Echocardiographic evaluation of the aortic valve

INTRODUCTION — Echocardiography is the most effective means of evaluating the aortic valve in normal and diseased states. For most conditions, transthoracic (surface) echocardiography (TTE) is sufficient. Congenital, degenerative, and inflammatory lesions are readily recognized and their severity graded. In addition, it is standard practice for TTE to be the sole method of serial evaluation of aortic stenosis and aortic regurgitation.

This topic will review echocardiography of the aortic valve. The diagnosis and management of aortic stenosis and aortic regurgitation are discussed separately in individual topic reviews including the following: (See "Clinical manifestations and diagnosis of aortic stenosis in adults" and "Indications for valve replacement for high gradient aortic stenosis in adults" and "Medical management of asymptomatic aortic stenosis in adults" and "Medical management of symptomatic aortic stenosis" and "Clinical manifestations and diagnosis of chronic aortic regurgitation in adults" and "Natural history and management of chronic aortic regurgitation in adults".)

ECHOCARDIOGRAPHY OF THE NORMAL AORTIC VALVE

Two-dimensional echocardiography — Two-dimensional (2D) imaging of the normal aortic valve in the parasternal long-axis view demonstrates two leaflets (right and noncoronary) (image 1), while the parasternal short axis demonstrates a symmetrical structure with three uniformly thin leaflets that open equally, forming a circular orifice during most of systole (figure 1). During diastole, the normal leaflets form a three pointed star with a slight thickening or prominence at the central closing point formed by the aortic leaflet nodules, known as the nodules of Arantius. The three aortic valve cusps may also be visualized in a subcostal view.

The aortic valve is composed of three cusps: the left, right, and noncoronary cusps. The left cusp guards the left sinus of Valsalva, with the left main coronary artery arising superior to and midway between the commissures of this cusp. The right cusp guards the right sinus of Valsalva, with the right coronary artery arising anteriorly and superiorly. It is the most anterior cusp and is positioned immediately just posterior to the right ventricular outflow tract. Its most rightward commissure is adjacent to the attachment of the anterior or septal leaflet of the tricuspid valve. The noncoronary cusp is located posteromedially, guards the noncoronary sinus of Valsalva, and is adjacent to the interatrial septum.

M-mode echocardiogram — M-mode echocardiography of the aortic valve is performed in conjunction with 2D imaging by targeting the M-mode beam through the aortic leaflets as displayed in the 2D cross sectional view. The M-mode image of a normal aortic valve and root includes a number of distinctive features:

●In the parasternal long-axis orientation, the aortic leaflets open and close at the midpoint of the space bounded by the anterior and posterior walls of the aortic root (image 2).

●After the opening motion, the leaflets are parallel to the aortic root and nearly appose its wall, where they remain until the end of systole. The net effect of these features is a "box-like" appearance of the M-mode wave form.

•Failure of the leaflets to open widely may be seen with aortic stenosis; a decreased stroke volume is suggested if they open widely but drift shut just after achieving maximum separation.

•If the leaflets close immediately and abruptly after achieving full opening, fixed subvalvular stenosis should be considered. If the leaflets close and reopen in the first third to one half of systole, dynamic subvalvular obstruction should be suspected. (See "Subvalvar aortic stenosis (subaortic stenosis)".)

●While in their open systolic position, it is normal for the leaflets to exhibit fine vibrations. The vibrations on the valve have the same timing and frequency of an early systolic low intensity ("functional") murmur.

●During diastole, the coapted leaflets move parallel to the aortic root.

•Vibrations during diastole are highly abnormal and are characteristic of rupture or disruption of the aortic valve.

OBSTRUCTION TO LEFT VENTRICULAR OUTFLOW — Obstruction to left ventricular (LV) outflow may be due to valvular aortic stenosis, fixed or variable subvalvular stenosis, or supravalvular stenosis. The most common cause is valvular aortic stenosis. (See "Clinical manifestations and diagnosis of aortic stenosis in adults".)

Valvular aortic stenosis — The normal aortic valve area in adults is 3 to 4 cm². As aortic stenosis develops with progressive thickening and calcification of the leaflets, a minimal valve gradient is present until the orifice area becomes less than half of normal. In general, symptoms in patients with aortic stenosis occur when the valve area is <1 cm² or the mean transvalvular gradient exceeds 40 mmHg. (See "Clinical manifestations and diagnosis of aortic stenosis in adults".)

Severe narrowing or obstruction of the aortic valve accompanied by dyspnea, angina, or syncope has a poor prognosis. Surgical (or percutaneous) relief by prosthetic valve implantation dramatically improves survival in such patients. (See "Indications for valve replacement for high gradient aortic stenosis in adults".)

