Review Article

Multimodality Imaging of Heart Valve Disease

Ronak Rajani1, Rajdeep Khattar2, Amedeo Chiribiri3, Kelly Victor1, John Chambers1
Department of Cardiology, St. Thomas’ Hospital1, London; Department of Cardiology, Royal Brompton Hospital2, London; Divisions of
Imaging Sciences, The Rayne Institute, St. Thomas’ Hospital3, London – United Kingdom

Glossary Echocardiography is the cornerstone of assessing heart

valve disease. It is affordable, accessible and backed by a
VENC – Velocity Encoding – a specialized technique for
strong evidence base (Table 1)2. However, cardiac magnetic
encoding flow-velocities on cardiac magnetic resonance imaging.
resonance imaging and cardiac computed tomography (CT)
SSFP – Steady-State Free Precession – a gradient echo are increasingly useful. This review addresses the roles and
magnetic resonance imaging pulse sequence in which a steady, limitations of each of these modalities for the assessment of
residual transverse magnetization is maintained between patients with heart valve disease.
successive cycles.

The aortic valve

Abstract
Unidentified heart valve disease is associated with a Echocardiography
significant morbidity and mortality. It has therefore become
important to accurately identify, assess and monitor patients
with this condition in order that appropriate and timely Aortic stenosis
intervention can occur. Although echocardiography has Aortic stenosis (AS) is differentiated from ‘sclerosis’ by a
emerged as the predominant imaging modality for this reduction in valve opening (Figure 1) with a peak transaortic
purpose, recent advances in cardiac magnetic resonance velocity > 2.5 m/s. It is graded using a minimum dataset of
and cardiac computed tomography indicate that they may the peak velocity, mean pressure gradient and effective orifice
have an important contribution to make. The current review area (EOA)a 3,4. (Table 1).
describes the assessment of regurgitant and stenotic heart Echocardiography provides information on left
valves by multimodality imaging (echocardiography, cardiac ventricular (LV) systolic and diastolic anatomy and
computed tomography and cardiac magnetic resonance) and function. It also assesses the rest of the heart especially
discusses their relative strengths and weaknesses. the aorta, the mitral valve and the right heart. Exercise
echocardiography may reveal indications for surgery in
patients with asymptomatic severe AS: symptoms (Class I),
Introduction a fall in blood pressure below baseline (Class IIa) or an
Heart valve disease causes significant morbidity and increase in mean gradient of > 20 mmHg (Class IIb)5.
premature death but also carries a sizeable health economic
burden. The population prevalence of moderate or severe
Discrepant measures of Aortic Stenosis severity
valve disease is 2.5% in industrially developed countries1,
but this rises to 13% at age ≥ 75 years. Therefore, as our It is relatively common to find that the velocity and gradient
population ages, clinicians will increasingly need to identify are discrepant with the EOA. The first step should be to review
and monitor valve disease. Judging the appropriateness and the measurements (Table 2) looking for errors. Transvalvular
timing of interventions will become progressively harder in the gradients in the severe range and the EOA in the moderate
face of cardiac and extracardiac comorbidities. range may be caused by erroneously low placement of the
pulsed sample volume and the diameter of the LV outflow tract
(LVOT) may be difficult to measure correctly. This situation
can also be a genuine effect of increased flow for example
Keywords as a result of sepsis, anaemia, or coexistent significant aortic
Diagnostic Imaging; Heart Valve Diseases; Cardiac Imaging; regurgitation (AR).
Techniques / trends; Magnetic Resonance Imaging; Tomography. If the velocity and gradient are moderate but the EOA is
Mailing address: Ronak Rajani • severe, the situation has a number of possible explanations.
Department of Cardiology, Westminster Bridge Road, St Thomas’ Hospital, There is evidence that the cut-points for orifice area may
London, SE1 7EH. United Kingdom.
E-mail: [email protected] not be valid and effective areas between 0.8 and 1.0 cm2
Manuscript received October 28, 2013; revised January 7, 2014; may sometimes be moderate rather than severe. The shape
accepted January 7, 2014. of the waveform and appearance and mobility of the valve
may help to differentiate moderate from severe and it
DOI: 10.5935/abc.20140057 may also help to index EOA to body surface area (BSA).
a

Where: AV: aortic valve; CSA: cross sectional area; EOA: effective orifice area; LVOT: left ventricular outflow tract; VTI: velocity-time integral.

251
 Rajani et al.
Multimodality Imaging of Heart Valve Disease

Review Article

Table 1 – Severity grading of heart valve disease

Mild Moderate Severe

Aortic stenosis
Peak velocity (m/s) <3 3-4 >4
Mean gradient (mmHg) < 25 (< 30*) 25-40 (30-50*) > 40 (> 50*)
Valve area (cm2) > 1.5 1-1.5 <1
Indexed valve area (cm /m )
2 2
> 0.85 0.60-0.85 < 0.60
Velocity ratio > 0.50 0.25-0.5 < 0.25

Aortic regurgitation
Colour Doppler width (%) < 25 25-65 > 65%
Regurgitant volume (mls/beat) < 30 30-59 ≥ 60
Vena contracta width <3 >6
Regurgitant fraction (%) < 30 30-49 ≥ 50
Pressure half-time (msec) > 500* 250-450 < 200*

Mitral stenosis
Valve area (cm2) > 1.5 1-1.5 <1
Mean gradient (mmHg) <5 5-10 > 10
Pulmonary artery pressure (mmHg) < 20 30-50 > 50

Mitral regurgitation
Vena contracta width (mm) <3 3-7 >7
Regurgitant volume (mls/beat) < 30 30-59 ≥ 60a / ≥ 30b
Regurgitant fraction (%) < 30 30-49 > 50
Regurgitant orifice area (cm2) < 0.2 0.2-0.39 ≥ 0.4a / ≥ 0.2b

Tricuspid stenosis
Valve area (cm2) <1
Tricuspid regurgitation
Vena contracta width (mm) 7
Flow reversal - hepatic veins Present

Pulmonary stenosis
Peak gradient (mmHg) > 60
Pulmonary regurgitation
Pressure half-time (msec) < 100
Adapted from: Bonow and cols. .2

* European Association of Echocardiography recommendations13.

