Echocardiographic Assessment of Aortic Regurgitation

 

Echocardiographic assessment of Aortic Regurgitation

Author

Dr Prathap Kanagala

BSE Education Committee

East Midlands Deanery

Acknowledgements

My sincere thanks to Dr Andrew R. Houghton (Consultant Physician & Cardiologist) and the Department of Medical Physics, Grantham & District Hospital for their valuable input in preparing this manuscript.

Abbreviations

2D              two dimensional

AR              aortic regurgitation

CABG          coronary artery bypass graft

CW             continuous wave

EF               ejection fraction

LV               left ventricle

LVEDD         left ventricular end diastolic diameter

LVEDP         left ventricular end diastolic pressure

LVEDV         left ventricular end diastolic volume

LVESD         left ventricular end systolic diameter

LVOT          left ventricular outflow tract

M-mode      motion mode

MR             mitral regurgitation

PISA           proximal isovelocity surface area

PW             pulsed-wave

RF              regurgitant fraction

ROA           regurgitant orifice area

RV             regurgitant volume

RWT          relative wall thickness

VC             vena contracta

VSD           ventricular septal defect

VTI            velocity time integral

 

Objectives

1. To understand the epidemiology, aetiology, pathophysiology and prognosis of aortic regurgitation

2. To review the qualitative and quantitative echocardiographic methods available to assess severity

3. To appreciate the role of echocardiography in management

 

Epidemiology

The incidence of clinically significant AR increases with age, typically peaking between the 4th and 6th decades of life. AR is more common in males. Reported prevalence is 4.9%, with moderate to severe cases accounting for 0.5%.

 

Aetiology

The causes of AR can be broadly categorised into disease affecting: the valvular apparatus (e.g. rheumatic, myxomatous), the aortic root (e.g. Marfan's  syndrome, sinus of valsalva aneurysm) or both (e.g. ankylosing spondylitis, bicuspid aortic valve).  In developing countries, rheumatic disease remains the leading cause of AR. In the Western World however, bicuspid valves and aortic root abnormalities predominate.

Valvular pathologies result in alterations in leaflet flexibility and shape with resultant inadequate coaptation. Regurgitation also results from leaflet perforation as seen in endocarditis or trauma. In aortic root disease, annular dilation causes malcoaptation as the valve leaflets become stretched further apart. In addition, a false channel created by dissection may directly distort valve structure causing flail leaflets.

Causes of Aortic Regurgitation

Valvular

Bicuspid

Rheumatic

Calcific

Myxomatous

*Endocarditis

Connective tissue disease e.g. Rheumatoid Arthritis, Systemic Lupus Erythematosus

*Trauma - leaflet rupture / perforation

VSD - supracristal type associated with cusp prolapse

Aortic Root

Hypertension

Cystic medial necrosis

Marfan's syndrome

Ehler's Danlos syndrome

Osteogenesis Imperfecta

*Aortic Dissection

Syphilis

Behcet's Disease

Sinus of Valsalva aneurysm

*Conditions  associated with acute regurgitation

 

Pathophysiology and haemodynamics

Acute AR is a medical emergency.  Untreated, LVEDP rises rapidly and effective stroke volume cannot be maintained despite intrinsic compensatory mechanisms (increasing heart rate and contractility) attempting  to cope with the regurgitant volume (preload).  Pulmonary oedema, cardiogenic shock and death usually develop quickly.

Chronic AR however allows the LV to adapt and remodel, delaying the onset of symptoms. A summary of the changes include:

Left ventricular volume and pressure overload

Increase in LV wall stress

Compensatory hypertrophy (concentric and eccentric) in an attempt to normalise wall stress

Systolic hypertension (often) as a consequence of increased stroke volume

Pulse pressure widening as aortic diastolic blood pressure drops due to regurgitation back into the LV

During initial stages, the regurgitant volume increases LVEDV without an increase in LVEDP as the LV dilates and compliance increases

Despite the compensatory mechanisms however, LVEDP eventually rises as systolic dysfunction supervenes and heralds the onset of symptoms. The end-stage heart often resembles a spherical, dilated LV with increased mass - the so called cor bovinum (bovine or ox heart).