Echocardiography in combination with continuous and pulse wave Doppler enables accurate evaluation of aortic stenosis severity (table 1) [1].

M-mode echocardiography — M-mode echocardiography remains useful in capturing the motion of the aortic valve; variations in motion patterns are often useful in differentiating severe from mild aortic stenosis [2]. In the setting of a trileaflet aortic valve, aortic valve M-mode excursion of at least 12 mm is generally not consistent with severe aortic stenosis.

Typically, most aortic stenosis presents on M-mode as dense, persistent echoes replacing the normal motion patterns described above; the echoes may no longer lie parallel to the aorta (figure 2) (see 'Echocardiography of the normal aortic valve' above). Aortic valve sclerosis without stenosis can mimic this pattern; dense echoes from sclerotic areas can obscure normal leaflet motion. Aortic valve sclerosis and stenosis can be differentiated by the 2D Doppler imaging.

Two-dimensional echocardiography — 2D echocardiographic findings in aortic stenosis include identification of the number of leaflets, the extent, and pattern of calcification, and the degree and pattern of leaflet motion (movie 1A-E). The aortic root (including the aortic ring) is also visualized.

Although the aortic valve area is usually calculated using the continuing equation as discussed below (see 'Doppler echocardiography' below), 2D planimetry of the aortic valve area is helpful when the transaortic valve gradient cannot be accurately ascertained (eg, in the setting of significant LV outflow tract [LVOT] obstruction) [3]. Transesophageal echocardiography (TEE) may be helpful when TTE images are inadequate for planimetry.

There are other findings on the echocardiogram that may help in the assessment of severity:

●Patterns of leaflet motion are helpful, and when leaflets demonstrate a systolic "doming" pattern, the possibility of significant obstruction (or bicuspid valve) is much greater. This is usually only present when the leaflets remain flexible and the pathology is related predominantly to commissural fusion.

●2D imaging can display the aorta distal to the valve. Dilatation may be present due to associated aortic disease in acquired aortic valve disease (image 3). Bicuspid aortic valves are associated with aortopathy and the extent of aortic dilation is not proportional to the severity of stenosis. (See "Clinical manifestations and diagnosis of bicuspid aortic valve in adults".)

●Varying degrees of concentric LV hypertrophy are seen in aortic stenosis. In the well-compensated patient with severe aortic stenosis, a resting echocardiogram will generally disclose significant LV hypertrophy with normal or even hyperdynamic contractile function. Use of strain analysis is discussed separately. (See "Tissue Doppler echocardiography" and "Clinical manifestations and diagnosis of aortic stenosis in adults".)

Doppler echocardiography — Although observations of two dimensional and M-mode findings are useful in the initial detection of aortic stenosis, Doppler quantitation of transaortic systolic pressure gradient and valve area are definitive diagnostically and are basic to noninvasive evaluation [4-8]. In fact, carefully obtained Doppler data are so reliable that diagnostic catheterization for the determination of the severity of aortic stenosis has been relegated to a secondary confirmatory role and for assessment of coexistent coronary artery disease (movie 2 and movie 3 and image 4 and image 5 and waveform 1). (See "Hemodynamics of valvular disorders as measured by cardiac catheterization".)

The critical components of the Doppler examination of aortic stenosis are based on the continuous wave Doppler and include the AS jet velocity, the mean AV gradient, and the AVA derived from the continuity equation [3].

In the evaluation of aortic stenosis with Doppler echocardiography, it is essential to employ continuous wave Doppler from a number of sites to sample flow signals arising from the jet across the stenotic aortic orifice so that the highest velocity can be recorded. Only continuous wave Doppler is acceptable because the velocities encountered in all grades of aortic stenosis are too high for pulsed wave Doppler to sample.

Peak velocity — To obtain the highest velocity, the angle of interrogation should be as parallel with flow as possible. Since the peak velocity is a function of the cosine of this angle, interrogation angles greater than 30 degrees result in major underestimation of the severity of obstruction. Since it is impossible to predict the orientation that will provide the highest peak velocity, the transaortic valve velocity is interrogated from several acoustic windows, including the apex, suprasternal notch, and right parasternal intercostal space. A peak velocity >4 m/s is strongly suggestive of severe stenosis and clinical outcomes related to stenosis, whereas a peak velocity <3 m/s usually indicates mild stenosis.

Using the highest recorded peak velocity, the simplified Bernoulli equation can be applied to obtain the peak instantaneous gradient:

It is important to note that the peak instantaneous systolic gradient, as measured by Doppler, may be higher than the "peak to peak gradient" obtained during invasive cardiac catheterization. The peak to peak gradient is derived by comparing peak ventricular and aortic pressures. (See "Hemodynamics of valvular disorders as measured by cardiac catheterization".)

