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Education in Heart
Valvular heart disease
The evolving role of multimodality imaging in valvular heart disease
  1. Darryl P Leong1,2,3,4,
  2. Majo X Joseph1,2,3,
  3. Joseph B Selvanayagam1,2,3
  1. 1Flinders Centre for Cardiovascular Magnetic Resonance Research, Adelaide, Australia
  2. 2Department of Cardiovascular Medicine, Flinders Medical Centre, Adelaide, Australia
  3. 3Discipline of Medicine, Flinders University, Adelaide, Australia
  4. 4Discipline of Medicine, University of Adelaide, Adelaide, Australia
  1. Correspondence to Professor Joseph B Selvanayagam, Department of Cardiovascular Medicine, Flinders Medical Centre, Bedford Park, Adelaide, South Australia 5042, Australia; Joseph.Selvanaygam{at}flinders.edu.au

https://doi.org/10.1136/heartjnl-2011-300919

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    The public health burden of valvular heart disease (VHD) is projected to grow over the ensuing years owing to the persistent spectre of rheumatic heart disease in developing countries,w1 and the increasing rate of degenerative VHD among the ageing population in developed countries.1 Morbidity and mortality associated with these conditions and their treatment are high.w2 Thus optimal evaluation of VHD is of clear importance.

    There are many approaches to the assessment of VHD.2 The aim of this article is first to provide a brief overview of the pathophysiology of the four most common valvular lesions: mitral regurgitation, mitral stenosis, aortic stenosis, and aortic regurgitation. The evolving role of cardiac imaging in the evaluation of these conditions will then be examined. The focus of this article is on multimodality imaging, and the complementary information these techniques provide on the most common valvular lesions (table 1). These imaging techniques are of increasing relevance given the invasive nature of cardiac catheterisation in the quantification of left ventricular (LV) function and VHD severity. The role of imaging in valvular intervention and in the assessment of the prosthetic valves (recently reviewed in Heartw3 w4) lies outside the scope of the present article.

    View this table:
    Table 1

    Strengths and limitations of the imaging modalities in the evaluation of valvular heart disease

    Mitral regurgitation

    The mitral valve (MV) apparatus is a complex structure. It comprises a fibrous annulus, whose saddle-like geometry has proven challenging to represent using older, two dimensional (2D) imaging approaches. Three dimensional (3D) imaging modalities, especially 3D echocardiography and multidetector row CT (MDCT), have allowed better characterisation of the mitral annulus, its dynamic nature, and the changes associated with mitral regurgitation (MR) (figure 1).w5 w6

    Figure 1
    Figure 1

    Three dimensional (3D) mitral valve (MV) reconstruction (A). AL, anterolateral mitral annulus; PM, posteromedial mitral annulus. (B) Orthogonal view of mitral annulus to (A). A, anterior mitral annulus; Ao, aortic annulus; Nadir, mitral leaflet coaptation nadir; P, posterior mitral annulus. (C) 3D MV model. A, anterior annulus; AL, anterolateral commissure; Ao, aorta; P, posterior annulus; PM, posteromedial commissure. (D) 3D volume rendered reconstruct of the MV as seen from the left atrium.

    The annulus supports the anterior and posterior mitral leaflets, which are anchored to the LV cavity via the papillary muscles and chordae tendinae. The interaction of these components of the mitral apparatus is critical in maintaining valvular competency. The coaptation of the mitral leaflets normally exhibits redundancy; however, disease processes affecting some or all of these components erode this redundancy, culminating in MR.

    Pathophysiology

    Chronic MR imposes a volume load on the left ventricle, which if of sufficient severity and duration results in adverse LV remodelling. This remodelling is classically eccentric in geometry (LV cavity dilatation is greater proportionally than the increase in LV wall thickness). Clinical symptoms in MR, the development of which forms a cornerstone of the intervention decision making algorithm,3 are not only predicated on lesion severity, but also on the time course with which it develops. Acute MR in the setting of papillary muscle rupture or infective endocarditis may present with precipitous pulmonary oedema in the absence of left atrial (LA) dilatation or a large colour Doppler signal characteristic of severe, chronic MR.2

    Imaging evaluation of MR

    Cardiac imaging evaluation is critical in the guideline driven management of MR.2 The role of imaging in the evaluation of MR entails diagnosis of its mechanism, as well as accurate quantification of its severity (figure 2). The distinction between MR aetiology, lesion (or pathology) and mechanism must be emphasised; diverse aetiologies can cause MR through similar mechanisms, and it is the mechanism of regurgitation that determines the choice of therapeutic approach adopted (figure 3). In contrast, assessment of MR severity in conjunction with symptoms is critical in dictating the timing of therapeutic intervention.