Prognosis

Acute AR is associated with high mortality rates without immediate surgical intervention. In chronic AR, predictors of poor outcome include increasing age, severe AR, symptoms, EF<50% and LVESD >55mm.

Echocardiographic assessment

The echo study should aim to confirm diagnosis, establish aetiology, categorise severity and consequences of AR.

Two dimensional imaging

2D imaging provides useful information regarding valve anatomy, valvular structure & deformity, aortic root dimensions and the adaptive LV response to regurgitant volume.

Useful pointers

Valve anatomy: Is the valve tricuspid? Is there evidence of eccentric coaptation? (unicuspid, biscuspid, quadricuspid)

Valve structure: Is there cusp thickening, calcification? Are other valves affected? (rheumatic) Is there evidence of perforation or vegetations? (endocarditis)

Valve function: Are the cusps thickened with redundant leaflets? Is there diastolic sagging into the LVOT? (myxomatous) Is leaflet motion restricted? (co-existent aortic stenosis) Is there leaflet prolapse? (false channel secondary to aortic dissection)

Aortic Root: Is there dilation with maintenance of normal contours and narrowing at the sinotubular junction? (degenerative disease) Is there effacement i.e. enlargement of the sinuses of valsalva accompanied by loss of narrowing at the sinotubular junction? (Marfan's syndrome) Is the aortic root extensively calcified? (syphilis) Is there evidence of a false channel / dissection flap? (aortic dissection)

Left Ventricle: Is there concentric hypertrophy i.e. increased LV mass & relative wall thickness? (typically seen with isolated hypertension and pressure overload) Is there eccentric hypertrophy i.e. increased LV mass but normal relative wall thickness? (typically as a consequence of volume overload) Is the LV dilated? (suggestive of chronicity of AR and increasing severity) Is LV function diminished? This implies haemodynamically severe AR although alternative causes of impaired function should be borne in mind.

Note Relative wall thickness (RWT) = 2 x posterior wall thickness ÷ LVEDD. In the presence of increased LV mass, RWT greater than 0.42 indicates concentric hypertrophy. On the other hand, RWT less than 0.42 defines eccentric hypertrophy.

Grading Severity

Colour Doppler

Vena Contracta (Quantitative)

VC width is the narrowest portion of colour flow at or just below the level of the aortic valve.

Calculation: Measure in parasternal windows since better axial resolution is offered compared to apical windows. Use zoom & colour M-mode to minimise errors in measurement.

Limitations: VC width is not reliable if there are multiple jets or the jet is irregularly shaped. VC is valid for eccentric jets however, if measurements are made perpendicular to the direction of the jet rather than to the long axis of the LVOT. Dealing with relatively small values of VC width (usually < 1cm) also means that even small measurement errors may result in large percentage errors and thus over/underestimating the degree of regurgitation.

Jet width / LVOT height (Quantitative)

The regurgitant jet width to LVOT diameter ratio refers to the maximal proximal jet width measured in the LVOT.

Calculation: Similar to VC width measurements, use parasternal windows with zoom & colour M-mode to maximise axial and temporal resolution.

Limitations:  Regurgitant jets expand unpredictably below the valve orifice often with differing shapes and are therefore a potential source of error. Measurement too far below the valve tends to overestimate severity as the jet spreads out.  In addition, central jets may overestimate (and conversely eccentric jets may underestimate) severity.

Jet area / length in LV cavity (Qualitative)

Calculation: In apical views, measure how far the regurgitation extends into the LV cavity using colour & PW Doppler. Regurgitation reaching the end of the anterior mitral valve leaflet is indicative of moderate severity. Jets extending beyond and into the body of the LV indicate severe disease. Set a Nyquist limit (aliasing velocity 50-60 cm/sec) and optimise colour gain such that random colour speckle from non-moving regions is just eliminated.