At times, relatively large peak systolic gradients can be confused with significant aortic obstruction but such confusion can be avoided in three ways.

●Inspection of the rate of rise of the Doppler wave form. If the wave rises rapidly with a short acceleration time, the stenosis is more likely to be mild, but if it rises more slowly with a long acceleration time, a high gradient is likely to connote severe obstruction (waveform 1).

●Using the mean gradient across the valve. Clinical echocardiography analysis packages display peak velocity, peak gradient, mean velocity, mean gradient, and the velocity time integral (VTI) after the spectral Doppler display of the continuous wave velocity signal is traced. There is a stronger correlation between mean gradients obtained by echocardiography and near-simultaneous invasive measurements than between the peak instantaneous gradient and the peak to peak gradient.

●The most effective method of quantitating the severity of aortic stenosis is to calculate the valve area (figure 3) using the continuity equation (see "Aortic valve area in aortic stenosis in adults"). This calculation is performed by using the continuity principle, which states that in a closed system the flow in one portion of the system is equal to the flow in another [9].

According to the continuity equation, flow in the LVOT is exactly equal to the flow across the stenotic aortic valve. Simply stated, flow volume (Q) measurements at serial sites in a closed system (such as the heart) should be identical. Planimetry of the pulsed wave Doppler flow signal from the LVOT derives theVTI, which is the distance the average red blood cell travels during systole in the outflow tract:

where Area_LVOT = cross-sectional area of the LVOT, VTI_LVOT = velocity time integral in the outflow tract, AVA = aortic valve area, and VTI_AV = velocity time integral across the aortic valve. The effective orifice area of the stenotic valve can therefore be calculated after simple equation rearrangement:

The cross-sectional area of the LVOT is derived from the diameter (d) of the LVOT measured at mid-systole on the parasternal long-axis view just proximal to the aortic valve hinge-points (area = ∏d²/4). The peak velocities in the LVOT and across the AV can be substituted for the respective VTIs in a simplified continuity equation [3]. The threshold for severe aortic stenosis is an aortic valve area of 1.0 cm². In contrast to invasive methods utilizing the Gorlin formula, the continuity equation is relatively insensitive to aortic regurgitation.

Other methods of estimating the severity of the aortic stenosis include measurement of aortic valve resistance. Aortic valve resistance (AVR) can be calculated using Doppler echocardiography based upon the following equation [3]:

where PkV_AV = peak velocity across the aortic valve, PkV_LVOT = peak velocity through the LVOT, and r_LVOT is the systolic radius of the LVOT. The cut-off for severe AS is 280 dynes/s/cm⁵. While aortic valve resistance was initially believed to be less dependent on flow, this claim turns out not to be true. Moreover, resistance is less predictive of prognosis than other measures such as the peak velocity through the valve.

Aortic stenosis complicated by LV dysfunction with low stroke volume is one cause of low gradient aortic stenosis. Determination of the role of aortic stenosis in this setting is difficult since low stroke volume, on its own, may falsely decrease the calculated valve area by the continuity equation. Identification and evaluation of low gradient aortic stenosis is discussed separately. (See "Clinical manifestations and diagnosis of low gradient severe aortic stenosis".)

Aortic valve sclerosis — Aortic valve thickening (sclerosis) without stenosis is common in older adults. It is often detected either as a systolic murmur on physical examination or on echocardiography. Aortic valve sclerosis may be important clinically as a marker for increased cardiovascular risk. Aortic and mitral annular calcification frequently accompany aortic sclerosis. (See "Aortic valve sclerosis and pathogenesis of calcific aortic stenosis".)

A variety of definitions have been used to identify aortic valve sclerosis. A proposed revised definition includes the following criteria [10]: irregular nonuniform thickening of portion of the aortic valve leaflets or commissure, or both; thickened portions of the aortic valve with an appearance (highly echogenic) suggesting calcification, nonrestricted or minimally restricted aortic cusp opening; and transvalvular peak continuous wave Doppler velocity <2 m/s. Tissue harmonic imaging and high gain settings should be avoided when evaluating for aortic sclerosis since these enhancements can accentuate the appearance of leaflet thickening.

Fixed subvalvular stenosis — Fixed subvalvular or subaortic stenosis, is a relatively uncommon congenital lesion that is often associated with other cardiovascular abnormalities. Patients with ventricular septal defects (repaired or unrepaired) appear to be at increased risk for acquiring this condition. This disorder should be considered whenever a high velocity jet through the LVOT is identified in the setting of visually mobile aortic leaflets. With fixed subvalvular stenosis, the early aortic valve closure is often seen. (See "Subvalvar aortic stenosis (subaortic stenosis)".)