    Figure 2
    Figure 2

    Flow diagram illustrating a clinical approach to the evaluation of mitral regurgitation (MR). The grey box contains parameters assessed. To its left are the imaging modalities used to assess these parameters, and to its right are the clinical implications of the imaging's findings. AF, atrial fibrillation; CAD, coronary artery disease; CMR, cardiovascular magnetic resonance; CTCA, CT coronary angiography; EROA, effective regurgitant orifice area; LV, left ventricular; LVEF, left ventricular ejection fraction; LVESD, left ventricular end-systolic diameter; MV, mitral valve; R Vol, regurgitant volume; SPAP, systolic pulmonary artery pressure; TOE, transoesophageal echocardiography; TTE, transthoracic echocardiography.

    Figure 3
    Figure 3

    Schematic diagram illustrating an aetiopathogenic classification of mitral regurgitation. Carpentier I, normal leaflet motion and length; Carpentier II, increased leaflet motion; Carpentier IIIa, restricted leaflet motion in ventricular diastole; Carpentier IIIb, restricted leaflet motion in ventricular systole; LV, left ventricular; MI, myocardial infarction; SAM, systolic anterior motion of anterior mitral valve leaflet.

    Diagnosis of MR mechanism

    Mechanistic contributors to MR may be dichotomised into those involving the leaflets, resulting in primary or organic MR, and those involving supportive structures, causing so-called functional or secondary MR. LV remodelling and dysfunction may permit functional MR through annular dilatation,4 w7 apical displacement of the papillary musclesw7 which exerts traction on the mitral leaflets, and increased MV tenting,4 w8 thus reducing its coaptation.

    A parallel classification system for MR, from work by Carpentier et al,w9 is based on mitral leaflet motion—whether normal (type I), exaggerated (type II), or reduced (type III). Although these classification schemes differ principally in semantics, it must be reiterated that the evaluation of MR should include description of its aetiology, pathophysiology, and severity.

    A wide array of clinical and imaging factors should be integrated to categorise accurately an individual's MR, and no one parameter should be taken in isolation. Owing to its real-time nature, echocardiography is suited to examination of the highly mobile mitral leaflets. Ben Zekry et al compared 3D transthoracic and 2D and 3D transoesophageal echocardiography (TOE) in the workup of patients undergoing MV surgery for MR of heterogeneous aetiology.w10 These authors found that these three echocardiographic modalities were comparable in recognising the MR aetiology, but that 3D TOE was superior in its ability to identify the scallop harbouring the MV pathology.

    Various imaging techniques can provide evidence of a functional MR mechanism. While 2D transthoracic echocardiography (TTE) can demonstrate LV dilatation, 3D techniques including 3D TTE and cardiac magnetic resonance (CMR) provide more accurate and reproducible LV chamber quantification.w11 Underlying ischaemic aetiology might be suggested by the identification of ischaemia on perfusion CMR imaging, or scar on late gadolinium enhancement CMR (which can involve the papillary musclesw12), or significant coronary disease on MDCT. Mitral annular dilatation can be illustrated with 3D TOE or indeed MDCT.w5

    With these diverse imaging options available, the diagnostic strategy should be individualised on the basis of the patient's clinical features, and also guided by local expertise.

    Quantification of MR severity

    Accurate quantification of MR has been demonstrated to be of powerful prognostic significance.5 Echocardiography is the mainstay of evaluating MR severity2 (table 2). Although a number of measures may be acquired,w13 the echocardiographic appraisal of MR severity should not be limited to a single approach, but should be a synthesis of multiple indices.2 Assessment of MR severity may include evaluation of regurgitant jet characteristics, measurement of the regurgitant volume, and identification of the beat-to-beat as well as chronic sequelae of the valvular incompetence.

    View this table:
    Table 2

    Echocardiographic indicators of severe valvular heart disease

    Regurgitant jet characteristics that suggest severe incompetence are a broad vena contracta (≥7 mm), a large effective regurgitant orifice area (EROA ≥40 mm2)—of which the vena contracta is a one dimensional analogue—and a substantial jet area on colour Doppler imaging of the left atrium (>10 cm2 or >40% of the left atrial area)w13 (figure 4). Regurgitant volume can be estimated echocardiographically either by the flow convergence technique (which may offer similar information to the EROA estimated by the same technique) or using a pulsed wave Doppler volumetric approach along with the continuity equation. This latter method is less helpful owing to its time consuming nature and its susceptibility to error at a number of stages.w14 In contrast, owing to its high signal-to-noise ratio, CMR measurement of regurgitant volume has been shown to be a robust approach in the research setting.w15

    Figure 4
    Figure 4

    Transthoracic echocardiographic images from a patient with severe mitral regurgitation (MR) from rheumatic heart disease. (A) Parasternal long axis view demonstrating failure of coaptation of the mitral leaflets. (B) Colour Doppler echocardiography in the parasternal long axis view, which shows a broad vena contracta. (C) Colour Doppler echocardiography in the apical four chamber view. (D) Colour Doppler echocardiography in the apical four chamber view with lowered colour baseline. Proximal isovelocity surface area (PISA) effective regurgitant orifice area (EROA) 0.5 cm2 consistent with severe MR.

