of the ascending aorta measured at the sinotubular junction (SAoA ). It can be quantified using the energy loss index (ELI) [31]:
 
 ELI = (SVAo •  SAoA  / SAoA  -  SVAo) / Scorp
 ELI < 0.5 for tight stenosis
 
Pressure recovery becomes significant when the aortic diameter is ≤ 3 cm, leading to an overestimation of the transvalvular gradient [4]. 
 
Reading cardiology reports often reveals differences in the calculated gradients; there are actually three different gradients (ΔP) (Figure 11.28B).
 
  • Peak-to-peak gradient (catheterisation): difference between the maximum ventricular and aortic pressures; these two pressures are not simultaneous; this gradient does not really exist in nature.
  • Maximum gradient (echo): pressure difference calculated at the highest transvalvular velocity occurring during the acceleration of the flow at the beginning of systole (maximum instantaneous gradient); it corresponds to the velocity in the vena contracta, which is the zone of maximum contraction of the flow just downstream of the minimal anatomical section of the stenosis. The area of the vena contracta (haemodynamically effective area) is slightly smaller than the area of the stenosis (geometric area).
  • Mean gradient (echo): average of the sum of the instantaneous gradients; the mean gradient is a better estimate of the degree of obstruction because it is less dependent on haemodynamic conditions and less prone to overestimating the stenosis.
 
Fig11 116 en 
 
Figure 11.116: Illustration of the continuity equation. A: The continuity equation expresses the law of conservation of kinetic energy; as velocity increases, pressure decreases and vice versa. Vmax is reached just distal to the constriction (called vena contracta because of the contraction of the flow); this is where the pressure is lowest and the pressure gradient is maximum. Pressure is recovered distally (pressure recovery, pr) as the velocity decreases as the duct widens; recovery is not complete because of head loss due to frictional forces and vortex formation [37,38]. B: The continuous Doppler spectral image across the aortic valve in the case of a tight stenosis shows a double envelope; superimposed on the base of Vmax (4.7 m/s, yellow arrow) across the valve is the image of the flow in the chasse chamber (1.2 m/s, green arrow). These two velocities correspond to V1 (plenum) and V2 (aortic valve) in Bernouilli's equation. 
 
 The discrepancy between preoperative (transthoracic echo) and intraoperative (TEE) measurements is due to the difference in loading conditions and sympathetic tone between the two situations. Vmax and ΔPm measured in the operating theatre were on average 0.6 m/s and 12.5 mmHg lower, respectively; in 45% of cases the severity of aortic stenosis was one degree lower. However, the velocity ratio (VLVOT / VVAo), see below) was identical in 83% of patients [34].
 
Aortic valve surface area
 
In echocardiography, the aortic valve surface area (SVAo ) is calculated using planimetry or the continuity equation. In TEE, the aortic valve orifice area is measured in a short-axis view at 40° (Figure 11.117). This view provides an immediate assessment of the valve orifice area; the measurement of this area has the advantage of being independent of haemodynamic conditions, but it has three major shortcomings [16].
 
  • Large calcifications create very strong echoes that saturate the image and shadow areas that obscure more distant structures; the perimeter of the orifice can be very difficult to draw accurately.

Video: Tight aortic stenosis of a tricuspid valve in 50° short-axis view. Although difficult, planimetry is feasible.


Video: 30° short-axis view of a tight calcified aortic stenosis with virtually motionless cusps. Planimetry is impossible here.
  • The valve may be so deformed that the echocardiographic short axis is not perpendicular to the axis of the tortuous canal between the calcifications.
  • The valve has the shape of a cone that dips into the aortic root; the appropriate section plane passes through the narrowest point, which is usually the most distal, but it cannot be excluded that the section plane is not further upstream and that the size of the orifice is significantly overestimated. 3D reconstruction provides greater accuracy and shows that 2D planimetry tends to overestimate the actual opening area [9].

Video: 130° long-axis view of a tight calcified aortic stenosis; the cusps hardly open at all.


Video: Three-dimensional view of a tight aortic stenosis, with only one cusp moving in systole.
.
 Fig11 117 en
 
 Figure 11.117: Two-dimensional TEE images of tight aortic stenosis and planimetry of the 40° short-axis orifice area; this measurement is independent of haemodynamics but can be difficult and inaccurate in the presence of extensive calcification. A: Planimetry of the 40° short-axis orifice area (tricuspid aortic valve); the area measured is 0.86 cm2. B: 150° long-axis view of a stenotic aortic valve; the orifice is very restricted. C: Planimetry of a bicuspid stenosis; the surface area is 0.78 cm2. D: Diagram illustrating the major problem of planimetry in aortic stenosis. The stenotic valve is deformed into a cone; it is impossible to know the exact level of this cone at which the 2D slice plane passes. Depending on the level, the area varies by a factor of two. Section 1: Sectional view correct at the narrowest point. Section 2: Sectional view overestimates the valve orifice area. MAL: anterior leaflet of the mitral valve. Se: interventricular septum. LVOT: LV outflow tract. E: Short-axis view in 3D reconstruction. F: Long axis view in 3D reconstruction.
 