Thresholds for primarya and secondaryb mitral regurgitation.

If the LVOT diameter is thought to be inaccurate, the use and the gradient only low moderate, a dobutamine stress
of the dimensionless velocity ratio may also give a guide. echocardiogram should be considered. This confirms severe
However it is increasingly recognised that this situation can AS if the mean gradient exceeds 30 to 40 mmHg during any
be caused by low flow. stage of the dobutamine infusion, provided that the EOA
Traditionally low flow AS was diagnosed by an EOA remains < 1.2 cm2 7-9. It also determines LV contractile reserve
< 1 cm2, mean gradient < 30 to 40 mmHg6 and LV ejection shown by an increase in stroke volume, velocity integral or
fraction < 40%. However a thick-walled LV with a small cavity ejection fraction by > 20%.
can eject a low stroke volume even with a normal ejection
fraction. Low flow may then be recognised with a subaortic
velocity integral of < 15 cm, indexed stroke volume 35 mL/m2 The effect of aortic physiology
or a calculated flow of < 200 mL/s. If the LV ejection Hypertension or the resulting decreased aortic compliance
fraction is low or if the EOA is just within the severe range adds to the resistance at the aortic valve (AV) to increase the

Arq Bras Cardiol. 2014; 103(3):251-263 252

 Rajani et al.
Multimodality Imaging of Heart Valve Disease

Review Article

Figure 1 – Echocardiographic appearances of the aortic valve in short axis. Figure 1A shows the three-dimensional appearance of a tricuspid aortic valve on
transoesophageal echocardiography; Figure 1B shows the appearance of a bicuspid aortic valve on transthoracic echocardiography; and Figures 1C and 1D shows the
appearances of a quadricuspid aortic valve in systole and diastole.

Table 2 – Resolving discrepant measurements of aortic stenosis severity

Assess valve opening

Severe area (< 1.0 cm2) Assess waveform shape (triangular = moderate)
Moderate gradient (< 30-40 mmHg) Index EOA to BSA (Table 1)
If EF <40% or VTI <15 consider stress echocardiogram
Check positioning of sub-aortic pulsed sample is away from the valve
Severe gradient (V max > 4m/s) Check measurement of LVOT diameter
Moderate area (> 1.0 cm2) Flow may be increased because of concomitant aortic regurgitation (assess valve
opening and waveform shape)
EOA: effective orifice area; BSA: body surface area; EF: ejection fraction; VTI: velocity-time integral; LVOT: left ventricular outflow tract.

total LV outflow impedance. This may result in severe LV it also depends on LV diastolic pressure, chamber compliance
systolic or diastolic dysfunction, even if the AS is moderate10-12. and systemic vascular resistance21. Severe AR is also confirmed
Blood pressure measurements should ideally be taken at the by the detection of pandiastolic flow reversal in the proximal
time of echocardiography to ensure valid comparison between descending aorta with an end-diastolic velocity typically > 20
serial studies13 using a number of indices of aortic and AV cm/s22 (Figure 2). The regurgitant volume (RVol) and fraction
combined impedance14-17. However, these are not in routine can be calculated by either pulsed wave (PW) Doppler or by
clinical use pending long-term outcome data. the proximal isovelocity surface area method. A RVol of ≥
60 mls and a regurgitant fraction of ≥ 50% are taken to be
indicative of severe AR2.
Aortic Regurgitation
The aetiology is shown on two-dimensional imaging and
may be valvar or secondary to aortic dilatation or both18,19. Evaluation of the left ventricle
Valve diseases include calcific disease, bicuspid AV, infective With chronic AR, the left ventricle dilates and there is
endocarditis and rheumatic disease. Colour Doppler provides eccentric hypertrophy to ameliorate the ensuing increase
a semi-quantitative assessment (Figure 2). Severe regurgitation in wall stress. Subendocardial fibrosis develops and as
is shown by a vena contracta width > 6 mm or the height of the LV ejection falls, LV failure will ultimately supervene,
the jet ≥ 65% LVOT diameter2,20. The pressure half-time of the if surgery is not performed. In asymptomatic severe AR,
continuous wave (CW) Doppler signal is less reliable because surgery is therefore indicated when the LVEF ≤ 50%

253 Arq Bras Cardiol. 2014; 103(3):251-263

 Rajani et al.
Multimodality Imaging of Heart Valve Disease

Review Article

(Class I indication) or with a left ventricular end diastolic There is no clear role for stress echocardiography in AR
dimension (LVEDD) > 70 mm, or left ventricular end although the evaluation of symptoms may be useful.
systolic diameter (LVESD) > 50 mm (or BSA indexed
LVESD > 25 mm/m 2) (Class IIa). Newer measures of Cardiac Computed Tomography
subclinical LV impairment (strain and tissue Doppler
imaging) have been proposed but are not in clinical use.
Aortic Stenosis
Coincidental AV calcification on a routine non-contrast
enhanced CT scan may alert clinicians to the need for
echocardiography (Figure 3)23-25. However, CT is not a first
line investigation because it cannot provide haemodynamic
data and requires ionising radiation and iodinated contrast
agents. Imaging of the AV must be performed in both systole
and diastole to permit reconstructions at every 5% to 10% of
the cardiac cycle. From these, the geometric orifice area can
be estimated by planimetry (Figure 3)26. CT can also provide
LV volume and function, and accurate measurements of the
ascending aorta. It can quantify calcium if a ‘porcelain’ aorta
is suspected on the echocardiogram or invasive coronary
angiogram. CT is essential for evaluating the aortic root before
transcatheter AV implantation27,28, and can detect pannus and
evaluate prosthetic valve function29. CT may also be used for
the assessment of concomitant coronary disease before AV
surgery especially in the presence of AV vegetations (Table 3).