    Beat-to-beat echocardiographic findings reflecting sequelae of severe MR include a prominent E wave (peak velocity ≥1.2 m/s being a sensitive but not specific sign) and systolic flow reversal within the pulmonary veins (a specific but insensitive marker).w13 Enlarged LA and ventricular volumes, and elevated resting pulmonary arterial systolic pressures, are hallmarks of severe, chronic MR. Indeed, resting systolic pulmonary pressure >50 mm Hg is an indication for MV intervention for severe MR.1

    An integrated approach to MR quantification that incorporates evaluation of its aetiology, pathology and mechanism is of increasingly recognised importance. Whereas an EROA by the flow of convergence method of ≥40 mm2 is indicative of severe MR, a threshold of ≥20 mm2 is more appropriate for ischaemic functional MRw14—this is but one example in which evaluation of MR severity using only one parameter, and without knowledge of the aetiology, pathology and mechanism, can lead to misclassification of its grade, which in turn may result in a deleterious delay in patient treatment.

    3D imaging approaches may come to play an important role in MR quantification. Each of the 2D echocardiographic measures of MR severity previously described have now been revisited using 3D echocardiography (vena contracta,w16 regurgitant volume derived from EROA estimated using 3D colour flow Doppler,w17 and from anatomic regurgitant orifice areaw18) with advantages demonstrated. These approaches will be more accessible with the advent of less cumbersome ultrasound probes that can achieve higher temporal resolution.

    In instances in which transthoracic echocardiographic evaluation of MR is doubtful due to limited image quality, TOE or CMR may deliver additional insights. CMR may be used to estimate mitral regurgitant volume by the difference between LV stroke volume, as measured by summation of axial LV slice volumes, and antegrade aortic flow volume by phase contrast magnetic resonance.w19 It can also examine the MV apparatus in a manner analogous to TOE.w20 TOE permits superior visualisation of the incompetent jet for more accurate quantification of its degree. Using TOE, Shanks et al have demonstrated that by 3D colour Doppler imaging of the regurgitant jet, estimation of the EROA yields comparable estimates of regurgitant volume to CMR, and that this approach is superior to 2D estimation.w15 TOE is also the modality of choice for imaging the dynamic function of the valve, allowing the best appreciation of organic valvular lesions. Specific lesions, such as ruptured chordae and flail segments, may be visualised, and the site of pathology (eg, scallop or commissural prolapse) may be more accurately localised using TOE.w21

    Evaluation of LV systolic function

    Deterioration in LV systolic function is a sign of decompensation of the left ventricle in the face of the sustained volume load imposed by significant MR. To this end, LV ejection fraction (LVEF) <60% has been recommended as an indication for MV surgery for severe, asymptomatic MR.3 The measurement of LV function by LVEF using 2D echocardiography is, however, hindered by issues of reproducibility.w22 Novel echocardiographic techniques (such as tissue Doppler, speckle tracking strain, and 3D imaging) and CMR assessment of LV volumes and regional function may offer valuable additional information.w22

    An important confounding factor in the evaluation of LV contractile performance in the setting of MR is the load dependence of most non-invasive indices of LV function. While there is ongoing research on less load dependent measures of LV contractility,w23 the role of these novel markers of LV function in risk stratification of patients with MR remains to be determined.

    Exercise echocardiography

    The correlation between the severity of MR at rest and its augmentation during exercise may be weak, especially in ischaemic MR.6 This observation is particularly pertinent in the assessment of patients whose symptoms on exertion appear excessive for the severity of MR identified on resting echocardiography. These individuals may be more accurately diagnosed using exercise echocardiography. Per-exercise echocardiography may play a role in identifying patients with MR of innocuous appearance on resting echocardiography but who in fact exhibit pronounced worsening with exercise. Lancellotti et al have shown in patients with ischaemic functional MR that an exercise induced increase in EROA of ≥13 mm2 is a significant predictor of mortality and heart failure hospitalisation.7 These investigators have also demonstrated similar findings among patients with organic MR, in whom an exercise induced increase in regurgitant volume ≥15 ml was associated with poorer outcome.w24 Further evidence is required, particularly demonstrating favourable outcomes of valvular intervention on the basis of per-exercise echocardiography when resting echocardiographic criteria for intervention are not met, before it can enter routine clinical practice.

    Mitral stenosis

    Pathophysiology

    Mitral stenosis (MS), which is generally caused by rheumatic heart disease, is characterised by progressive reduction in MV area from the norm of 4–5 cm2 until symptoms develop, usually at valve areas <1.5 cm2 (although tachycardia may precipitate symptoms at larger valve areas owing to truncation of diastolic filling).2 ,8 Significant MS is associated with an increase in LA pressure, resulting in LA dilatation, and ultimately pulmonary congestion and pulmonary arterial hypertension.

