how to interpret an echocardiography report (for the non

1733Bansal M, Sengupta PP. Heart 2017;103:1733–1744. doi:10.1136/heartjnl-2016-309443

IntroductIonEchocardiography is the most widely used cardiac imaging modality. Its ability to permit compre-hensive assessment of cardiac structure and func-tion combined with its safety, wide availability and ease of application render it indispensable in the management of most patients with a suspected or known cardiac illness. It is therefore not surprising that the use of echocardiography, when performed for appropriate clinical indications, has been shown to be associated with decreased odds of in-hospital mortality.1

However, the wide applicability of echocar-diography has resulted in an increasing number of non-cardiologists and non-imagers being involved in its use for clinical purposes. Since many of them are not well familiar with the echo-cardiography findings, they often find it difficult to navigate through and interpret an echocardi-ography report. Moreover, echocardiography is a dynamic field with constant addition of newer imaging modalities (eg, three-dimensional (3D) echocardiography), newer measurements (eg, strain) or changes in interpretation algorithms (eg, recent revision of the left ventricular (LV) diastolic function assessment guidelines2). The reporting format, terminologies used and the technologies available at disposal also vary across echocardiography laboratories, further adding to the complexity of the whole process. This review therefore describes a systematic approach to help enable non-imagers extract clinically relevant information from an echocardiography report and effectively apply it for clinical deci-sion making in their patients.

InterpretIng an echocardIography reportEchocardiography tends to generate a large amount of structural and functional data, but not all the information contained within an echocardiography report has similar impact on clinical outcomes. Therefore, the primary goal for the treating physicians is to promptly recognise those echocardiography findings that directly impact clinical decision making. Tables 1 and 23summarise key echocardiography findings that maximally impact clinical deci-sion making, whereas table 3 outlines an approach to reach the aetiological diagnosis in various clinical presentations. Additionally, a suggested approach for further diagnostic evaluation based on different echocardiographic findings is also provided in figure 1.

To maximally benefit from echocardiography, it is important that the ordering physicians clearly specify the indication for performing the test to enable the echocardiographer extract relevant information from the test. At the same time, the echocardiographers reporting the study should also ensure that all the relevant details are provided in the echocardiography report. They should also provide an overall interpretation of the echo-cardiographic findings, instead of just reporting the individual findings. If the echocardiography report does not adequately answer the clinical question or if there is a discrepancy between the clinical assessment and the echocardiographic findings, it is desirable that the treating physician reaches out to the echocardiographer directly and discusses the implications of various echocardio-graphic findings and the need for either a repeat echocardiogram or an alternate diagnostic testing.

Specific echocardiographic findingsWhen interpreting an echocardiography report, the attention should first be given to the clinical indication for which the study was performed, the nature of the study performed (ie, transthoracic or transesophageal, focused or complete), haemo-dynamics at the time of the study and the echo-cardiographer’s impression of the image quality. Acoustic image quality is a major determinant of the diagnostic accuracy of transthoracic echocar-diography (TTE) and when image quality is poor, all echocardiographic findings need to be viewed with caution. The use of ultrasound contrast or performance of transoesophageal echocardiog-raphy (TOE) help overcome these challenges in the majority of the cases, but alternate imaging modalities such as nuclear scan, computed tomog-raphy (CT) or magnetic resonance imaging (MRI) may be needed in difficult cases.

How to interpret an echocardiography report (for the non-imager)?Manish Bansal,1 Partho P Sengupta2,3

education in heart

to cite: Bansal M, Sengupta PP. Heart 2017;103:1733–1744.

1Department of Cardiology, Medanta – The Medicity, Gurgaon, India2Division of Cardiology, Heart and Vascular Institute, West Virgina University, Morgantown, WV, USA3West Virginia University

correspondence toDr Partho P Sengupta, Heart and Vascular Institute, West Virginia University, 1 Medical Center Drive Morgantown, WV 26506, USA; Partho. Sengupta@ wvumedicine. org

Published Online First 7 September 2017

Learning objectives

► To be able to interpret findings from an echocardiographic study in a systematic manner.