Aortic Regurgitation
The role of cardiac CT in the assessment AR is limited.
If appropriate phase reconstructions from the cardiac cycle are
available from a cardiac CT scan performed for other reasons
(e.g. coronary imaging), then it is reasonable to use multiplanar
reformatted images to assess the configuration and morphology
of the AV and to look for areas of malcoaptation of the valve
leaflets. Although malcoaptation on cardiac CT has been shown
to have a sensitivity of 95% and specificity of 95% to 100%
for the detection of moderate-severe AR, measurements of
the AR area by planimetry are less reliable when compared to
transthoracic echocardiography (TTE) as a gold standard30,31.

Cardiac magnetic resonance

Aortic Stenosis
AS may be detected on cardiovascular magnetic resonance
(CMR) by the identification of flow turbulence on bright blood
sequences within the LVOT and into the ascending aorta
(Table 4 and Figure 4). The valve can be imaged using bright
blood sequences. The geometric orifice area, measured by
planimetry, correlates well, but systematically underestimates
compared with TEE (Figures 5 and 6)32-35. The main reasons
for this are the complex three-dimensional shape of the
stenotic orifice, the leaflet calcification and the associated
jet turbulence making an accurate visualization of the true
stenotic orifice difficult. CMR has the added benefit of being
able to measure flow and velocity across any tubular structure
Figure 2 – Two-dimensional transthoracic appearances of severe aortic using velocity encodinged (VENC) contrast sequences. With
regurgitation. Figure 2A shows the aortic regurgitant jet occupying 100% of optimal plane selection at the aortic root, the peak transaortic
the left ventricular outflow tract diameter in the parasternal long axis view and
Figure 2B, 100% of the left ventricular outflow tract in the apical three chamber velocity can be obtained from which the peak instantaneous
view. Figure 2C shows pandiastolic flow reversal in the proximal descending gradient can be derived, using the simplified Bernoulli
aorta on colour M-Mode. equation (4V2). This technique requires careful mapping of

Arq Bras Cardiol. 2014; 103(3):251-263 254

 Rajani et al.
Multimodality Imaging of Heart Valve Disease

Review Article

Table 3 – Cardiac computerized tomography and the assessment of

the aortic valve

Cardiac computerized tomography

Valve morphology
Aortic valve calcification
Accurate aortic annulus size
Aortic stenosis Aortic dimensions
Aortic valve planimetry
TAVI assessment
Coronary assessment
Valve morphology
Leaflet mal-coaptation
Aortic regurgitation
Aortic dimensions
Coronary assessment
Aortic root abscesses
Suspected endocarditis
Localised aneurysm formation
TAVI: transcatheter aortic heart valve.

Cardiac magnetic resonance is the gold standard method

of measuring LV mass and volume and can also assess systolic
and diastolic LV function. It can differentiate sub-valvular and
supravalvular stenosis by inplane velocity mapping. It can assess
the whole aorta, which may be important in patients with a
bicuspid AV, in whom the echocardiographic window does not
permit adequate imaging above the root. New studies suggest
that CMR detects myocardial fibrosis using late Gadolinium
enhancement, which may portend a worse clinical outcome39.

Aortic Regurgitation
This can be identified by the detection of diastolic backwards
flow into the LVOT upon steady-state free precession (SSFP)
cine imaging in the three-chamber/LVOT view (Figure 5).
An accurate quantification of RVol and fraction can then be
obtained using inplane flow imaging which is able to measure
both the forward flow and the regurgitant flow across the AV.
From this, the regurgitant fraction can be derived [(RVol/forward
flow) x 100]. This technique is dependent upon careful tracing
around the area of interest of each frame of the cardiac cycle
and the selection of the correct plane at which to measure the
forward and regurgitant flows (Figure 5)40. CMR’s excellent
Figure 3 – Cardiac computed tomography of a bicuspid aortic valve. reproducibility for AR flow and LV volumes is useful for serial
Figure 3A shows the morphology and distribution of aortic valve calcium in examinations when determining the timing of surgery41,42.
a patient with a bicuspid aortic valve on a multiplanar reformatted image.
Figure 3B shows planimetry of the bicuspid aortic valve and Figure 3C the
ascending aorta anatomy. The mitral valve

Echocardiography
the area of interest for each frame of the cardiac cycle and an
appropriate selection of maximum velocity to be programmed
into the pulse sequence to avoid aliasing. Peak gradients across Mitral Regurgitation
the AV by VENC correlate well, but slightly underestimate, the Mitral Regurgitation (MR) may be primary (organic)
peak gradient obtained CW Doppler on TTE36-38. or secondary (functional). Primary causes include mitral

255 Arq Bras Cardiol. 2014; 103(3):251-263

 Rajani et al.
Multimodality Imaging of Heart Valve Disease

Review Article

Table 4 – Imaging principles for heart valve disease using cardiac magnetic resonance imaging

Electrocardiogram gating
Breath hold acquisitions
Balanced steady-state free precession imaging for cine sequencing in multiple imaging planes (two, three and four chamber’s views)
Velocity encoded cine phase contrast imaging in plane and through plane for velocity and flow data
Short axis stack for quantification of regurgitant volume and left ventricular systolic volumes and function
Late gadolinium enhancement for the detection of myocardial fibrosis

Figure 4 – Cardiac magnetic resonance imaging of a bicuspid aortic valve in diastole (A) and systole (B). Turbulence through the aortic valve is seen as white. Figure 4C
shows the use of cardiovascular magnetic resonance at also looking at the aortic root in the same patient in who an aortic coarctation was detected (black arrow).