    Imaging evaluation of MS

    A critical role of imaging in MS is the assessment of its severity (table 2). TTE has formed the cornerstone of non-invasive evaluation of MS grade. Continuous wave Doppler echocardiography across the MV may be used to estimate the transmitral gradient through the Bernouilli equation, and the MV area by the half-time method. Significant (at least moderate) MS is suggested by a gradient ≥5 mm Hg or MV area ≤1.5 cm2. Planimetry of the MV area at the leaflet tips is a cardinal measure of MS severity, particularly in the presence of atrial fibrillation or significant MR, when the half-time approach may be less reliable.w25 Accurate MV area planimetry requires correct imaging plane orientation, which may prove challenging using 2D approaches. 3D echocardiography permits imaging in any plane (figure 5), and thus allows superior measurement of the MV area.w26

    Figure 5
    Figure 5

    Offline analysis of a three dimensional transoesophageal echocardiographic dataset from a patient with mitral stenosis. Panels A and B depict orthogonal long axis views of the mitral apparatus. Panel C demonstrates an en face view of the stenotic mitral valve cropped for accurate planimetry of the valve area at the leaflet tips in the plane of the valve orifice. Panel D is a multiplanar representation of the dataset.

    Beyond assessment of MS severity, TTE permits identification of adverse sequelae of longstanding significant MS—LA dilatation and pulmonary hypertension. Estimated systolic pulmonary artery pressure >50 mm Hg at rest or >60 mm Hg with exercise is considered a class I indication for percutaneous balloon valvotomy if feasible.3

    Finally, TTE is important in guiding the choice of therapy (percutaneous or surgical) when required for MS. Scoring systems based on MV characteristics, such as leaflet mobility, thickening, calcification, and subvalvular involvement, can help identify individuals likely to benefit from percutaneous mitral commissurotomy.w27 w28 In addition, the presence of MR≥2+ has been shown to predict subsequent adverse outcome following percutaneous mitral commissurotomy, and is considered a relative contraindication to this approach.w28

    In the majority of cases, TTE suffices for the evaluation of MS. TOE may possess a particular role in instances of poor transthoracic image quality, however. In addition, MDCT displays promise in the planimetry of MV area.9 Although a clear role for MDCT in MS has yet to be defined, its ability to quantify calcification (a prognostic factor before percutaneous balloon valvotomy) as well as to identify concomitant coronary artery disease make it an appealing alternative.

    Aortic stenosis

    Pathophysiology

    Aortic stenosis (AS) results most frequently from calcific degeneration of the normal valve. Such a degenerative process may be accelerated in individuals with congenital bicuspid aortic valve (AV). Chronic and pronounced afterload excess in severe AS causes concentric LV hypertrophy and diffuse myocardial fibrosis, which lead initially to diastolic and ultimately systolic LV dysfunction, and heart failure.

    Imaging evaluation of AS

    While the most important role of imaging in AS is the assessment of its severity, attention must also be directed towards its underlying cause. The presence of congenital bicuspid AV should signal the presence of coexistent aortopathy, and has implications for subsequent intervention.

    Assessment of AS severity

    TTE remains the mainstay in the grading of AS severity (table 2). Guidelines quote peak AV velocity >4 m/s, mean gradient >40 mm Hg, aortic valve area (AVA) <1 cm2, and AVA indexed to body surface area <0.6 cm2/m2 as markers of severe AS.3 These criteria form the cornerstone of assessment of AS. Recent evidence raises the possibility that these cut-offs in isolation oversimplify the complexity of AS, and may result in under-referral of patients for AV surgery who are likely to benefit.8 In addition to the evaluation of AS severity, Dumesnil et al8 recommend quantification of vascular and haemodynamic load, as well as LV geometry and LV function. More novel indices to this end include valvulo-arterial impedance, ZVA, which is calculated asEmbedded Image

    where SAP is systolic arterial pressure in mm Hg, ΔP is the mean AV gradient in mm  Hg, and SVi is the stroke volume indexed to body surface area.w29 A ZVA >5 mm Hg/ml/m2 has been associated with adverse prognostic factors and outcome.10w29 Whereas ZVA is a measure of valvulo-arterial impedance, systemic arterial compliance (defined as SVi/arterial pulse pressure) may be a purer measure of vascular stiffness. Systemic arterial compliance has been shown to increase following transcatheter AV implantation,w30 although its prognostic value before AV intervention remains to be determined.

    There has been some research towards the potential for MDCT assessment of AS by planimetry of the AVA.11 The appeal of MDCT in the patient with AS is its high negative predictive value for the co-occurrence of coronary artery disease before valve replacement or transcatheter valve implantation, as well as its ability to visualise the proximal aorta. Available evidence suggests that MDCT tends to yield marginally larger AVA compared with echocardiographic approaches.w31 This may be due in part to the fact that in a given patient the anatomic AVA (as measured by planimetry) tends to be greater than the effective AVA (which is what is measured by echocardiographic Doppler techniques), depending on LV outflow tract geometry.w32

    The asymptomatic patient with severe AS

    Current indications for aortic valve replacement (AVR) in the asymptomatic individual with severe AS include the development of symptoms or hypotension on exercise testing, resting LVEF <50%, severe valvular calcification or rapid disease progression (increment in peak AV velocity >0.3 m/s per year).12 Clearly, therefore, serial imaging on a 6–12 monthly basis is warranted in these patients.