► To be able to appreciate relative clinical value of various echocardiographic findings in different clinical scenarios and recognise those directly impacting clinical decision making.

► To be able to integrate echocardiographic findings with those of clinical examination and other investigations.

► To be able to integrate echocardiography in the overall patient care.

on 17 October 2018 by guest. P

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1734 Bansal M, Sengupta PP. Heart 2017;103:1733–1744. doi:10.1136/heartjnl-2016-309443

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table 1 Key echocardiographic findings that impact clinical decision making in various common cardiac conditions

clinical condition echocardiographic findings therapeutic implications

Coronary artery disease LVEF LVEF influences almost every therapeutic decision in these patients

Distribution and severity of RWMA Need for and the choice of coronary intervention

Presence and severity of secondary mitral regurgitation Choice of coronary intervention; need for concomitant mitral valve surgery during coronary artery bypass surgery

PASP Optimisation of medical management; need for advanced heart failure therapies such as mechanical circulatory support

Non-ischaemic dilated cardiomyopathy LVEF Medical management; need for ICD and CRT; advanced heart failure therapies

Presence and severity of secondary mitral regurgitation Medical management; need for MR intervention (eg, mitra-clip)

PASP Optimisation of medical management; need for advanced heart failure therapies

Mitral regurgitation Severity of mitral regurgitation Need for mitral valve surgery

Valve morphology Timing and the nature of mitral valve surgery

LV dimensions and EF Timing and the nature of mitral valve surgery

PASP Need for mitral valve surgery

Other valve lesions Timing and the nature of mitral valve surgery

Mitral stenosis Severity of mitral stenosis (valve area, gradients) Timing and the choice of mitral valve intervention

Valve morphology, subvalvular apparatus Timing and the choice of mitral valve intervention

Concomitant mitral regurgitation, other valve lesions Timing and the choice of mitral valve intervention

PASP Need for mitral valve intervention

LA/LA appendage clot Choice of mitral valve intervention

Aortic stenosis Severity of aortic stenosis (valve area, gradients) Need for and the timing of aortic valve intervention

LVEF Need for and the timing of aortic valve intervention

Other valve lesions Need for and the timing of aortic valve intervention

Aortic root/ascending aorta dimensions Need for concomitant aortic root replacement during aortic valve surgery

Aortic regurgitation Severity of aortic regurgitation Need for aortic valve surgery

Valve morphology Need for and the type of aortic valve surgery

LV dimensions and EF Timing of aortic valve surgery

Aortic root/ascending aorta dimensions Need for concomitant aortic root replacement during aortic valve surgery

Other valve lesions Need for and the timing of aortic valve intervention

Infective endocarditis Size, location and mobility of the vegetations Need for surgical management for endocarditis

Nature of the underlying valve lesion, severity of valve dysfunction

Need for and the timing of surgical management

Intracardiac abscess, other complications of infective endocarditis

Need for and the timing of surgical management

Hypertrophic cardiomyopathy Location and severity of LV hypertrophy Need for surgical myomectomy or alcohol septal ablationNeed for ICD

Systolic anterior motion of mitral apparatus and LV outflow tract obstruction

Need for surgical myomectomy or alcohol septal ablationNeed for mitral valve surgery

Severity of mitral regurgitation Need for mitral valve surgery

Restrictive cardiomyopathy Any echocardiographic features suggestive of the underlying aetiology (eg, LV/RV apical obliteration in endomyocardial fibrosis or hypereosinophillic syndrome; significant LV hypertrophy with altered myocardial echotexture, thickened interatrial septum and so on in amyloidosis)

Steroids, antithrombotics and haematological therapy in hypereosinophilic syndromeEvaluation and management of underlying plasma cell dyscrasia in amyloidMainly supportive treatment in most other cases

PASP Optimisation of medical management; need for advanced heart failure therapies

Left and right heart filling pressures Optimisation of medical management; need for advanced heart failure therapies

Pericardial effusion Location and size of effusion Need for and the modality for pericardiocentesis

Haemodynamic features of tamponade (RA/RV diastolic collapse, respiratory variation in mitral and tricuspid inflow velocities, dilated and non-collapsing inferior vena cava)