 The aforementioned continuity equation states that kinetic energy remains constant throughout a continuous vascular system. The flow per unit time through a wide zone S1 is equal to that through a narrow zone S2, but the velocity (V) increases as the surface area (S) decreases. The stroke volume through the LVOT is the same as through the aortic valve, but is accelerated by the aortic valve. The stroke volume (SV) is the product of the cross-sectional area and the integral of the velocities (ITV, see above).
 
Continuity equation:  S1 · VTI1 =  S2 · VTI2
For simplicity S1 · V1max = S2 · V2max
 
For greater accuracy, it is preferable to use the integral of velocities (VTI) rather than the maximum velocity, as it is less dependent on momentary haemodynamic conditions and represents the whole systole. For the aortic valve we obtain
 
SVAo · VTIVAo = SLVOT · VTILVOT
SVAo (cm2) = (SLVOT · VTILVOT) /  VTIVao
SVAo (cm2 ) = (d2 · 0.785 · VTILVOT) /  VTIVao
             
where: d = diameter of the LV outflow tract 
VTILVOT = integral of the velocities in the LV plenum (pulsed Doppler flow)
VTIVao = integral of velocities across the aortic valve (continuous Doppler flow)
 
Pulsed Doppler sampling is performed in the centre of the LVOT a few millimetres upstream of the aortic annulus, avoiding the zone of concentric flow acceleration (PISA), which gives a wide dispersion of velocities, and the zone close to the septum, where the flow accelerates significantly. The diameter of the LVOT is measured in systole at the same level as the flow measurement, below the aortic valve, between the septum and the base of the anterior leaflet of the mitral valve. In a tight stenosis, the surface area of the aortic valve is < 1 cm2 .
 
However, the cross section of the LVOT is not circular but oval, and the echocardiographic view measures the small diameter of this oval, resulting in a 17% underestimation of the true diameter; this error is then squared in the calculation of the surface area, resulting in a 24% underestimation of the degree of stenosis of the aortic surface [5,12,29]. Direct planimetry of the 3D LVOT will certainly increase the accuracy of the measurements, as that of the outlow tract diameter is the main source of error in the continuity equation [17]. 
Based on the measurement of aortic transvalvular velocity, the continuity equation provides the hemodynamically effective orifice area (EOA) rather than the anatomically effective orifice area (AOA), which is slightly larger [31]. However, the effective orifice area is the one that best represents true LV afterload and is the most accurate predictor of clinical prognosis [4].
 
One way to simplify the continuity equation and minimise the effect of Doppler axis misalignment is to calculate the ratio between Vmax in the LVOT and Vmax across the aortic valve: VLVOT / VVAo. This ratio of velocities (RV) is normally > 0.8; it is < 0.25 in a tight stenosis, meaning that the blood flow is accelerated more than 4 times as it passes through the narrowed valve. RV is a dimensionless index that remains valid when measured velocities are low (misalignment, LV dysfunction). It is also more reliable than the measurements themselves when comparing intraoperative TEE with preoperative transthoracic echocardiography [34].
 
 Functional indices
 
The usual indices of systolic function, such as ejection fraction, are very sensitive to preload and afterload and are therefore of little relevance in the context of aortic stenosis. As the ventricular cavity is small in concentric LVH, it is mathematically normal for the EF to be high as it tends towards 1 (or 100%) as the telesystolic volume tends towards zero. Circumferential velocity of shortening (Vcf), on the other hand, is lower because ejection velocity is reduced because LV afterload is excessive and it takes time for stroke volume to pass through the stenosis:
 
Vcf = (CTD · CTS ) / CTD · téj 
 
Where: CTD : short-axis LV end-diastolic circumference
CTS : LV short-axis telesystolic circumference
Tej: duration of ejection (n = 220-280 msec)
 
Introducing time into the formula, which is the same for circumference as the ejection fraction for volume, gives a result equivalent to power (work per unit time). The ejection time in narrow aortic stenosis is 300-350 msec (normal 220-280 msec). The most reliable criterion for ventricular dysfunction is the short-axis LV end-diastolic diameter; if it is > 4 cm2 /m2, the LV is in systolic failure. Irrespective of inotropic function, diastolic function is always impaired because of ventricular hypertrophy, which makes the cavity very non-compliant.
 