    Emerging imaging approaches include more sensitive techniques to detect subtle LV systolic dysfunction and even myocardial fibrosis. Delgado et al found among patients with severe AS and preserved LVEF that myocardial strain by speckle tracking echocardiography is impaired.w33 Indeed, this group has demonstrated that these perturbations in LV strain appear to worsen in parallel with AS severity.w34 In a study combining both late gadolinium enhancement CMR and echocardiographic speckle tracking strain, Weidemann et al13 showed that AVR did not appear to reverse myocardial fibrosis, but that myocardial strain was predictive of symptomatic improvement following surgery. These studies offer promise that advances in imaging techniques can refine the selection of asymptomatic patients with severe AS who may benefit from valve surgery, although this hypothesis requires confirmation in prospective clinical studies.

    Low flow/low gradient AS

    A non-severe transvalvular gradient can mask the presence of severe AS in those with LV contractile impairment. In these instances a reduced AVA and morphological valve characteristics will be suggestive of this diagnosis, which may be confirmed by low dose dobutamine stress echocardiography (figure 6). Should the valve area increase by ≥0.2 cm2 or to >1 cm2 with no change in gradient, it is likely that the valve is not anatomically severely stenotic, whereas preservation of a severely reduced AVA with an increase in the transvalvular gradient indicates true severe AS. Furthermore, a lack of contractile reserve (failure of LV stroke volume to augment by ≥20% with dobutamine) has been associated with adverse surgical outcomes.

    Figure 6
    Figure 6

    Flow diagram illustrating a clinical approach to the evaluation of aortic stenosis (AS). The grey box contains the parameters assessed. To its left are the imaging modalities used to assess these parameters, and to its right are the clinical implications of the imaging's findings. AV, aortic valve; AVA, aortic valve area; AVR, aortic valve replacement; CAD, coronary artery disease; CMR, cardiovascular magnetic resonance; CTA, CT angiography; CTCA, CT coronary angiogram; DSE, dobutamine stress echocardiogram; LF/LG, low flow/low gradient; LV, left ventricular; LVEF, left ventricular ejection fraction; MDCT, multidetector row CT; MG, mean gradient; PG, peak gradient; TAVI, transcatheter aortic valve implantation; TOE, transoesophageal echocardiography; TTE, transthoracic echocardiography. aParadoxical low flow AS is an emerging diagnosis that must be made, taking other potential causes of symptoms into consideration.

    Paradoxical low flow aortic stenosis

    Paradoxical low flow severe AS has been defined as the presence of indexed AVA<0.6 cm2/m2, with LVEF>50% and SVi<35 ml/m2.8 Its presence has been linked with features of a more advanced disease stage and a greater burden of myocardial fibrosis than severe AS with normal flow.10 ,14 w35 In addition, one multicentre cohort study of patients with severe, asymptomatic AS has recently shown that low flow is associated with subtle LV dysfunction when measured using the more sensitive speckle tracking strain, as well as poorer outcome, compared with preserved flow.15 w36 This report is tempered by findings from another multicentre study indicating a similar prognosis of low gradient, severe AS patients and moderate AS patients.16 The reasons for the discrepant findings are not clear, but highlight the importance of more studies with generalisable imaging techniques before strong recommendations can be made. Differences in how stroke volume is measured may account for some variation in how paradoxical low flow AS is diagnosed; however, awareness of this condition is important because the disproportionately low AV gradients observed may mislead the clinician into the erroneous diagnosis of a lesser grade of AS severity. The ensuing delay to therapy might be especially undesirable given the later stage of disease associated with paradoxical low flow, juxtaposed against the favourable outcome for this entity following surgery.

    Evaluation of the left ventricle

    Current imaging techniques are able to characterise the effect of chronic, severe AS on LV structure and function. Early signs may include echocardiographic evidence of diastolic dysfunction, progressing to concentric LV hypertrophy and LA dilatation. The development of myocardial fibrosis is a well recognised feature of significant AS. While there exist a number of imaging approaches to its identification,w37 recent evidence suggests that its recognition using late gadolinium enhancement CMR may be of important prognostic value.17

    Aortic regurgitation

    Pathophysiology

    Although the spectrum of causes of aortic regurgitation (AR) differs from MR, the two left sided regurgitant valve conditions share much in common in their pathophysiology, and thus in their evaluation. As with MR, acute severe AR can present with calamitous and sudden heart failure. Secondly, in chronic AR, a volume and pressure loadw38 is placed on the left ventricle, which if severe enough for sufficient time culminates in eccentric LV remodelling, chamber dilatation, and eventually heart failure.