Need for pericardiocentesis

Any echocardiographic features of underlying constriction (pericardial thickening, septal bounce and so on)

Evaluation and management of constrictive pericarditis if evolves later on

Ventricular tachyarrhythmia LVEF, any RWMA Need for coronary intervention; ICD

RV size, systolic function and aneurysms Need for ICD

Suspected cardioembolic Stroke Any LA/LA appendage clot Need for anticoagulation

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clinical condition echocardiographic findings therapeutic implications

Any LV clot Need for anticoagulation, surgical removal of clot

Any other intracardiac mass (location, size, nature) Need for surgery; treatment of underlying condition

Patent foramen ovale/atrial septal defect Closure of patent foramen ovale/atrial septal defect

CRT, cardiac resynchronisation therapy; EF, ejection fraction; ICD, implantable cardioverter defibrillator; LA, left atrial; LV, left ventricular; LVEF, left ventricular ejection fraction; PASP, pulmonary artery systolic pressure; RA, right atrial; RV, right ventricular; RWMA, regional wall motion abnormality.

table 1 Continued

LV systolic functionLV systolic function, traditionally measured as LV ejection fraction (LVEF), is a key information sought from echocardiography. LVEF is pivotal in the management of all patients with cardiac dysfunction, regardless of whether such dysfunction is due to a primary cardiac disease or is secondary to a systemic illness. Management of fluids and inotropic support, decisions regarding myocardial revascularisation,4 timing and the choice of valve interventions,3 need for cardiac resynchronisation therapy (CRT) and/ or an implantable cardioverter defibrillator (ICD)5 are some of the decisions that are largely dependent on LV systolic function and thus LVEF. Additionally, the recognition of impaired LV systolic function in patients presenting with dyspnoea, haemodynamic compromise, stroke, and so on, helps in triaging them into appropriate management pathways.

While there are several methods for estimation of LVEF by echocardiography, modified biplane Simpson’s method is the recommended method.6 However, in real-life practice, LVEF is often assessed visually by eyeballing, which has been shown to have high degree of accuracy in case of experienced readers.7 8 When available, 3D echo-cardiography provides a more accurate assessment of LVEF and LV volumes.9

Two important points need to be considered when interpreting LVEF report. First, echocardi-ography has certain degree of inherent measure-ment variability. Although in most patients, this measurement variability has little practical signifi-cance, it becomes relevant when LVEF value is near the threshold for defining the need for a specific cardiac intervention (e.g. LVEF ≈50% in patients with aortic stenosis (AS) or aortic regurgitation (AR), ≈60% in patients with mitral regurgitation (MR), ≈35% in patients potentially requiring CRT). In these circumstances, one should always corroborate LVEF with other echocardiographic findings and the overall clinical picture. 3D echo-cardiography, as mentioned above, provides more accurate and reproducible measurements,9 10 but if the uncertainty still persists, cardiac MRI may be needed to confirm LV volumes and EF (figure 1).

Second, as LVEF is a global measure of LV systolic function, it is not sensitive enough to detect subtle impairment of LV contractile function during the early stages of the diseases. Myocardial strain imaging offers a promising solution in this regard. Speckle-tracking echocardiography (STE), which is a greyscale-based technique, is the current modality of choice for this purpose.11 Technical details of

STE and strain measurement are provided else-where11 12 but suffice is to mention that of all the available strain measurements, global longitudinal strain (GLS) is the most robust and reproducible enough for routine clinical use.6 GLS is more repro-ducible than even LVEF. The normal value of GLS varies with the equipment and the software used for obtaining and analysing the images, but a value more negative than −16% to 18% is generally considered to be normal.