valve prolapse (‘degenerative’ disease), endocarditis regurgitant orifice area (EROA), volume (RVol) and
and rheumatic disease. Secondary causes include any regurgitant fraction using the PISA method (Table 1) 2.
causes of LV dysfunction most commonly ischaemic Severe MR is likely if the vena contract width is > 7 mm
heart disease, hypertension and dilated cardiomyopathy. and is supported by a peak transmitral velocity > 1.5 m/s
These can all be detected by echocardiography. and a mitral VTI: aortic VTI ratio > 1.443. Three-dimensional
Colour Doppler detects MR and quantifies its severity TTE or transoesophageal echocardiography may provide
(Figure 6) from the vena contracta width or effective additional anatomical and quantitative information in

Arq Bras Cardiol. 2014; 103(3):251-263 256

 Rajani et al.
Multimodality Imaging of Heart Valve Disease

Review Article

Figure 6 – Two-dimensional and three-dimensional echocardiographic

assessment of mitral regurgitation. Severe mitral regurgitation is seen on
colour Doppler imaging in the apical four-chamber view (6A) and on spectral
Doppler imaging (6B). Figures 6C and D show the use of three-dimensional
transoesophageal echocardiography to model the mitral valve anatomy in an
individual with severe function mitral regurgitation.

patients with complex mitral valve lesions (Figure 6).

Exercise echocardiography may be useful in patients with
discordant symptoms to provide information on changes
in MR, LV systolic function and pulmonary artery pressure.
An exercise-induced increase in pulmonary artery systolic
pressure to > 60 mmHg is a criterion for surgery if repair is
feasible. In functional MR caused by ischaemic disease, an
exercise-induced increase in EROA ≥ 13 mm2 is associated
Flow (ml/s) with a much worse prognosis in those with ischaemic MR.
Flow (ml/s) In asymptomatic patients with severe primary MR
600 surgery is indicated when: the LVEF ≤ 60% (Class I)2,5,
500 or LVESD ≥ 45 mm (Class I)5, or even ≥ 40 mm (Class I)2
provided the valve is repairable. For patients with
400 Stroke volume
secondary MR undergoing coronary artery bypass grafting
300 mitral repair usually with a small annuloplasty ring is
200 recommended if there is moderate or severe regurgitation.
Regurgitant volume (41%) However, if surgery is being considered for breathlessness
100 as a result of the MR rather than for ischaemic heart
0 disease, the recommended indications are5: (1) if the LVEF
–100 is < 30% and there is both evidence of significant viability
and the possibility of revascularisation or (2) if there is
–200 no viability provided the LVEF is > 30%, full medical
0 200 400 600 800 1000 Time (ms)
treatment including cardiac resynchronization therapy has
been ineffective and there is no significant comorbidity.
Figure 5 – Cardiac magnetic resonance imaging of aortic regurgitation using
steady-state free precession imaging. The aortic regurgitation is seen as a Mitral stenosis
black jet projecting into the left ventricular cavity in the coronal (5A) and apical
five-chamber views (5B). Figure 5C shows a flow/volume curve derived from Rheumatic heart disease results in a typical appearance
velocity encoding imaging to calculate the regurgitant volume. on two-dimensional echocardiography. The leaflet tips are

257 Arq Bras Cardiol. 2014; 103(3):251-263

 Rajani et al.
Multimodality Imaging of Heart Valve Disease

Review Article

thickened and commissural fusion results in diastolic bowing Cardiac magnetic resonance imaging
of the leaflets in a hockey-stick shaped deformity. The chordae
tendinae are also thickened and become matted together.
Mitral Regurgitation
Planimetry of the mitral valve orifice area should be performed
using the parasternal short axis on a zoomed mid-diastolic MR is initially seen as a net loss of signal across the mitral
frame13. Three-dimensional transthoracic or transoesophageal valve representing flow turbulence on SSFP and gradient
echocardiography may be useful to select the correct plane for echo sequences. For a complete anatomical assessment of the
planimetry. A CW Doppler recording across the mitral valve mitral valve bright blood cine sequences should be acquired
enables the measurement of the mean transmitral gradient in the two, three and four chamber planes, along with a
and the pressure half-time. The pulmonary artery systolic full LV short-axis stack. Following this, a basal slice from the
pressure is estimated using the tricuspid regurgitation (TR) short axis stack should be selected where the mitral valve is
peak velocity (4 x TR V max) added to an estimated of right seen. Oblique slices may then be taken perpendicular to the
atrial mean pressure provided by the size and response of the line of coaptation working down from the A1-P1 juncture
IVC to a sniff. From the pressure half-time, an estimation of inferiorly down to the A3-P3 juncture every 5 mm with no
valve area can be madeb 44. inter-slice gap48. This system permits the accurate localisation
of regurgitant jets and helps to localise dysfunctional mitral
The grade of mitral stenosis (MS) can then be estimated valve leaflet scallops. The RVol can be estimated using the
(Table 1). LV stroke volume and forward flow within the aorta at the
Valve EOA can be estimated using the continuity level of the sinus of valsalva using VENC contrast mapping.
equation or proximal isovelocity surface area method. The regurgitant fraction is then calculated as the [(RVol/LV
Exercise echocardiography is indicated in patients with stoke volume) x 100]49,50.
severe symptoms despite apparently only moderate MS.
Exercise-induced increases in mean gradient to ≥ 15 mmHg
or pulmonary artery systolic pressures to ≥ 60 mmHg are Mitral stenosis
indications for intervention provided that balloon mitral Cardiac magnetic resonance imaging is not used routinely
valvuloplasty is feasible2. This is possible in the absence of for the assessment of mitral stenosis. Mitral inflow turbulence
bicommissural or severe single commissural calcification, may be seen on SSFP in-plane imaging and the mitral valve
severe chordal involvement, calcification and immobility of area may be measured using carefully placed through-plane
the valve, more than mild MR, left atrial thrombus and the SSFP imaging. Although this technique has been shown to
requirement for intervention for severe involvement of other correlate well with echo derived areas51,52 it is often limited
valves or the coronary arteries45. by the presence of atrial fibrillation and problems with
electrocardiogram gating.
Cardiac Computed Tomography
The tricuspid valve
Mitral Regurgitation
Echocardiography
The EROA can be measured by planimetry and this has
been shown to correlate well with TEE46. Additional information Causes of primary (organic) tricuspid valve disease include
available from cardiac CT includes mitral annulus size, mitral valve rheumatic disease, endocarditis, prolapse and carcinoid.
leaflet length and calcification, chordae tendinae thickening, left Secondary (functional) TR is caused by abnormalities of the RV
atrial size and the detection of pulmonary oedema. Although either as a result of infarction, volume or pressure overload.
cardiac CT with cine imaging can reliably detect and localise Colour Doppler imaging is the mainstay for quantification with
segmental leaflet prolapse, this is not routinely performed. severe TR shown by a vena contracta width ≥ 7 mm. Although
a vena contracta width < 6 mm is suggestive of less than
moderate regurgitation, there are no well validated cut-offs for
Mitral stenosis differentiating mild from moderate TR53. Additional markers
Cardiac CT is particularly suited to the detection of mitral of severe TR are a pulsed Doppler peak E velocity ≥ 1 m/s, a
valve leaflet, commissural and annulus calcification. For an dense CW signal with a fast upstroke (Figure 7) and prominent
evaluation of the valve components, a reconstruction at 65% of flow reversal in the hepatic veins54. In severe compensated TR,
the R-R interval for the open mitral valve and a reconstruction the RV may be normal in size but hyperdynamic. With time,
at 5% of the R-R interval are recommended for the closed the RV dilates progressively and may become hypodynamic as
mitral valve. The geometric orifice area is measured by direct shown by a tricuspid annulus excursion < 15 mm or a systolic
planimetry and has been shown to correlate well with TEE maximum tissue Doppler velocity at the base of the RV free
(R = 0.88; p < 0.001)47. Additional information obtainable is wall of < 11 cm/s55.
left atrial size, left atrial appendage thrombus, right ventricular In severe tricuspid stenosis (TS), the leaflets will be
(RV) hypertrophy and radiographic evidence of pulmonary restricted although there may be relatively little thickening
oedema and pulmonary hypertension. compared with left-sided rheumatic disease. Severe stenosis
b
MVA = 220
PHalf-time
Where: MVA: mitral valve area; PHalf-time: pressure half-time.