The most prominent echocardiographic feature of the condition is a linear density crossing the LVOT just proximal to the junction of the aortic root with the septum. On 2D echocardiography, a subvalvular membrane appears to arise from the membranous septum. The degree of obstruction to outflow in subvalvular aortic stenosis cannot be determined by 2D TTE, and Doppler examination is indicated. Color flow Doppler usually demonstrated flow acceleration originating proximal to the aortic valve at the site of obstruction.

The picture of fixed subvalvular obstruction may be further obscured and complicated by associated severe asymmetrical septal thickening that extends to just under the fibrous ring, mimicking classic hypertrophic obstructive myopathy. There may also be ectopic mitral chordae attached in and around the narrowed area.

It is important to define each of these elements when planning interventional (surgical or transcatheter) therapy; this task is best accomplished with TEE. When evaluating cases of hypertrophic cardiomyopathy by echocardiography, the possibility of a subvalvular membrane should always be considered. Failure to recognize this condition could lead to inappropriate use of alcohol ablation or a poor surgical result.

Supravalvular aortic stenosis — Supravalvular aortic stenosis is rarely seen in adults. It is rarely present in isolation and is most frequently found with Williams syndrome or homozygous familial hypercholesterolemia. When encountered, there is a narrowing directly above and usually affixed to the valve leaflets. Features include aortic regurgitation, enlarged coronary arteries, which are sometimes obstructed, and severe hypertrophy. Doppler measurement of the aortic gradient may be useful to distinguish those patients who are candidates for surgical correction [11]. Cross sectional imaging with magnetic resonance imaging or computed tomography angiography can better define the aortic anatomy. (See "Valvar aortic stenosis in children".)

ECHOCARDIOGRAPHIC DIFFERENTIATION AMONG THE CAUSES OF AORTIC STENOSIS — Most aortic stenosis presenting in later life is associated with a considerable amount of thickening and calcification in and around the aortic root and valve leaflets. These degenerative changes are nonspecific and do not serve to differentiate among the possible causes of aortic stenosis.

Congenital bicuspid aortic valve — Congenitally bicuspid aortic valves are common precursors of progressive aortic stenosis and are among the most common congenital cardiac anomalies in the adult (see "Clinical manifestations and diagnosis of bicuspid aortic valve in adults"). Visualization of three commissures is not sufficient to establish the presence of a trileaflet valve; in most functionally bicuspid valves in adults, three commissures are present but one is fused. The fused commissure can be easily seen echocardiographically and hence the valve may appear tricuspid, especially during diastole. Fusion of the right and left cusps is most common and may be associated with coarctation of the aorta [12]. Less common is fusion of the right and non-coronary cusps followed by the left and non-coronary cusps [13]. Clues to the true nature of these valves include apparent inequality in the size of the leaflets, ovoid opening shape of the orifice, and eccentricity in its position (image 6 and movie 4 and movie 5 and movie 6). A true (anatomically) bicuspid valve without a fused commissure is uncommon.

Rheumatic aortic stenosis — Rheumatic aortic stenosis is a rare cause of aortic stenosis in developed countries and is usually accompanied by significant mitral disease, which dominates the clinical and echocardiographic picture.

In general, milder forms of rheumatic aortic valve disease seem to involve the leaflet commissures with very little, if any, involvement of the aortic ring and commissural ring attachments. The thickening and calcification occurs mostly at the edges of the cusps [3].

Degenerative aortic stenosis — The most commonly encountered abnormality associated with aortic stenosis is chronic degeneration of the leaflets that occurs with advanced age. (See 'Aortic valve sclerosis' above and "Aortic valve sclerosis and pathogenesis of calcific aortic stenosis".)

●With this type of valve disease, the echocardiogram initially demonstrates the greatest concentration of calcification or thickening at the point where the commissures meet the aortic ring.

●At times, one of the leaflets may become immobile or frozen while the others move freely. When only one leaflet is immobile, there is usually only a mild increase in transaortic velocity (minimal aortic stenosis). The severity of aortic regurgitation in this setting is usually mild.

The natural history of aortic stenosis and risk factors for progression are discussed separately. (See "Natural history, epidemiology, and prognosis of aortic stenosis".)

ECHOCARDIOGRAPHIC EVALUATION OF THE AORTIC VALVE FOR TRANSCATHETER AORTIC VALVE REPLACEMENT — Imaging, including echocardiography, is important for determining eligibility for transcatheter aortic valve implantation (TAVI), for guidance during the procedure, and for follow-up after the procedure. These issues are discussed in detail separately. (See "Imaging for transcatheter aortic valve implantation".)