The main clinical application of GLS is in the recognition of subclinical LV systolic dysfunction, which is common during the early stages of several cardiac and non-cardiac disorders such as treatment with potentially cardiotoxic cancer chemothera-pies,13 valvular heart diseases,14 cardiomyopathies,15 heart failure with preserved LVEF,15 16 hyperten-sion,17 obesity18 and so on. Reduced GLS in these conditions indicates worse prognosis. However, the therapeutic implications of such a finding are not yet well established as studies linking strain-guided management with improvement in clin-ical outcomes are currently lacking. Nevertheless, in some clinical conditions, such as in patients receiving potentially cardiotoxic cancer chemother-apies, GLS is now being increasingly used for thera-peutic decision making as well.13

Regional versus global LV systolic dysfunctionIn patients with reduced LVEF, the distinction between global and regional LV systolic dysfunc-tion has major clinical implications. Global LV hypokinesia without any significant regional vari-ation generally indicates non-ischaemic aetiology, whereas regional wall motion abnormalities are considered to be the sine qua non of the underlying coronary artery disease. However, exceptions are not uncommon as the patients with severe isch-aemic LV systolic dysfunction may present with global hypokinesia whereas regional variations are known to occur even in the absence of coronary artery disease (box 1). In patients with regional LV systolic dysfunction, the location of the wall motion abnormalities provides useful clue about the culprit artery (figure 2), which has prognostic and therapeutic implications. Additionally, echocar-diographers often also comment on the segmental myocardial thickness. A thinned-out segment is likely to be scarred and is unlikely to recover regardless of the treatment.19

Cardiac chamber sizesCardiac chamber dimensions are routinely reported in echocardiography reports. In case of ventricles,



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table 2 Clinically relevant threshold values for common echocardiographic measurements

parameter clinically relevant threshold values and their implications remarks

LVEF <60% Threshold for intervention in chronic severe MR3 33 Three-dimensional echocardiography more accurate than two-dimensional echocardiography; cardiac MRI may be needed when LVEF value is close to a clinically relevant threshold

<50% Indication for AVR in severe AS, severe AR3 33

Threshold above which heart failure is classified as ‘heart failure with preserved EF’34

<40% Used for diagnosing ‘heart failure with reduced EF’34

<35% Indication for CRT in appropriately selected patients34 35

<30%–35% Indication for ICD implantation for primary prevention of sudden cardiac death, depending on functional class and underlying aetiology34 35

<30% Only a class IIb indication for surgery in chronic severe MR3 33

LV end-systolic dimension >50 mm (>25 mm/m2) Class IIa indication for AVR in severe AR3 33 Three-dimensional echocardiography more accurate than two-dimensional echocardiography; cardiac MRI may be needed when values close to a clinically relevant threshold

>40 mm Class I indication for surgery in chronic severe MR3

>45 mm Class I indication for surgery in chronic severe MR33

LV end-diastolic dimension >65 mm Class IIb indication for AVR in severe AR3

>70 mm Class IIa indication for AVR in severe AR33

Left atrial volume >34 mL/m2 Threshold for defining as increased left atrial volume6

Mitral stenosis

Mitral valve area <1.5 cm2 Indicates significant MS; is a threshold for intervention in appropriately selected patients3

Planimetry more accurate than pressure half-time method, provided image quality is good

Mean gradient >10 mm Hg Indicates severe MS3 20 Dependent on heart rate, other haemodynamic variables

Aortic stenosis

Mean gradient >40 mm Hg Consistent with a diagnosis of severe AS;Class I indication for AVR in symptomatic patients3 33

Velocity and gradient may be low despite aortic valve area being <1.0 cm2—this is termed as low-gradient severe AS (refer to section on low-gradient severe AS)

>60 mm Hg Class IIa indication for AVR in asymptomatic AS3

Peak jet velocity >4 m/s Class I indication for AVR in symptomatic patients3

>5 m/s Class IIa indication for AVR in asymptomatic AS3

>5.5 m/s Class IIa indication for AVR in asymptomatic AS33

Aortic valve area <1 cm2 Used for diagnosing severe AS; threshold for intervention in appropriately selected patients3 33

Usually derived using continuity equation, which is prone to errors

Proximal aorta (aortic root/ascending aorta) dimensions

≥45 mm Class IIa indication for aortic root surgery for patients with Marfan’s syndrome with additional risk factors33

Class IIa indication for aortic root surgery in patients undergoing AVR, especially if with bicuspid aortic valve disease26 36