Arq Bras Cardiol. 2014; 103(3):251-263 258

 Rajani et al.
Multimodality Imaging of Heart Valve Disease

Review Article

Cardiac Computed Tomography

Cardiac CT is of limited use in tricuspid valve disease. It
can show secondary effects such as right atrial and ventricular
dilatation and reflux of contrast into the hepatic veins.
Occasionally cardiac CT can identify primary lung causes for
TR induced by pulmonary hypertension such as pulmonary
fibrosis or pulmonary embolic disease.

Cardiac magnetic resonance imaging

Significant tricuspid valve disease can be identified by
turbulent flow across the tricuspid valve with in-plane SSFP
imaging. As with MR, TR can be quantified by measuring RVol
and regurgitant fraction from the forward stroke volume in the
main pulmonary artery and the measured RV stroke volume
on SSFP imaging.

The pulmonary valve

Echocardiography
Two-dimensional imaging may provide clues as to the
aetiology of pulmonary valve dysfunction e.g. congenital,
endocarditis, carcinoid syndrome. Coexistent congenital
anomalies e.g. atrial septal defect (ASD) should be sought
since isolated congenital pulmonary valve disease is
uncommon. Severe pulmonary valve regurgitation (PR) is
shown by a wide jet on colour Doppler (Figure 8) originating
in the distal main pulmonary artery or branches, a pressure
half-time < 100 ms on CW (Figure 8) and a dilated
hyperdynamic RV. For pulmonary stenosis (PS), the primary
means for detecting stenosis is the visualisation of calcified
leaflets or reduced leaflet excursion on two-dimensional
imaging. A peak trans-pulmonary gradient on CW Doppler
of > 60 mmHg is taken to usually represent severe PS2.

Cardiac Computed Tomography

Cardiac CT may be useful in defining complex congenital
heart anatomy and for detecting secondary effects of
pulmonary valve disease. Dilatation of the pulmonary valve
annulus, pulmonary artery dilatation and RV dilatation may
be seen with PR, and dilatation of the main pulmonary artery
and left and right pulmonary arteries, RV hypertrophy, right
atrial enlargement and bowing of the interatrial septum to
the left with PS.

Cardiac magnetic resonance imaging

Figure 7 – Two-dimensional transthoracic echocardiographic appearances
Cardiac MR is considered to be the gold standard for the
of severe tricuspid regurgitation. In the parasternal tricuspid inflow view,
there is mal-coaptation of the anterior and posterior tricuspid valve leaflets assessment of PR. With visualisation of PR using cine SSFP
(7A) that gives rise to a severe jet of regurgitation seen on colour Doppler imaging and the ability to accurately measure RVol and
imaging 7B. Figure 7C shows the continuous wave Doppler appearance of regurgitant fractions with flow imaging, it has now become the
severe tricuspid regurgitation (dagger shape). technique of choice for the serial evaluation of patients with
congenital heart disease, in which progressive RV dilatation
and RV dysfunction is important for the timing of pulmonary
is shown by a mean gradient ≥ 5 mmHg and pressure valve intervention. In patients with PS, turbulent flow can
half‑time ≥ 190 ms on CW Doppler and a valve area ≤ 1 cm2 be seen across the pulmonary valve with SSFP cine imaging.
by the continuity equation. Other surrogate measures of Although planimetry of the pulmonary valve is of limited use,
significant TS include a dilated right atrium and inferior vena CMR is able to provide accurate peak velocity data across the
cava reflecting elevated right atrial pressures. pulmonary valve.