AORTIC REGURGITATION — In contrast to the mitral, tricuspid, and pulmonic valves, trivial aortic regurgitation is far less common in healthy young adults. As the aortic valve becomes thickened or sclerotic, mild degrees of aortic regurgitation may develop. Pathologic aortic regurgitation may arise from a variety of aortic valve and aortic root abnormalities. It may coexist with aortic stenosis. (See "Clinical manifestations and diagnosis of chronic aortic regurgitation in adults" and "Acute aortic regurgitation in adults".)

Many of these pathologic entities can be identified by echocardiographic imaging and the severity or degree of regurgitation can be measured.

M-mode echocardiogram — Diastolic fluttering of the anterior mitral valve leaflet, which occurs when the regurgitant jet is directed posteriorly, was the first M-mode echocardiographic observation permitting the detection of aortic regurgitation [14]. This sign is less relevant today since Doppler is more accurate for all degrees of aortic regurgitation, including the most trivial.

Chronic aortic regurgitation — In asymptomatic patients with hemodynamically significant aortic regurgitation, it is important to obtain accurate linear measurements of LV dimensions at end-diastole (LVIDd) and end-systole (LVIDs). It is preferable to make the measurements directly on the 2D image to ensure that they are perpendicular to the long axis of the ventricle. Indications for aortic valve surgery (including LVIDs and LVIDd thresholds) are discussed separately. (See "Natural history and management of chronic aortic regurgitation in adults", section on 'Aortic valve surgery'.)

Acute aortic regurgitation — Causes of acute severe aortic regurgitation include aortic valve endocarditis, aortic dissection involving the aortic valve and chest trauma/deceleration injury. Echocardiographic signs of rapid equilibration of aortic and LV diastolic pressures include premature closure of the mitral valve before the onset of the QRS as seen on M-mode. Premature mitral valve closure is a sign indicating that valve closure is caused by an inappropriate rise in LV diastolic pressure due to filling from aortic regurgitation rather than by pressure generated by isovolumic contraction [15]. (See "Acute aortic regurgitation in adults", section on 'Echocardiography'.)

Two-dimensional echocardiography — The 2D echocardiogram is important for establishing the etiology and mechanism for the aortic regurgitation (movie 7). Aortic regurgitation may be due to valvular pathology or aortic root pathology. Important features of the valve include: the number of leaflets, the presence of cusp prolapse, leaflet destruction or perforation, or vegetations interfering with leaflet closure. The aortic root may be dilated due to annuloaortic ectasia, connective tissue disease, the aortopathy associated with bicuspid aortic valve, or inflammatory disease. In aortic dissection, aortic regurgitation may be due to the intimal flap interfering with cusp closure, root dilation, or loss of valve support with extension of the dissection to the annulus. When TTE is inadequate, TEE may provide additional information.

Quantitation of total LV stroke volume from two dimensional echocardiography planimetry of the LV or from the LV outflow tract (LVOT) flow can be compared with the effective forward systemic flow as estimated from transmitral or transpulmonic flow so that regurgitant volume and regurgitant fraction can be calculated from their difference [14,16-18]. Using the continuity principle, effective regurgitant orifice can also be computed [19]. Use of strain imaging in patients with aortic regurgitation is discussed separately. (See "Tissue Doppler echocardiography" and "Natural history and management of chronic aortic regurgitation in adults".)

Doppler echocardiography — Doppler echocardiography is the principal method for evaluation of the patient suspected of having aortic regurgitation (table 2) [1]. Color flow Doppler of the aortic valve from the parasternal long- and short-axis views is highly sensitive to aortic regurgitation and will demonstrate very mild to severe regurgitation (movie 8 and movie 9 and movie 10 and image 7).

The width of the vena contracta, the jet width and area, the rate of decay of the continuous wave diastolic velocity (as measured by the pressure half-time), the density of the continuous wave jet, and the duration of reverse flow in the descending aorta are semiquantitative methods of grading the severity of aortic regurgitation (image 8 and waveform 2) [20-22]. Quantitative methods include the effective regurgitant orifice area (EROA) and the regurgitation volume [19,21-23]. These methods are summarized in the 2017 American Society of Echocardiography (ASE) recommendations on evaluation of valvular regurgitation. However, a study comparing the EROA and semiquantitative methods (including pressure half-time, diastolic flow reversal, and vena contracta) using standard thresholds found that the vena contracta had good sensitivity and specificity for severe aortic regurgitation but the other methods were specific but less sensitive [24].

Evidence of aortic and LV diastolic pressure equilibration seen with acute severe aortic regurgitation includes a short aortic regurgitation pressure half-time, a short mitral deceleration time (waveform 2), as well as premature closure of the mitral valve as mentioned above.