Measurements on echocardiography (uses leading edge-to-leading edge approach) approximately 2 mm larger than the same on CT (uses inner edge-to-inner edge approach)≥50 mm Class I indication for aortic root surgery in Marfan’s syndrome33

Class IIa indication for aortic root surgery for patients with bicuspid valve with additional risk factors33 36

≥55 mm Class I indication for aortic root surgery for all patients (regardless of the aortic valve morphology and severity of AR)26 36

Class IIa indication for aortic root surgery for all patients (regardless of the aortic valve morphology and severity of AR)33

Tricuspid regurgitation

Peak gradient at rest >30 mm Hg Threshold for defining as abnormal

>50 mm Hg Class IIa indication for MVR in chronic severe MR3 33

Tricuspid annulus size >4 cm (>21 mm/m2) Generally indicates need for concomitant tricuspid valve surgery in patients with any degree of functional TR undergoing mitral valve surgery3 33 37 38

LV diastolic function

Mitral E/A ratio >2 Generally indicates restrictive mitral filling pattern with raised left atrial pressure2

LV diastolic function parameters should not be viewed in isolation and should always be corroborated with other clinical and echocardiographic findings

Mitral E/e’ (average) >14 Generally indicates raised left atrial pressure2

A, mitral inflow late diastolic velocity; AR, aortic regurgitation; AS, aortic stenosis; AVR, aortic valve replacement; CRT, cardiac resynchronisation therapy;; E, mitral inflow early diastolic velocity; e’, mitral annular early diastolic velocity; EF, ejection fraction; ICD, implantable cardioverter defibrillator; LV, left ventricular; LVEF, left ventricular ejection fraction; MR, mitral regurgitation; MS, mitral stenosis; MVR, mitral valve replacement.

the end-diastolic measurements provide an estimate of chamber enlargement, whereas the end-systolic dimensions serve as a surrogate for systolic function.

In contrast, the atrial size is generally measured at the end of ventricular systole only because that is the time in the cardiac cycle when the atria are at



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table 3 Approach to interpretation of echocardiography findings in relation to the clinical presentation*

clinical presentation Likely aetiology corroborative findings

Chest pain Coronary artery disease ► Regional wall motion abnormalities (sometimes global LV systolic dysfunction) ► Wall thinning, scarring

Pulmonary embolism ► Raised PASP ► RV dilatation/dysfunction ► Sometimes, visible thrombus in main pulmonary artery or right-side cardiac

chambers

Aortic dissection ► Visible dissection flap ► Dilated aortic root/ascending aorta ► Differential flow pattern in aorta ► Sometimes AR, pericardial effusion ► Aortic valve may be bicuspid

Pericarditis ► Variable extent of pericardial effusion and/or pericardial thickening ► Haemodynamic features of constriction in case of effuso-constrictive pericarditis

Dyspnoea LV systolic dysfunction ► Reduced myocardial contractile function, regional or global ► Wall thinning, scarring ► Evidence of raised LV filling pressure ► Secondary MR

Heart failure with preserved ejection fraction ► LV hypertrophy of variable extent ► Usually small size LV cavity ► Normal or near normal LV ejection fraction, GLS often reduced ► Significant LV diastolic dysfunction with raised LV filling pressures, PASP

Significant aortic or mitral valve disease ► Structural abnormality of the valve ► Doppler evidence of significant valve dysfunction (MS, MR, AS or AR) ► Cardiac chamber enlargement depending on the valve lesion

Hypertrophic cardiomyopathy ► Significant LV hypertrophy, often asymmetrical ► Altered myocardial echotexture ► Systolic anterior motion of mitral valve apparatus with variable severity of MR ► LV outflow tract obstruction ► LV diastolic dysfunction

Restrictive cardiomyopathy ► Normal-sized ventricles, with or without hypertrophy ► Usually normal LV ejection fraction, GLS almost invariably reduced ► Doppler evidence of raised intracardiac filling pressures, elevated PASP ► Specific abnormalities in certain diseases (eg, LV/RV apical obliteration

in endomyocardial fibrosis or hypereosinophillic syndrome; significant LV hypertrophy with altered myocardial echotexture, thickened interatrial septum, and so on, in amyloidosis)