259 Arq Bras Cardiol. 2014; 103(3):251-263

 Rajani et al.
Multimodality Imaging of Heart Valve Disease

Review Article

Figure 8 – Bidimensional transthoracic echocardiographic appearances of severe pulmonary regurgitation. In diastole, the colour Doppler jet is seen to occupy the
entirety of the right ventricular outflow tract (8A). On continuous wave Doppler imaging, the pressure half-time is < 100 ms in keeping with severe regurgitation (8B).

Conclusions Author contributions

Echocardiography is the mainstay for the assessment Conception and design of the research: Rajani R, Khattar
of patients with valve disease. Where image quality is R, Chiribiri A, Victor K, Chambers J; Acquisition of data:
poor, cardiac magnetic resonance imaging and cardiac Victor K, Chambers J; Analysis and interpretation of the
computed tomography can both image all valves and data: Victor K, Chambers J; Writing of the manuscript:
provide geometric orifice areas. The ascending aorta is Rajani R; Khattar R, Chiribiri A; Victor K; Critical revision of
often suboptimally imaged on echocardiography and the manuscript for intellectual content: Rajani R, Khattar R,
cardiac magnetic resonance imaging or cardiac computed Chiribiri A, Victor K, Chambers J; Supervision/ as the major
tomography are commonly needed to fill this deficiency. Both investigator: Rajani R, Victor K, Chambers J.
cardiac magnetic resonance imaging and cardiac computed
tomography are useful for the assessment of complex
anatomy in patients with congenital heart disease. Computed Potential Conflict of Interest
tomography may be used for evaluating coronary disease No potential conflict of interest relevant to this article
often before valve surgery. However, it is not indicated for was reported.
routine valve disease assessment owing to its inability to
provide haemodynamic information and its inherent need
for iodinated contrast agents and ionising radiation. Cardiac Sources of Funding
magnetic resonance imaging is valuable for its ability to There were no external funding sources for this study.
provide haemodynamic data and also accurate reproducible
measurements of ventricular volumes, mass and function. It is
considered to be the technique of choice for the assessment Study Association
of pulmonary valve disease and for detecting myocardial scar. This study is not associated with any thesis or dissertation work.

References
1. Nkomo VT, Gardin JM, Skelton TN, Gottdiener JS, Scott CG, Enriquez-Sarano Heart Association Task Force on Practice Guidelines (Writing Committee
M. Burden of valvular heart diseases: a population-based study. Lancet. to revise the 1998 guidelines for the management of patients with valvular
2006;368(9540):1005-11. heart disease). Endorsed by the Society of Cardiovascular Anesthesiologists,
Society for Cardiovascular Angiography and Interventions, and Society of
2. Bonow RO, Carabello BA, Chatterjee K, de Leon AC Jr, Faxon DP, Freed
Thoracic Surgeons. J Am Coll Cardiol. 2008;52(13):e1-142.
MD, et al; American College of Cardiology/American Heart Association
Task Force on Practice Guidelines. 2008 focused update incorporated into 3. Otto CM, Pearlman AS, Comess KA, Reamer RP, Janko CL, Huntsman LL.
the ACC/AHA 2006 guidelines for the management of patients with valvular Determination of the stenotic aortic valve area in adults using Doppler
heart disease: a report of the American College of Cardiology/American echocardiography. J Am Coll Cardiol. 1986;7(3):509-17.

Arq Bras Cardiol. 2014; 103(3):251-263 260

 Rajani et al.
Multimodality Imaging of Heart Valve Disease

Review Article

4. Zoghbi WA, Farmer KL, Soto JG, Nelson JG, Quinones MA. Accurate 20. Lancellotti P, Tribouilloy C, Hagendorff A, Moura L, Popescu BA, Agricola
noninvasive quantification of stenotic aortic valve area by Doppler E, et al; European Association of Echocardiography. European Association
echocardiography. Circulation. 1986;73(3):452-9. of Echocardiography recommendations for the assessment of valvular
regurgitation. Part 1: aortic and pulmonary regurgitation (native valve
5. Vahanian A, Alfieri O, Andreotti F, Antunes MJ, Barón-Esquivias G, disease). Eur J Echocardiogr. 2010;11(3):223-44.
Baumgartner H, et al; Joint Task Force on the Management of Valvular
Heart Disease of the European Society of Cardiology (ESC); European 21. Griffin BP, Flachskampf FA, Siu S, Weyman AE, Thomas JD. The effects of
Association for Cardio-Thoracic Surgery (EACTS). Guidelines on the regurgitant orifice size, chamber compliance, and systemic vascular resistance
management of valvular heart disease (version 2012): The Joint Task Force on aortic regurgitant velocity slope and pressure half-time. Am Heart J.
on the Management of Valvular Heart Disease of the European Society of 1991;122(4 Pt 1):1049-56.
Cardiology (ESC) and the European Association for Cardio‑Thoracic Surgery
(EACTS). Eur Heart J. 2012;33(19):2451-96. 22. Tribouilloy C, Avinee P, Shen WF, Rey JL, Slama M, Lesbre JP. End
diastolic flow velocity just beneath the aortic isthmus assessed by pulsed
6. Chambers J. Low “gradient”, low flow aortic stenosis. Heart. Doppler echocardiography: a new predictor of the aortic regurgitant
2006;92(4):554-8. fraction. Br Heart J. 1991;65(1):37-40.

7. Monin JL, Quere JP, Monchi M, Petit H, Baleynaud S, Chauvel C, et al. 23. Messika-Zeitoun D, Aubry MC, Detaint D, Bielak LF, Peyser PA, Sheedy
Low-gradient aortic stenosis: operative risk stratification and predictors PF, et al. Evaluation and clinical implications of aortic valve calcification
for long-term outcome: a multicenter study using dobutamine stress measured by electron-beam computed tomography. Circulation.
hemodynamics. Circulation. 2003;108(3):319-24. 2004;110(3):356-62.