    Imaging evaluation of AR

    Similar to MR, imaging in AR is vital in determining its aetiology and mechanism, quantifying its severity, and assessing its deleterious effects on LV structure and function.

    Classification of AR mechanism

    A classification scheme to describe the AR mechanism has been proposed.w39 According to this system, AR may be categorised as type 1 (enlargement of the aortic root with normal cusps), type 2 (cusp prolapse or fenestration), or type 3 (poor cusp or tissue quality). This scheme was shown to predict the intraoperative approach (valve repair or replacement) and give an indication of the likelihood of successful repair.w39 Notably, however, this classification approach was evaluated using TOE. It is uncertain whether it can be extrapolated to TTE.

    Quantification of AR severity

    The quantification of AR remains a challenging undertaking. Markers of severe AR include a vena contracta width >6 mm, EROA ≥30 mm2, and regurgitant volume ≥60 ml.w40 Furthermore, rapid equilibration between aortic and LV pressures during diastole, as reflected by a diastolic half-time <200–300 ms on continuous wave Doppler echocardiography across the AV,3 w40 as well as diastolic flow reversal in the proximal descending aorta (particularly at velocities >20 cm/s throughout diastolew40), may be seen in significant AR. These signs tend to be specific but relatively insensitive,w41 and in keeping with the clinical approach to any valvular abnormality, the assessment of AR severity should be based on the integration of these measures.

    Aortic regurgitant volume may also be measured with use of phase contrast CMR in the proximal aorta. This may be combined with stroke volume evaluated in the conventional CMR manner, by summation of axial sections of the left ventricle, to estimate the aortic regurgitant fraction. A recent seminal study by Myerson et al,18 involving 113 asymptomatic patients with echocardiographic features of moderate or severe AR, showed that CMR quantified regurgitant fraction >33% (especially when combined with an LV end diastolic volume (LVEDV) >246 ml) was associated with a future need for surgery. The follow-up period was relatively short (mean 2.6 years) and this work needs further validation in a larger clinical trial.

    3D colour Doppler echocardiographic measurement of EROA has shown promise in comparison with CMR evaluationw42; however, the adoption of this approach into mainstream practice awaits further research, particularly involving clinical end points.

    Evaluation of LV function and remodelling

    According to current guidelines, LVEF ≤50% or significant LV dilatation (systolic and diastolic diameters >55 mm and >75 mm, respectively) are indications for AVR in chronic, severe AR.3 As mentioned above, 3D imaging modalities, such as CMR, permit more accurate and reproducible quantification of adverse LV chamber dilatation, remodelling and systolic dysfunction. In addition, speckle tracking global longitudinal strain appears to constitute a more sensitive tool for detecting subtle LV dysfunction in AR.19

    Visualisation of the aortic root

    Accurate and reproducible evaluation of the aortic root is an important part of the assessment and follow-up of the patient with AR. These measurements should be taken at several different levels. Root dilatation may be significant as the cause of the AR, but may also, if severe or rapid enough, merit surgical intervention independent of the degree of AR, and can govern the type of operation undertaken. An aortic root calibre >50 mm is a surgical indication; however, diameters >45 mm, particularly in conditions such as Marfan syndrome, or progressive aortic dilatation ≥5 mm per year should prompt consideration of root replacement surgery.3 w43

    While 2D TTE is generally used for initial evaluation and follow-up of the aortic root, 3D techniques such as CMR are likely to provide more reproducible measurements of this structure (see online supplemental video). When coupled with CMR's ability to quantify LV volumes accurately, this makes CMR an appealing imaging modality for AR with aortic root dilatation.

    Other considerations

    While the emphasis of this article has been on the most common valvular lesions, mass lesions and hereditary/developmental sub- or supravalvular abnormalities can cause apparent mitral stenosis or AS. Valvular abnormalities frequently coexist. Such concurrence may reflect the underlying VHD aetiology, as in mixed MV disease secondary to rheumatic heart disease, or in particular instances one valve lesion may give rise to the other valvular dysfunction (eg, severe AS causing MR). Evaluation of VHD severity under these circumstances should take into account haemodynamics and pathophysiology. For example, severe MR may result in underestimation of AV gradients through loss of antegrade blood flow, disguising severe AS.

    Conclusion and future directions

    With respect to echocardiography, ongoing advancement in 3D imaging may arguably revolutionise the approach to quantification of valve lesion severity, particularly in the future if echocardiographic hardware and software can be streamlined to fit into usual workflow. Novel techniques, such as speckle tracking strain imaging and myocardial longitudinal relaxation time mapping using CMR,20 will also enable earlier identification of adverse sequelae of VHD. At the present time, these approaches may provide supportive information to conventional patient work-up. For them to merit routine clinical use, long term outcome studies are awaited.

    Other 3D imaging modalities—CMR and MDCT—offer valuable ancillary information to echocardiography. Additionally, novel approaches such as quantification of myocardial fibrosis by CMR T1 mapping may allow more refined assessment of the effects of VHD. Although multimodality imaging is instinctively appealing, in an environment of finite healthcare resources, the challenge for CMR, MDCT, and 3D TOE will be to demonstrate their incremental value and cost efficacy. In the meantime their use is governed by local expertise and resource availability.