Pulmonary hypertension ► Raised PASP ► RV hypertrophy, dilatation and dysfunction ► Dilatation of the pulmonary artery

Fever Infective endocarditis ► Vegetations, location depending on the predisposing factors (TOE may be needed)

► ntracardiac abscess ► Structural and functional abnormality of the valves

Pericarditis ► Variable extent of pericardial effusion and/or pericardial thickening ► Haemodynamic features of constriction in case of effuso-constrictive pericarditis

Stroke Intracardiac thrombi ► Visible intracardiac thrombus may or may not be present. TOE required to rule out LA/LA appendage thrombus

► Evidence of predisposing condition—LV systolic dysfunction/ aneurysm, mitral valve obstruction, and so on, but may be completely normal if AF is the only issue

Intracardiac tumour ► Visible intracardiac mass, usually on the left side

Paradoxical embolism ► Atrial septal defect or patent foramen ovale (agitated saline injection often required)

► Evidence of persistent or intermittent right to left shunt (Valsalva manoeuvre often required)

Vegetation ► Visible vegetation in the left-side cardiac chambers (right-sided endocarditis may also cause stroke in presence of interatrial communication)

► May be infective or non-infective

Mitral annular calcification ► Visible mitral annular calcification with or without mobile components

► Variable degree of mitral valve dysfunction

Swelling of feet Pulmonary hypertension ► Raised PASP ► RV hypertrophy, dilatation and dysfunction ► Dilated inferior vena cava ► Evidence of left-side cardiac pathology if that is the primary disease

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table 3 Continued

clinical presentation Likely aetiology corroborative findings

Primary RV systolic dysfunction ► RV dilatation and systolic dysfunction ► Dilated inferior vena cava ► Usually normal pulmonary pressures

Primary tricuspid valve disease ► Structural abnormality of tricuspid valve ► Doppler evidence of significant tricuspid stenosis or regurgitation ► RA/RV dilatation with or without RV systolic dysfunction ► Dilated inferior vena cava

Restrictive cardiomyopathy ► Findings as described above

Constrictive pericarditis ► Thickened pericardium, may be calcified ► Evidence of exaggerated ventricular interdependence (septal bounce, significant

respiratory variation in mitral and tricuspid inflow velocities) ► Preserved mitral annular velocities despite raised LV filling pressure (annulus

paradoxus) ► Dilated inferior vena cava

Haemodynamic collapse Several possibilities such as sudden severe LV systolic dysfunction, RV infarction, mechanical complication of MI, infective endocarditis with acute valve dysfunction, prosthetic valve thrombosis, pericardial effusion with tamponade, massive pulmonary embolism, and so on.

► Echocardiographic features will vary according to the aetiology (as discussed above)

*This table describes commonly encountered aetiologies and clinical presentations and is not exhaustive. In addition, exceptions may occur, and therefore clinical judgement is warranted in each individual case.AF, atrial fibrillation; AR, aortic regurgitation; AS, aortic stenosis; GLS, global longitudinal strain; LA, left atrial; LV, left ventricular; MI, myocardial infarction; MR, mitral regurgitation; MS, mitral stenosis; PASP, pulmonary artery systolic pressure; RV, right ventricular; TOE, transoesophageal echocardiography.

Figure 1 Approach to referral for further diagnostic evaluation based on common echocardiographic findings. AR, aortic regurgitation; AS, aortic stenosis; echo, echocardiography; LV, left ventricular; LVEF, left ventricular ejection fraction; MR, mitral regurgitation; MS, mitral stenosis; RWMA, regional wall motion abnormality; TOE, transoesophageal echocardiography; TTE, transthoracic echocardiography.

their largest sizes. For accurate interpretation, all the chamber size measurements should preferably be indexed to body surface area and compared with the predefined age-specific, gender-specific and ethnic-specific normal ranges.6

Cardiac chamber dimensions provide useful supportive evidence for the severity of other cardiac lesions. Thus, significant LV enlargement in a patient with chronic MR or AR indicates that the valve lesion is severe, unless there is some other