8. Nishimura RA, Grantham JA, Connolly HM, Schaff HV, Higano ST, 24. Cowell SJ, Newby DE, Burton J, White A, Northridge DB, Boon NA, et al.
Holmes DR Jr. Low-output, low-gradient aortic stenosis in patients with Aortic valve calcification on computed tomography predicts the severity of
depressed left ventricular systolic function: the clinical utility of the aortic stenosis. Clin Radiol. 2003;58(9):712-6.
dobutamine challenge in the catheterization laboratory. Circulation.
2002;106(7):809-13. 25. Koos R, Kuhl HP, Muhlenbruch G, Wildberger JE, Gunther RW, Mahnken
AH. Prevalence and clinical importance of aortic valve calcification detected
9. Takeda S, Rimington H, Chambers J. The relation between transaortic incidentally on CT scans: comparison with echocardiography. Radiology.
pressure difference and flow during dobutamine stress echocardiography 2006;241(1):76-82.
in patients with aortic stenosis. Heart. 1999;82(1):11-4.
26. Shah RG, Novaro GM, Blandon RJ, Whiteman MS, Asher CR, Kirsch
10. Aronow WS, Schwartz KS, Koenigsberg M. Correlation of serum lipids, J. Aortic valve area: meta-analysis of diagnostic performance of
calcium and phosphorus, diabetes mellitus, aortic valve stenosis and history multi‑detector computed tomography for aortic valve area measurements
of systemic hypertension with presence or absence of mitral anular calcium as compared to transthoracic echocardiography. Int J Cardiovasc Imaging.
in persons older than 62 years in a long-term health care facility. Am J Cardiol. 2009;25(6):601-9.
1987;59(4):381-2.
27. Willson AB, Webb JG, Labounty TM, Achenbach S, Moss R, Wheeler M,
11. Antonini-Canterin F, Huang G, Cervesato E, et al. Symptomatic aortic et al. 3-dimensional aortic annular assessment by multidetector computed
stenosis: does systemic hypertension play an additional role? Hypertension. tomography predicts moderate or severe paravalvular regurgitation after
2003;41(6):1268-72. transcatheter aortic valve replacement: a multicenter retrospective analysis.
J Am Coll Cardiol. 2012;59(14):1287-94.
12. Kadem L, Dumesnil JG, Rieu R, Durand LG, Garcia D, Pibarot P. Impact
of systemic hypertension on the assessment of aortic stenosis. Heart. 28. Jilaihawi H, Kashif M, Fontana G, Furugen A, Shiota T, Friede G, et al.
2005;91(3):354-61. Cross-sectional computed tomographic assessment improves accuracy
of aortic annular sizing for transcatheter aortic valve replacement and
13. Baumgartner H, Hung J, Bermejo J, Chambers JB, Evangelista A, Griffin BP, et al. reduces the incidence of paravalvular aortic regurgitation. J Am Coll Cardiol.
Echocardiographic assessment of valve stenosis: EAE/ASE recommendations 2012;59(14):1275-86.
for clinical practice. Eur J Echocardiogr. 2009;10(1):1-25. Erratum in: Eur J
Echocardiogr. 2009;10(3):479. 29. Konen E, Goitein O, Feinberg MS, Eshet Y, Raanani E, Rimon U, et al. The role
of ECG-gated MDCT in the evaluation of aortic and mitral mechanical valves:
14. Garcia D, Pibarot P, Dumesnil JG, Sakr F, Durand LG. Assessment of aortic initial experience. AJR Am J Roentgenol. 2008;191(1):26-31.
valve stenosis severity: a new index based on the energy loss concept.
Circulation. 2000;101(7):765-71. 30. Feuchtner GM, Dichtl W, Schachner T, Müller S, Mallouhi A, Friedrich
GJ, et al. Diagnostic performance of MDCT for detecting aortic valve
15. Briand M, Dumesnil JG, Kadem L, Tongue AG, Rieu R, Garcia D, et al. regurgitation. AJR Am J Roentgenol. 2006;186(6):1676-81.
Reduced systemic arterial compliance impacts significantly on left ventricular
afterload and function in aortic stenosis: implications for diagnosis and 31. Feuchtner GM, Dichtl W, Muller S, Müller S, Jodocy D, Schachner T, et al.
treatment. J Am Coll Cardiol. 2005;46(2):291-8. 64-MDCT for diagnosis of aortic regurgitation in patients referred to CT
coronary angiography. AJR Am J Roentgenol. 2008;191(1):W1-7.
16. Lancellotti P, Donal E, Magne J, Moonen M, O’Connor K, Daubert JC, et al.
Risk stratification in asymptomatic moderate to severe aortic stenosis: 32. Debl K, Djavidani B, Seitz J, Nitz W, Schmid FX, Muders F, et al. Planimetry
the importance of the valvular, arterial and ventricular interplay. Heart. of aortic valve area in aortic stenosis by magnetic resonance imaging.
2010;96(17):1364-71. Invest Radiol. 2005;40(10):631-6.

17. Hachicha Z, Dumesnil JG, Bogaty P, Pibarot P. Paradoxical low-flow, 33. John AS, Dill T, Brandt RR, Rau M, Ricken W, Bachmann G, et al.
low-gradient severe aortic stenosis despite preserved ejection fraction Magnetic resonance to assess the aortic valve area in aortic stenosis:
is associated with higher afterload and reduced survival. Circulation. how does it compare to current diagnostic standards? J Am Coll Cardiol.
2007;115(22):2856-64. 2003;42(3):519-26.

18. Wan CK, Suri RM, Li Z, Orszulak TA, Daly RC, Schaff HV, et al. Management 34. Kupfahl C, Honold M, Meinhardt G, Vogelsberg H, Wagner A, Mahrholdt H,
of moderate functional mitral regurgitation at the time of aortic valve et al. Evaluation of aortic stenosis by cardiovascular magnetic resonance
replacement: is concomitant mitral valve repair necessary? J Thorac imaging: comparison with established routine clinical techniques. Heart.
Cardiovasc Surg. 2009;137(3):635-40. 2004;90(8):893-901.