Tissue Doppler examination of the rate of movement of the mitral annulus towards the apex in systole (S') is a more sophisticated observation of myocardial function. This systolic descent of the mitral annulus is due to contraction of the longitudinal myocardial bundles in the subendocardium, the area most at risk in the event of overload or ischaemia. If it decreases (normal value of S': 10-12 cm/s), it is a finer and earlier sign of ventricular dysfunction than the decrease in ejection fraction. Tissue Doppler can also assess a portion of the myocardium and measure its deformation in systole and diastole (strain) and the rate of this deformation (strain rate) [5]. 
 
The heterogeneity of myocardial echoes makes it possible to isolate small areas of 20-40 pixels, known as speckles, which have a particular configuration in their ultrasound reflection that does not change during the cardiac cycle. Using shape recognition algorithms, the processor can track the movement of these natural acoustic markers, a process called speckle tracking (see Doppler echocardiography). By tracking several of them, the computer can continuously assess the distance between them and the deformation of the observed tissue segment (strain and strain rate) [5]. This type of study makes it possible to quantify subtle changes in LV function, such as the degree of longitudinal shortening, which are not apparent in the ejection fraction [1].
 
In addition to the assessment of longitudinal contraction, measurement of valvular-arterial impedance (VaI) appears to be a reliable indicator of the effect of aortic obstruction on LV performance. Valvular-arterial impedance is the ratio between LV systolic pressure, obtained by adding the mean transaortic gradient and systolic arterial pressure, and indexed stroke volume: Zva = (APsyst + ΔPm) / VSi. This represents the haemodynamic load on the LV. When it is greater than 4.5 mmHg/mL/m2, it is an independent predictor of mortality [14].
 
 Tight stenosis and low gradient

Ventricular failure (EF < 0.50) can reduce the mean gradient to < 30 mmHg if the valve area is less than 1.0 cm2 (low flow/low gradient). However, low ventricular ejection may also mean that a simply sclerosed aortic valve cannot open properly, giving the impression that the opening is smaller than it actually is (pseudostenosis). A dobutamine stress echo (dose < 10 mcg/kg/min) can be used to differentiate between these two situations (Figure 11.118) [3,28]. In narrow aortic stenosis, Vmax and pressure gradient increase with dobutamine (≥ 4 m/s and > 30-40 mmHg, respectively), but not the valve area, which remains fixed due to calcifications. In cardiomyopathy, however, the measured valve area increases because improved LV function allows stroke volume to increase and the valve to open further, but the gradient does not change [21,27,28,30]. The ratio between the velocity in the LVOT ( VTILVOT ) and the velocity across the aortic valve ( VTIVao ) is < 0.25 in narrow aortic stenosis (normal: > 0.8). With dobutamine, this ratio increases further in tight stenosis because  VTIVao increases more than VTILVOT. In cardiomyopathy and functional stenosis, however, the ratio increases because the acceleration in the LVOT is much greater than through the valve, which increases its opening and adapts to the increase in stroke volume without changing its gradient [8].

Fig11 118 en

 Figure 11.118: Dobutamine stress echo to differentiate fixed aortic stenosis (top) from functional stenosis (bottom) in the presence of ventricular dysfunction and low gradient. A: The transvalvular gradient is low despite a tight, highly calcified stenosis on planimetry. B: In a tight aortic stenosis, the pressure gradient on dobutamine increases by >18 mmHg, but not the valve surface, which remains fixed due to calcification. C: The transvalvular gradient is low despite a tight stenosis on planimetry, but the valve is simply sclerosed and the LV is unable to open it properly. D: in the case of cardiomyopathy, the measured valve area increases because the functional improvement in the LV allows the stroke volume to increase and the valve to open further; Vmax remains unchanged. In both cases, the surface area of the LVOT does not change, but its velocity increases. LVOT: LV outflow tract.

 A pressure rise of <20 mmHg and an ejection volume of <20% during the dobutamine test are associated with a poor prognosis [2]. This inadequate inotropic response stigmatises irreversible ventricular failure, which increases the mortality of surgical intervention to 20-30% [20]. Stress echocardiography is also useful in unmasking symptoms in patients with tight stenosis who are asymptomatic or hide their condition by limiting their activity. However, it is contraindicated in symptomatic patients with a high gradient [35].

A paradoxical situation of low gradient (ΔPmoy < 40 mmHg) and tight stenosis (S < 1.0 cm2 ) can sometimes occur in the presence of normal ventricular function (EF > 50%). These are usually elderly patients with concentric hypertrophy, a particularly restrictive ventricular cavity and a stroke volume < 35 mL/m2 [28]. However, more detailed investigations, such as measurement of LV longitudinal shortening (strain and strain rate), actually show deterioration in contractile function and advanced fibrosis [1,18].