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Box 1 non-coronary causes of regional left ventricular systolic dysfunction

conditions ► Non-ischaemic dilated cardiomyopathy (disproportionate hypokinesia of inferior wall and interventricular septum is common)

► Stress cardiomyopathy or Takatsubo cardiomyopathy ► Abnormal electrical conduction

– Conduction system abnormalities such as left bundle branch block – Ventricular pacing – Ventricular ectopics – Ventricular pre-excitation

► Postpericardiotomy state ► Pericardial constriction ► Right ventricular pressure and volume overload ► Systemic diseases such as sarcoidosis, haemochromatosis and so on ► Normal variants

– Early relaxation – Tardokinesis

► External compression

Figure 2 Typical left ventricular myocardial distribution of coronary arterial supply. Reproduced from: Lang RM, Bierig M, Devereux RB, et al. J Am Soc Echocardiogr. 2005;18:1440–1463. LAD, left anterior descending; LCx, left circumflex; RCA, right coronary artery.

cause for LV enlargement. Similarly, the enlarge-ment of right atrium and right ventricle in a patient with apparently normal left-side structures raises the possibility of a haemodynamically significant atrial septal defect. Apart from these diagnostic considerations, chamber dimensions have thera-peutic implications also, as summarised in tables 1 and 2.

Valve lesionsValve lesions constitute the second most common indication for echocardiography, after assessment of LV systolic function. Echocardiography provides comprehensive information about the valve struc-ture and function and is pivotal in the management of valve diseases. TOE often provides incremental information and is frequently required for the eval-uation of valve lesions, esp. the mitral valve lesions (figure 1).

The severity of valvular dysfunction is assessed on the basis of a combination of 2D and Doppler-de-rived parameters.20–22 For stenotic lesions, valve area and transvalvular gradients are the key param-eters (table 4)20 and both should be considered together for accurate interpretation. The severity of regurgitant lesions is based on a combination of qualitative and quantitative parameters including jet size (planimetered jet area, jet width or vena contracta, as appropriate), effective regurgitant orifice area, regurgitant volume and fraction and the impact of regurgitation on upstream and down-stream cardiac chambers (table 5).21 22

Caution needs to be exercised when interpreting Doppler-based measurements as they are influenced by haemodynamics and can lead to erroneous inter-pretation if viewed in isolation. Valve gradients are typically exaggerated in presence of tachycardia and increased cardiac output state, whereas regur-gitant lesions are suppressed when systolic blood pressure is reduced. Table 6 summarises common conditions that affect echocardiographic assessment of valve lesion severity. Apart from these consider-ations, careful evaluation of the valve morphology is also very helpful in determining the severity of the valve dysfunction. For example, in a patient with increased LV outflow gradient, normally opening aortic valve leaflets would exclude valvular AS as the cause of increased gradients and would warrant search for an alternate explanation for the same (eg, subvalvular obstruction, high cardiac output state and so on). Conversely, a markedly thickened and calcific aortic valve with reduced opening strongly suggests the possibility of significant AS, even if the transvalvular gradient is not particularly high. Simi-larly, the presence of a ruptured chordae with flail mitral valve leaflet strongly suggests the possibility of severe MR even if the colour flow Doppler is not much impressive.

When a significant valve lesion is reported, the treating physician should then look for other echo-cardiographic characteristics that determine the need for, the timing of,and the nature of the valvular intervention. These include valve morphology, LV systolic function, intracardiac haemodynamics, coexisting valvular and non-valvular pathologies and so on. Balloon mitral valvotomy in rheumatic mitral stenosis, mitral valve repair or replacement in MR, concomitant aortic root replacement in a patient with aortic valve disease and so on are some of the decisions that are significantly influenced by the valve morphology.3

Low gradient severe AS is a unique entity that often poses diagnostic dilemma and merits specific mention. Traditionally, severe AS is diagnosed when aortic valve area is <1 cm2 and the mean transval-vular gradient is >40 mm Hg (or peak velocity >4 m/s). However, a sizeable proportion of the patients with aortic valve area <1 cm2 present with trans-valvular gradients much below the threshold for severity. This is often because of reduced stroke volume (<35 mL/m2) and may occur even when the LVEF is preserved. This entity is common in elderly hypertensive individuals with small LV cavity size.