Width of the vena contracta — The vena contracta is the narrowest neck of the color flow jet as it passes from the aortic valve and enters the LVOT (receiving chamber). The width of the vena contracta correlates with the severity of aortic regurgitation [20-22]. Mild aortic regurgitation is present when the vena contracta width is less than 0.3 cm and severe regurgitation is present when the vena contracta width is greater than 0.6 cm [21]. This method may be more robust than jet width, particularly in the presence of eccentric jets. In the above cited study comparing vena contracta with effective regurgitant orifice area, a vena contracta ≥0.6 cm was 81 percent sensitive and 83 percent specific for severe aortic regurgitation [24].

Jet width — A related but distinct parameter is the ratio of the jet width to the width of the LVOT. The width of the jet is measured just proximal to (below) the vena contracta within 1 cm of the aortic valve leaflets. A ratio of less than 25 percent is considered mild and 65 percent or greater is considered severe [21,25]. A ratio of the cross-sectional area of the jet to the cross-sectional area of the LVOT of <5 percent is categorized as mild and ≥60 percent is categorized as severe. The accuracy of jet width and area estimates may be limited when an eccentric jet is present.

Reversal of aortic flow — Normally, when flow is sampled in the descending aorta, most flow occurs during ventricular systole and is antegrade. Using magnetic resonance (MR) imaging phase velocity methods, forward flow is seen to stop in the descending aorta during diastole. On pulsed wave Doppler of the descending aorta in normal individuals, there is brief early diastolic reversal of flow. In aortic regurgitation, retrograde flow can be detected and its quantity and duration is proportional to the degree of severity of the lesion (image 8). The retrograde flow signal may become holodiastolic and the velocity time integral of retrograde diastolic flow may approach that of systolic flow.

There are several pitfalls in using this sign for evaluating AR severity. Diastolic flow reversal may become more prominent with decreases in aortic compliance as occurs with normal aging. Diastolic flow reversal in the descending thoracic aorta may also be due to an upper extremity arteriovenous fistula for dialysis or a cerebral arteriovenous malformation. In the above cited study comparing diastolic flow reversal with effective regurgitant orifice area, a diastolic flow reversal ≥18 cm/s was 45 percent sensitive and 87 percent specific for severe aortic regurgitation [24]. Thus, the presence of this finding must be integrated with other measures of AR severity.

In the quantitative application of relative antegrade and retrograde flows, one must also account for changes in aortic diameter which must be measured in diastole and systole [26].

Continuous wave Doppler — Continuous wave Doppler of the regurgitant jet acquired from the apical five chamber or apical three long axis can be used to qualitatively grade the severity of aortic regurgitation (figure 4 and waveform 3). The flow signal velocity is determined throughout diastole by the gradient between the aortic root and the LV. Ordinarily, the diastolic pressure in the LV is much lower than the aortic root pressure (12 versus 80 mmHg). Thus, the velocity of the aortic regurgitation jet at early diastole is generally at least 4 m/s and subsequently slowly declines. In mild regurgitation, the deceleration time for that decline usually exceeds 500 ms. In severe aortic regurgitation, the pressure gradient between aortic root and LV becomes very small because the diastolic systemic pressure falls and the LV pressure rises. As the gradient is abolished, the retrograde flow ceases and the velocity of the diastolic signal falls towards zero. The more rapidly the signal decays, the more severe the regurgitation [27]. A deceleration time of less than 200 ms or a decay slope greater than 3 m/s² is indicative of severe aortic regurgitation.

However, the pressure half-time has limited sensitivity for detection of severe aortic regurgitation, particularly in the chronic setting. In the above cited study comparing pressure half time with effective regurgitant orifice area, a pressure half time <200 ms was 12 percent sensitive and 100 percent specific for severe aortic regurgitation [24].

The pressure half-time can be confounded in situations such as severe heart failure, where the filling pressure in the LV is elevated and mean aortic pressure reduced. It can also be influenced by changes in systemic vascular resistance and LV compliance. Increasing the systemic vascular resistance increases the rate of decay without any change in valve orifice; reduced LV compliance produces a more rapid rise in LV pressure, which influences the diastolic slope without reflecting the severity of aortic regurgitation. In patients with compensated chronic severe aortic regurgitation, the dilated ventricle may have near normal filling pressures and the rate of diastolic velocity decline is often intermediate.