    Multimodality imaging in valvular heart disease: key points

    • Thorough characterisation of a diseased valve requires not only assessment of the lesion severity, but also the aetiology and mechanism, which may influence the severity grading.

    • Accurate evaluation of the severity of a valve lesion is an amalgamation of direct quantitative indices of lesion severity with markers of the effects of the valvular abnormality, such as left ventricular (LV) remodelling and function, and pulmonary artery pressures. Clinical decision making should not be founded entirely on a single echocardiographic parameter, but on a synthesis of available clinical and imaging information.

    • Three dimensional imaging of abnormal valves by echocardiography, multidetector row CT, or cardiac MRI has a growing role in the diagnosis of both the severity and mechanism of valvular lesions.

    • Evolving imaging techniques, such as speckle tracking strain and cardiac MRI, are likely to help in identifying subtle abnormalities in LV function, early LV remodelling, and myocardial fibrosis.

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    References

    1. ↵
      1. Nkomo VT,
      2. Gardin JM,
      3. Skelton TN,
      4. et al
      . Burden of valvular heart diseases: a population-based study. Lancet 2006;368:1005–11.
      OpenUrlCrossRefPubMedWeb of Science
      Authoritative paper on VHD epidemiology in the developed world.
    2. ↵
      1. Vahanian A,
      2. Alfieri O,
      3. Andreotti F,
      4. et al
      . Guidelines on the management of valvular heart disease: the joint task force on the management of valvular heart disease of the European Society of Cardiology and the European Association for Cardio-Thoracic Surgery. Eur Heart J 2012;33:2451–96.
      OpenUrlFREE Full Text
      Complete and contemporary evidence based recommendations on the approach to VHD.
    3. ↵
      1. Bonow RO,
      2. Carabello BA,
      3. Chatterjee K,
      4. et al
      . ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association task force on practice guidelines (writing committee to revise the 1998 guidelines for the management of patients with valvular heart disease) developed in collaboration with the Society of Cardiovascular Anesthesiologists endorsed by the Society for Cardiovascular Angiography and Interventions and the Society of Thoracic Surgeons. J Am Coll Cardiol 2006;48:e1–148.
      OpenUrlCrossRefPubMedWeb of Science
      Complete evidence based recommendations on the approach to VHD.
    4. ↵
      1. Watanabe N,
      2. Ogasawara Y,
      3. Yamaura Y,
      4. et al
      . Quantitation of mitral valve tenting in ischemic mitral regurgitation by transthoracic real-time three-dimensional echocardiography. J Am Coll Cardiol 2005;45:763–9.
      OpenUrlCrossRefPubMedWeb of Science
      Early study employing 3D echocardiography to characterise ischaemic mitral regurgitation.
    5. ↵
      1. Enriquez-Sarano M,
      2. Avierinos JF,
      3. Messika-Zeitoun D,
      4. et al
      . Quantitative determinants of the outcome of asymptomatic mitral regurgitation. N Engl J Med 2005;352:875–83.
      OpenUrlCrossRefPubMedWeb of Science
      Landmark paper demonstrating the prognostic value of measurement of effective regurgitant orifice area in MR.
    6. ↵
      1. Lancellotti P,
      2. Lebrun F,
      3. Pierard LA
      . Determinants of exercise-induced changes in mitral regurgitation in patients with coronary artery disease and left ventricular dysfunction. J Am Coll Cardiol 2003;42:1921–8.
      OpenUrlCrossRefPubMedWeb of Science
      Mechanistic study distinguishing MR at rest from MR during exertion.
    7. ↵
      1. Lancellotti P,
      2. Gerard PL,
      3. Pierard LA
      . Long-term outcome of patients with heart failure and dynamic functional mitral regurgitation. Eur Heart J 2005;26:1528–32.
      OpenUrlAbstract/FREE Full Text
      Important study highlighting the role of exercise echocardiography in evaluating the dynamic nature of MR.
    8. ↵
      1. Dumesnil JG,
      2. Pibarot P,
      3. Carabello B
      . Paradoxical low flow and/or low gradient severe aortic stenosis despite preserved left ventricular ejection fraction: implications for diagnosis and treatment. Eur Heart J 2010;31:281–9.
      OpenUrlAbstract/FREE Full Text
      Review article addressing an emerging facet to the assessment of AS.
    9. ↵
      1. Messika-Zeitoun D,
      2. Serfaty JM,
      3. Laissy JP,
      4. et al
      . Assessment of the mitral valve area in patients with mitral stenosis by multislice computed tomography. J Am Coll Cardiol 2006;48:411–3.
      OpenUrlCrossRefPubMedWeb of Science
      CT study illustrating its potential value in evaluation of MS.
    10. ↵
      1. Hachicha Z,