19. Unger P, Dedobbeleer C, Van Camp G, Plein D, Cosyns B, Lancellotti P. Mitral 35. Reant P, Lederlin M, Lafitte S, Serri K, Montaudon M, Corneloup O,
regurgitation in patients with aortic stenosis undergoing valve replacement. et al. Absolute assessment of aortic valve stenosis by planimetry
Heart. 2010;96(1):9-14. using cardiovascular magnetic resonance imaging: comparison with

261 Arq Bras Cardiol. 2014; 103(3):251-263

 Rajani et al.
Multimodality Imaging of Heart Valve Disease

Review Article

transesophageal echocardiography, transthoracic echocardiography, and 46. Alkadhi H, Wildermuth S, Bettex DA, Plass A, Baumert B, Leschka S, et al.
cardiac catheterisation. Eur J Radiol. 2006;59(2):276-83. Mitral regurgitation: quantification with 16-detector row CT--initial experience.
Radiology. 2006;238(2):454-63.
36. Kilner PJ, Manzara CC, Mohiaddin RH, Pennell DJ, Sutton MG, Firmin DN,
et al. Magnetic resonance jet velocity mapping in mitral and aortic valve 47. Messika-Zeitoun D, Serfaty JM, Laissy JP, Berhili M, Brochet E, Iung B, et al.
stenosis. Circulation. 1993;87(4):1239-48. Assessment of the mitral valve area in patients with mitral stenosis by multislice
computed tomography. J Am Coll Cardiol. 2006;48(2):411-3.
37. Eichenberger AC, Jenni R, von Schulthess GK. Aortic valve pressure gradients
in patients with aortic valve stenosis: quantification with velocity-encoded 48. Chan KM, Wage R, Symmonds K, Rahman-Haley S, Mohiaddin RH, Firmin
cine MR imaging. AJR Am J Roentgenol. 1993;160(5):971-7. DN, et al. Towards comprehensive assessment of mitral regurgitation using
cardiovascular magnetic resonance. J Cardiovasc Magn Reson. 2008;10:61.
38. Caruthers SD, Lin SJ, Brown P, Watkins MP, Williams TA, Lehr KA, et al. Practical
value of cardiac magnetic resonance imaging for clinical quantification 49. Kon MW, Myerson SG, Moat NE, Pennell DJ. Quantification of regurgitant
of aortic valve stenosis: comparison with echocardiography. Circulation. fraction in mitral regurgitation by cardiovascular magnetic resonance:
2003;108(18):2236-43. comparison of techniques. J Heart Valve Dis. 2004;13(4):600-7.
39. Dweck MR, Joshi S, Murigu T, Alpendurada F, Jabbour A, Melina G, et al. 50. Kizilbash AM, Hundley WG, Willett DL, Franco F, Peshock RM, Grayburn
Midwall fibrosis is an independent predictor of mortality in patients with PA. Comparison of quantitative Doppler with magnetic resonance
aortic stenosis. J Am Coll Cardiol. 2011;58(12):1271-9. imaging for assessment of the severity of mitral regurgitation. Am J Cardiol.
40. Myerson SG. Heart valve disease: investigation by cardiovascular magnetic 1998;81(6):792-5.
resonance. J Cardiovasc Magn Reson. 2012;14:7. 51. Djavidani B, Debl K, Lenhart M, Seitz J, Paetzel C, Schmid FX, et al.
41. Aurigemma G, Reichek N, Schiebler M, Axel L. Evaluation of aortic Planimetry of mitral valve stenosis by magnetic resonance imaging. J Am
regurgitation by cardiac cine magnetic resonance imaging: planar analysis and Coll Cardiol. 2005;45(12):2048-53.
comparison to Doppler echocardiography. Cardiology. 1991;78(4):340-7. 52. Djavidani B, Debl K, Buchner S, Lipke C, Nitz W, Feuerbach S, et al. MRI
42. Honda N, Machida K, Hashimoto M, Mamiya T, Takahashi T, Kamano T, et al. planimetry for diagnosis and follow-up of valve area in mitral stenosis
Aortic regurgitation: quantitation with MR imaging velocity mapping. Radiology. treated with valvuloplasty. Rofo. 2006;178(8):781-6.
1993;186(1):189-94.
53. Lancellotti P, Moura L, Pierard LA, Agricola E, Popescu BA, Tribouilloy C,
43. Tribouilloy C, Shen WF, Rey JL, Adam MC, Lesbre JP. Mitral to aortic et al. European Association of Echocardiography recommendations
velocity‑time integral ratio: a non-geometric pulsed-Doppler regurgitant for the assessment of valvular regurgitation. Part 2: mitral and tricuspid
index in isolated pure mitral regurgitation. Eur Heart J. 1994;15(10):1335-9. regurgitation (native valve disease). Eur J Echocardiogr. 2010;11(4):307-32.

44. Thomas JD, Weyman AE. Doppler mitral pressure half-time: a clinical tool 54. Gonzalez-Vilchez F, Zarauza J, Vazquez de Prada JA, Martín Durán R, Ruano
in search of theoretical justification. J Am Coll Cardiol. 1987;10(4):923-9. J, Delgado C, et al. Assessment of tricuspid regurgitation by Doppler color
flow imaging: angiographic correlation. Int J Cardiol. 1994;44(3):275-83.
45. Wilkins GT, Weyman AE, Abascal VM, Block PC, Palacios IF. Percutaneous
balloon dilatation of the mitral valve: an analysis of echocardiographic 55. Haddad F, Doyle R, Murphy DJ, Hunt SA. Right ventricular function in
variables related to outcome and the mechanism of dilatation. Br Heart J. cardiovascular disease, part II: pathophysiology, clinical importance, and
1988;60(4):299-308. management of right ventricular failure. Circulation. 2008;117(13):1717-31.

Arq Bras Cardiol. 2014; 103(3):251-263 262

 Review Article

263 Arq Bras Cardiol. 2014; 103(3):251-263