Severity of aortic regurgitation — Severe aortic regurgitation is considered to be present if at least four of the following findings are present on echocardiography [28]:

●Vena contracta width >6 mm

●Flail valve

●Central jet width ≥65 percent of LVOT

●Prominent holodiastolic flow reversal in the descending aorta

●Large flow convergence

●Enlarged LV with normal systolic function

●Pressure half-time <200 ms

If only two or three of the above criteria are present, quantitation is performed to determine if one or more of the following criteria for severe aortic regurgitation are present [28]:

●A regurgitant fraction ≥50 percent

●A regurgitant volume ≥60 mL

●An effective regurgitant orifice area ≥0.30 cm²

When these criteria are not met on TTE but there is a suspicion for hemodynamically significant regurgitation, cardiac magnetic resonance or TEE should be considered for further confirmation. An algorithm for assessing the severity of aortic regurgitation is proposed in the recent guidelines (algorithm 1) [28]. (See "Clinical manifestations and diagnosis of chronic aortic regurgitation in adults".)

Echocardiography and the timing of surgery for aortic regurgitation — The role of echocardiography in the timing of surgery for aortic regurgitation is discussed separately. (See "Natural history and management of chronic aortic regurgitation in adults".)

ECHOCARDIOGRAPHIC DETERMINATION OF THE ETIOLOGY OF AORTIC REGURGITATION — Any process that interferes with the integrity of the aortic valve leaflets can result in aortic incompetence. (See "Clinical manifestations and diagnosis of chronic aortic regurgitation in adults".)

Aortic root disease — Aortic root dilatation is a common cause of aortic regurgitation. Aortic root dilation is often idiopathic. Causes of aortic root dilation include dilation associated with bicuspid aortic valve, Marfan syndrome, sinus of Valsalva aneurysm (with and without fistulous connection), annuloaortic ectasia, luetic aortitis, and aortic root dilation in association with ankylosing spondylitis. (See "Clinical manifestations of axial spondyloarthritis (ankylosing spondylitis and nonradiographic axial spondyloarthritis) in adults" and "Syphilis: Epidemiology, pathophysiology, and clinical manifestations in patients without HIV".)

The echocardiographic findings in these various conditions can be nonspecific, and differentiation must rest on clinical or pathological grounds. Dilation of the aortic root and thickening of its walls are, however, common echocardiographic findings.

Marfan syndrome — The Marfan syndrome is associated with aortic regurgitation due to aortic dilatation as well as mitral valve prolapse. In Marfan syndrome, the appearance of the aortic valve and root may be distinctly different from that in other conditions (image 9 and image 10). In the Marfan patient, isolated dilation of the sinuses of Valsalva with sparing of the ascending aorta and a nonprolapsing aortic valve are typical, although diffuse fusiform dilatation may be present [29]. (See "Genetics, clinical features, and diagnosis of Marfan syndrome and related disorders".)

Aortic dissection — Dissection of the proximal aorta is a major cause of acute severe aortic regurgitation. TEE, computed tomography, and magnetic resonance imaging are the methods of choice for the emergency diagnosis of aortic dissection [30-32]. By TTE, the intimal flap can be very difficult to image, but some degree of root dilation is usually present. Some studies have suggested that the sensitivity of TTE for detecting an aortic dissection is in the range of 65 percent. (See "Clinical features and diagnosis of acute aortic dissection".)

Sinus of Valsalva aneurysm — Sinus of Valsalva aneurysm, a form of aortic root aneurysm, is characterized by asymmetric dilation involving one of the sinuses. The dilated sinus will often bulge in systole, facilitating detection. In the setting of a sinus of Valsalva aneurysm, a Doppler examination should be performed and both aortic regurgitation and an intracardiac communication at the site of the aneurysm sought.

Bicuspid aortic valve — Aortic regurgitation commonly arises in non-stenotic bicuspid aortic valves. These valves can often be recognized by two dimensional imaging of the aorta in the precordial short-axis view (image 6 and movie 4 and movie 5 and movie 6). The mechanism for aortic regurgitation in the setting of bicuspid aortic valve may be due to associated aortic root dilatation, endocarditis, or cusp prolapse.

Rheumatic disease — Aortic regurgitation in association with rheumatic mitral involvement can be readily appreciated by Doppler echocardiography. In this setting, the aortic valve leaflet edges are thickened along their entire border and the aortic ring is small and normal in appearance. While this type of aortic regurgitation is often mild, it can occasionally be moderate or even severe.

Endocarditis — Endocarditis of the aortic valve is a leading cause of acute severe aortic regurgitation. Classically, dense mobile echoes prolapsing into the LV outflow tract are diagnostic when present. However, approximately 25 percent of patients with clinically diagnosed infective endocarditis have no vegetations detected by TTE. The presence of a pre-existing abnormality serving as a nidus for infection, especially if calcified, can make vegetation detection difficult by TTE (image 11 and image 12 and movie 11 and movie 12 and movie 13). TEE, with its superior resolution, has greatly improved the detection rate of vegetations of the aortic valve [33].