Limitations:  Colour Doppler is heavily dependent on PRF and colour gain. Jet area includes both turbulent (aliased) and laminar flow which may result in overestimation of central jets. Increasing the scale may underestimate jet area. The length of the regurgitant jet is similarly influenced by the above factors.

PISA or flow convergence (quantitative)

Whilst this method is theoretically measurable (as in MR assessment) and has been shown to provide accurate quantification in severity of AR, it is not routinely practiced. Limitations include suboptimal images in the presence of aortic valvular calcification and underestimation in aortic aneurysms. Validity is questionable for multiple/eccentric jets.

CW & PW Doppler

Pressure half-time and jet deceleration rate (qualitative)

Calculation: In apical 5- or 3-chamber views, align CW Doppler (aided by colour flow mapping) along the direction of the jet as it originates from the regurgitant orifice. Measure peak velocity and the slope of the flat part of the spectral trace i.e. deceleration slope. Pressure half-time corresponds to the rate of deceleration of the jet i.e. time taken for pressure across the aortic valve to fall by half. Typically, with increasing severity of regurgitation, aortic diastolic pressure falls more rapidly. Therefore, the late-diastolic velocity is lower and a steep deceleration slope & short pressure half-time result.

Limitations: Factors affecting the significance of pressure half-time values  include changes in LV compliance (e.g. chronic AR), LV diastolic pressure (e.g. systolic dysfunction, ischaemia) and aortic diastolic pressure (e.g. sepsis, patent ductus arteriosus, vasodilators).

Acute versus Chronic severe regurgitation

Pressure half-time is more useful as a marker of severity in acute regurgitation since LV compliance will not have adapted so quickly. With chronic cases, LV function and aortic compliance change to accommodate the larger regurgitant volumes.  These processes slow down the equalisation of trans-aortic pressures and lead to misleadingly longer pressure half-time values.

Similarly, normal LV dimensions, often with vigorous function point towards acute regurgitation. In chronic cases, a dilated LV with eccentric hypertrophy often results due to the process of LV remodelling. Systolic function may also become impaired.

Other relevant pointers of acute onset include evidence of dissection, endocarditis and trauma.

Regurgitant Volume / Regurgitant Fraction /  Regurgitant Orifice Area

Calculation: The volume of blood entering the LV via the mitral valve during diastole should equal the volume leaving the LV via the LVOT during systole (stroke volume). In AR, LV outflow exceeds mitral inflow since LVOT outflow also comprises blood that has entered the LV via AR during diastole. Therefore, Aortic Regurgitant Volume (ml) = Stroke volume of LVOT - Stroke Volume of MV in the absence of significant MR or a VSD.

Stroke volume of LVOT

= cross sectional area of LVOT x VTI of LVOT

 

= 0.785 x (LVOT diameter) 2 x VTI of LVOT

Measure LVOT diameter in Parasternal long axis view

Measure VTI using PW Doppler in Apical 5- chamber view

Stroke volume of MV

= cross sectional area of MV annulus x VTI of MV

 

= 0.785 x (MV annulus diameter) 2 x VTI of MV

Measure MV annulus diameter in Apical 4-chamber view

Measure VTI using PW Doppler in Apical 4-chamber view at mitral annulus level

Regurgitant Fraction (%) = (Regurgitant Volume ÷ Stroke Volume of LVOT) x 100

Regurgitant Orifice Area is the average size of the orifice in the aortic valve during diastole through which regurgitation occurs.

Regurgitant Orifice Area (cm2) = Regurgitant Volume ÷ VTI of AR Doppler trace

Measure VTI of the AR Doppler trace using CW Doppler in Apical 3- or 5-chamber views

Limitations: The above Doppler derived flow calculations are fraught with potential pitfalls. Calculations are not valid in the presence of more than mild mitral regurgitation. In addition, even small errors in measurements of either LVOT/MV annulus diameters are greatly magnified as the results are squared.