      2. Dumesnil JG,
      3. Bogaty P,
      4. et al
      . Paradoxical low-flow, low-gradient severe aortic stenosis despite preserved ejection fraction is associated with higher afterload and reduced survival. Circulation 2007;115:2856–64.
      OpenUrlAbstract/FREE Full Text
      Key paper characterising low flow, low gradient, severe AS.
    11. ↵
      1. Pflederer T,
      2. Achenbach S
      . Aortic valve stenosis: CT contributions to diagnosis and therapy. J Cardiovasc Comput Tomogr 2010;4:355–64.
      OpenUrlCrossRefPubMed
      Excellent technical review of the role of CT in AS.
    12. ↵
      1. Rosenhek R,
      2. Binder T,
      3. Porenta G,
      4. et al
      . Predictors of outcome in severe, asymptomatic aortic stenosis. N Engl J Med 2000;343:611–7.
      OpenUrlCrossRefPubMedWeb of Science
      Important paper emphasising that intervention for severe AS may be warranted for particular asymptomatic individuals.
    13. ↵
      1. Weidemann F,
      2. Herrmann S,
      3. Stork S,
      4. et al
      . Impact of myocardial fibrosis in patients with symptomatic severe aortic stenosis. Circulation 2009;120:577–84.
      OpenUrlAbstract/FREE Full Text
      Interesting paper examining the relationship between myocardial fibrosis and deformation using late gadolinium enhancement CMR and strain imaging with echocardiography in severe AS.
    14. ↵
      1. Herrmann S,
      2. Stork S,
      3. Niemann M,
      4. et al
      . Low-gradient aortic valve stenosis myocardial fibrosis and its influence on function and outcome. J Am Coll Cardiol 2011;58:402–12.
      OpenUrlCrossRefPubMedWeb of Science
      Multimodality characterisation of low gradient AS.
    15. ↵
      1. Lancellotti P,
      2. Magne J,
      3. Donal E,
      4. et al
      . Clinical outcome in asymptomatic severe aortic stenosis. Insights from the new proposed aortic stenosis grading classification. J Am Coll Cardiol 2012;59:235–43.
      OpenUrlCrossRefPubMedWeb of Science
      Recent study that shows the clinical relevance of evaluating flow in severe, asymptomatic AS.
    16. ↵
      1. Jander N,
      2. Minners J,
      3. Holme I,
      4. et al
      . Outcome of patients with low-gradient “severe" aortic stenosis and preserved ejection fraction. Circulation 2011;123:887–95.
      OpenUrlAbstract/FREE Full Text
      The counterfactual study to the one above.
    17. ↵
      1. Dweck MR,
      2. Joshi S,
      3. Murigu T,
      4. et al
      . Midwall fibrosis is an independent predictor of mortality in patients with aortic stenosis. J Am Coll Cardiol 2011;58:1271–9.
      OpenUrlCrossRefPubMedWeb of Science
      Valuable study demonstrating the prognostic importance of myocardial fibrosis as detected by CMR in AS.
    18. ↵
      1. Myerson SG,
      2. d'Arcy J,
      3. Mohiaddin R,
      4. et al
      . Clinical outcome in aortic regurgitation with cardiovascular magnetic resonance. Circulation 2012;126:1452–60.
      OpenUrlAbstract/FREE Full Text
      Seminal paper demonstrating the prognostic value of CMR evaluation of AR.
    19. ↵
      1. Smedsrud MK,
      2. Pettersen E,
      3. Gjesdal O,
      4. et al
      . Detection of left ventricular dysfunction by global longitudinal systolic strain in patients with chronic aortic regurgitation. J Am Soc Echocardiogr 2011;24:1253–9.
      OpenUrlCrossRefPubMed
      Study demonstrating the presence of subtle abnormalities in LV contractile function using speckle tracking strain echocardiography, despite preserved LVEF.
    20. ↵
      1. Mewton N,
      2. Liu CY,
      3. Croisille P,
      4. et al
      . Assessment of myocardial fibrosis with cardiovascular magnetic resonance. J Am Coll Cardiol 2011;57:891–903.
      OpenUrlCrossRefPubMedWeb of Science
      Thorough state-of-the-art review on myocardial fibrosis and its evaluation using CMR.
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    Footnotes

    • Contributors DPL was involved in manuscript drafting and image editing. MXJ was involved in manuscript editing and image procurement. JBS was involved in manuscript design, drafting and editing.

    • Funding Dr Leong is supported by the National Health and Medical Research Council of Australia (grant no. 1016627), the National Heart Foundation of Australia (grant no. O 10A 5372), and the Royal Australasian College of Physicians. Dr Selvanayagam is supported by the National Heart Foundation.

    • Competing interests In compliance with EBAC/EACCME guidelines, all authors participating in Education in Heart have disclosed potential conflicts of interest that might cause a bias in the article. The authors have no competing interests.

    • Provenance and peer review Commissioned; externally peer reviewed.

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