Secondary involvement of the mitral valve in patients with primary aortic valve endocarditis has been demonstrated on TEE in 10 percent of patients. This can arise from large aortic vegetations (>6 mm) that prolapse into the LV during diastole and contact the anterior mitral leaflet, causing it to be secondarily infected (mitral kissing vegetation) [34]. Mitral valve involvement can also result from direct extension of infection through the continuous central fibrous body.

Subaortic stenosis — Aortic regurgitation can arise in association with jet lesions from subaortic stenosis. In this situation, dynamic or fixed outflow tract narrowing produces a jet of high velocity blood that strikes the aortic valve. The resulting damage may alter the valve architecture and produce aortic regurgitation. (See "Subvalvar aortic stenosis (subaortic stenosis)".)

Myxomatous disease — Aortic regurgitation in association with mitral valve prolapse can be due either to myxomatous changes in the leaflets themselves or to aortic root disease. Although very uncommon, aortic valve prolapse due to myxomatous degeneration can be seen in association with mitral prolapse.

The most common manifestation of aortic root disease is general dilatation of the sinuses. Dilatation limited to one sinus is called a sinus of Valsalva aneurysm, which is a form of aortic root aneurysm. (See 'Sinus of Valsalva aneurysm' above.)

Aortic valve sclerosis — As discussed above, aortic valve sclerosis is a degenerative process that may progress to aortic stenosis. When aortic regurgitation is present, it is usually mild. (See "Aortic valve sclerosis and pathogenesis of calcific aortic stenosis".)

Rheumatoid arthritis — Rarely, aortic regurgitation can arise from a rheumatoid nodule on the valve. (See "Overview of the systemic and nonarticular manifestations of rheumatoid arthritis".)

Leaflet fenestrations — Leaflet fenestrations are said to be common among post mortem specimens. They can be inferred by color flow Doppler detection of an unusual site of regurgitation.

Ventricular septal defect — Small ventricular septal defects in the perimembranous region frequently close during childhood. They can be associated with aortic regurgitation that can persist after closure. Infundibular (also known as supracristal) ventricular septal defects are also associated with aortic regurgitation and are more likely to be associated with hemodynamically significant aortic regurgitation due to undermining of the right coronary cusp, resulting in prolapse.

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Cardiac valve disease".)

SUMMARY AND RECOMMENDATIONS

●The left, right, and noncoronary cusps of the aortic valve are visualized by transthoracic echocardiography (TTE) in the parasternal short-axis view (as well as in a subcostal short-axis view): the left cusp is adjacent to the main pulmonary artery, the right cusp is adjacent to the right ventricular outflow track, and the noncoronary cusp is adjacent to the interatrial septum.

●Aortic valve motion can be visualized in M-mode and two-dimensional (2D) views. Failure of the leaflets to open widely may be seen with aortic stenosis; a decreased stroke volume is suggested if they open widely but drift shut just after achieving maximum separation.

●Transesophageal echocardiography (TEE) may be required in some patients to distinguish valvular stenosis from subvalvular or supravalvular obstruction. (See 'Obstruction to left ventricular outflow' above.)

●Doppler echocardiography enables quantification of aortic valve gradients. The continuity equation can be used to calculate aortic valve area (figure 3). (See 'Doppler echocardiography' above and "Aortic valve area in aortic stenosis in adults", section on 'Echocardiography'.)

●When aortic regurgitation is acute and severe (often due to active aortic valve endocarditis, aortic dissection involving the aortic valve, or chest trauma/deceleration injury), M-mode is of value in detecting premature closure of the mitral valve, which is defined as valve closure that occurs on or before the onset of the QRS and indicates that the valve did not close because of isovolumic contraction but rather because of an inappropriate rise in left ventricular (LV) pressure due to filling from aortic regurgitation.

●Assessment of aortic regurgitation requires an integrative approach including the width of the vena contracta, the rate of decay of the continuous wave diastolic velocity (pressure half-time), the degree of reverse flow in the descending aorta (image 8), as well as the presence of LV enlargement and hypertrophy (algorithm 1).

●In asymptomatic patients with chronic severe aortic regurgitation, echocardiography is used to determine whether LV dilatation and LV dysfunction meet criteria for aortic valve replacement. (See "Natural history and management of chronic aortic regurgitation in adults", section on 'Aortic valve surgery'.)

●Echocardiography enables determination of the cause of aortic regurgitation. (See 'Echocardiographic determination of the etiology of aortic regurgitation' above.)