A positive stress test response is a good indication for surgery, as removal of the obstruction improves LV performance; an increase in stroke volume of >20% suggests a contractile reserve favourable to surgery [4]. In the case of pseudostenosis, the benefit of AVR is likely to be negligible compared with the risk, although some patients may improve [11]. In the former, the one-year mortality is less than 15%, whereas in the latter it is more than doubled [22]. In these high-risk circumstances, a minimally invasive technique such as TAVI is preferable.

These various discrepancies between gradient, velocity and area occur in 30% of cases of tight aortic stenosis [26]. What should the echocardiographer do when faced with this problem [4]?

  • Check for simple measurement errors: Doppler axis misalignment, LVOT diameter measurement error. Adolescents and short people have smaller aortic valves, so it is advisable to index the valve surface area to the body surface area.
  • Ensure good haemodynamic stability during the examination. Variations in stroke volume alter the velocity and gradient across the aortic valve.
    • High flow: sympathetic stimulation, anaemia, fever, arteriovenous shunt (dialysis), vasodilatation, IABP; in these circumstances Vmax in the LVOT is excessive.
    • Reduced flow: hypovolemia, hypertension, myocardial depression (anaesthesia).
  • Look for associated pathologies: aortic insufficiency (high SV), mitral insufficiency (transfer of part of the SV to the mitral valve), mitral stenosis (low SV), severe arterial hypertension (reduced gradient). On Doppler, the jet of a severe MI can be confused with that of aortic stenosis, although their morphology is different.
  • Perform a stress echo in a low-flow/low-gradient situation with an apparently narrow stenosis.
    • Differentiate between true stenosis with LV dysfunction (indication for AVR) and pseudostenosis (doubtful indication).
    • Differentiation between positive functional reserve (indication for AVR) and absence of functional reserve (high mortality, preference for TAVI).
  • Complement echocardiography with an additional test.
    • 3D echo: planimetry of aortic valve orifice, planimetry of LVOT.
    • CT scan: precise measurement of LVCC, calcium index.
    • MRI: myocardial function, fibrosis.
  • Evaluate the factors that favour AVR, even in an asymptomatic patient.
    • Vmax ≥ 5 m/s.
    • Massive calcification.
    • Mean pressure gradient increased > 20 mmHg with dobutamine.

The anaesthetist may be faced with this type of assessment in the operating theatre during coronary artery bypass grafting (CABG) or polyvalvulopathy and the discovery of unexpected or greater than expected aortic stenosis. This occurs in 2.3% of coronary artery bypass graft (CABG) operations [23]. The mortality rate in CABG is directly proportional to the degree of stenosis: it increases 2.5-fold when the aortic surface area is 1.0-1.25 cm2 [24], and spontaneous progression to tight stenosis is faster the older the patient [19]. Therefore, concomitant AVR is recommended for moderate to severe or severe stenosis [4,28].

 

Echocardiography in aortic stenosis 
 Two-dimensional features of severe AS :

- Low cusp mobility
- Planimetric orifice area ≤ 0.6 cm2 /m(difficulty in measuring the minimum orifice)
- Concentric LVH (thickness of subaortic septum)
- Dilatation of the LA (diastolic dysfunction)
Planimetry of the orifice surface is independent of haemodynamics, but often inaccurate (calcifications, cross-sectional plane).

Colour Doppler (narrow stenosis) :
- PISA upstream (LVOT side)
- Reduced flow through the valve
- Downstream vortex flow, with central jet in the root of the aorta
- Frequent concomitant MI
Vmax and gradient increase when:↑ systolic orifice,↑ LV contractility,↑ stroke volume, ↓ aortic pressure (vasoplegia, IABP).

Continuity equation: S = (SLVOT · VTILVOT ) /  VTIVao

Pressure gradient: ΔP= 4 (V2VAo - V2LVOT)
Severe aortic stenosis
- S ≤ 0.6 cm2 /m2

- Vmax > 4 m/s, VTI ≥ 100 cm, ratio VTILVOT /   VTIVao ≤ 0.25

- ΔPmoy- ≥ 40 mmHg

Tight aortic stenosis with low pressure gradient in LV dysfunction is an indication for a dobutamine stress test:
- Fixed stenosis: Vmax ↑ in LVOT and ↑ in VAo, opening area unchanged; ad AVR.
- Functional stenosis: Vmax ↑ in LVCC, orifice surface ↑ , Vmax VAo unchanged; no indication for surgery.

 

 
© CHASSOT PG, BETTEX D, August 2011, last update November 2019

 

References

 

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