CW Doppler AR jet density (qualitative)

The intensity of the regurgitant signal seen on CW spectral display in apical 3- or 5-chamber views reflects the volume of regurgitation compared to forward flow through the aortic valve.  Whilst a weak regurgitant signal compared to forward flow is consistent with minimal AR, greater degrees of regurgitation produce equal density of retrograde and antegrade flow signals.  Reliable discrimination between moderate and severe grades of regurgitation however is not possible based on signal intensity alone.

Diastolic flow reversal - Descending Aorta (Semi-quantitative)

Calculation: Using a suprasternal view, PW Doppler interrogation of the upper descending aorta may detect brief (early) reversal of diastolic aortic flow even in normal individuals. As regurgitation becomes more severe however, flow reversal occupies a greater period of diastole and indeed diastolic flow velocities increase. Descending thoracic aortic holodiastolic flow reversal indicates at least moderate regurgitation.

Limitations: Varying degrees of flow reversal may also be seen with age related changes in rigidity and diminishing compliance of the aortic wall.

Severity of AR (BSE Education Committee Guidelines for Valve Quantification)

Mild

Moderate

Severe

VC width (cm)

<0.3

 

>0.6

 

Jet width/LVOT diameter (%)

<25

 

>65

 

Regurgitant Volume (ml/beat)

<30

31-59

=60

Regurgitant Fraction (%)

<30

31-49

=50

Regurgitant Orifice Area (cm2)

<0.10

0.11-0.29

=50

VTI diastolic flow reversal (cm) (upper descending aorta)

 

 

15

Pressure Half Time (ms)

>500

 

<250

Management

Echo monitoring

Mild to moderate AR may be managed with annual review and echo assessment every 2 years. Severe AR & normal LV function typically necessitates 6 monthly patient review (annual if stable). Dilated aortic roots require echo monitoring on an annual basis or more frequently if rapid rate of growth is seen.

Treatment

Whilst standard anti-heart failure medication is the mainstay of medical therapy, the use of vasodilators in asymptomatic patients is unproven. Additionally, beta-blockers may be helpful in peri- & post-operative patients with Marfan's syndrome.  Surgical options include valve replacement or repair with grafting of the aortic root as appropriate.

 

Surgical indications include:

1. Acute symptomatic AR

2. Chronic severe AR

Symptoms

Asymptomatic patients with LVEF = 50%

Asymptomatic  patients with LVEF > 50% and severe LV dilation (LVEDD > 70mm, LVESD > 50mm)

Patients undergoing other surgery (CABG, ascending aorta, other valvular)

3. Regardless of severity of AR, patients with aortic root disease

Aortic Root > 45mm in Marfan's syndrome

Aortic Root > 50mm in Bicuspid valves

Aortic root > 55mm in other patients

 

 

Suggested reading

1. Houghton AR. Making sense of echocardiography: a hands-on guide. London: Hodder Arnold, 2009. ISBN: 978-0-3409-4688-6.

2. The Task Force on the Management of Valvular heart Disease of the European Society of Cardiology. Guidelines on the management of valvular heart disease. Eur Heart J 2007; 28: 230-68.

3. Maurer G. Aortic Regurgitation. Heart 2006; 92:994-1000.

4. Otto CM. Textbook of Clinical Echocardiography, 3rd edn. Edinburgh: Elsevier Saunders, 2004. ISBN-13: 9780721607894.

5. Zoghbi WA, Enriquez-Sarano M, Foster E, et al. American Society of Echocardiography: recommendations for evaluation of the severity of native valvular regurgitation with two-dimensional and Doppler echocardiography. J Am Soc Echocardiogr 2003; 16:777-802.

Last Updated (Fri 08 November 2013)

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