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table 4 Echocardiographic criteria for grading severity of mitral and aortic stenosis20

parameter Mild Moderate Severe

Mitral stenosis

Specific findings

Mitral valve area (cm2) >1.5 1.0–1.5† <1.0†

Supportive findings

Mitral valve mean gradient (mm Hg)* <5 5–10 >10

Pulmonary artery systolic pressure (mm Hg) <30 30–50 >50

aortic stenosis

Aortic jet peak velocity (m/s) 2.6–2.9 3.0–4.0 >4.0

Aortic valve mean gradient (mm Hg) <20 20–40 >40

Aortic valve area (cm2) >1.5 1.0–1.5 <1.0

Indexed aortic valve area (cm2/m2) >0.85 0.60–0.85 <0.60

Velocity ratio >0.50 0.25–0.50 <0.25

*At heart rates between 60 beats/min and 80 beats/min and in sinus rhythm.†The 2014 American college of Cardiology/American Heart Association guideline for the management of patients with valvular heart disease (J Am Coll Cardiol. 2014;63:e57-185) considers mitral valve area <1.5 cm2 as severe mitral stenosis. When mitral valve area is >1.5 cm2, it is termed as progressive mitral stenosis.

table 5 Echocardiographic criteria for diagnosing chronic severe mitral and aortic regurgitation21 22

parameters chronic severe primary mitral regurgitation chronic severe aortic regurgitation

Structural parameters

Left atrial size Usually dilated –

Left ventricular size Usually dilated Usually dilated

Valve apparatus Abnormal Abnormal

doppler parameters

Colour flow jet area (cm2)* Large central jet (usually >10 cm2, or >40% of left atrial area) or variable size wall hugging jet in left atrium

–

Colour flow jet width in LVOT* – Large in central jets; variable in eccentric jets

Jet deceleration rate- continuous wave (Pressure half-time, ms)† – Steep <200

Diastolic flow reversal in descending aorta—pulsed wave – Prominent holodiastolic reversal (end-diastolic velocity >20 cm/s)

Mitral inflow (pulsed wave) E wave dominant (E usually >1.2 m/s) –

Jet density (continuous wave) Dense Dense

Jet contour (continuous wave) Early peaking triangular –

Pulmonary vein flow Systolic flow reversalc –

Quantitative parameters

Vena contracta width (cm)* >0.7 ≥0.6

Jet width/LVOT width, %* – ≥65

Jet CSA/LVOT CSA, %* – ≥60

Regurgitant volume (mL/beat) ≥60 ≥60

Regurgitant fraction (%) ≥50 ≥50

Effective regurgitant orifice area (cm2) ≥0.40 ≥0.30

CSA, cross sectional area; LVOT, left ventricular outflow tract. *At a Nyquist limit of 50–60 cm/s. †Pressure half-time is shortened with increasing left ventricular diastolic pressure and vasodilator therapy.‡Pulmonary venous systolic flow reversal is specific but not sensitive for severe mitral regurgitation.

Recognition of this entity is clinically important as the long-term prognosis of these patients is not necessarily benign.23 24 Such patients will require more comprehensive evaluation and should be referred to a valve specialist.

Intracardiac haemodynamicsPulmonary artery systolic pressure (PASP) has been one of the most popular haemodynamic parameters derived from echocardiography. It is estimated from tricuspid regurgitation (TR) jet, using the modified Bernoulli’s principle. Since this method has some

limitations, many echocardiography labs have now resorted to reporting only peak TR velocity without mentioning PASP. Regardless of these tech-nical issues, estimated PASP (or TR jet velocity) has proved to be a useful measure of intracardiac haemodynamic status. In patients with right-sided lesions, PASP helps in distinguishing between primary versus secondary right heart failure, whereas in cases of left-sided cardiac lesions such as LV systolic dysfunction, aortic and mitral valve diseases, cardiomyopathies and so on, PASP serves as a measure of the overall haemodynamic burden imposed by these lesions and therefore has prog-nostic and therapeutic implications. For example, an elevated PASP, either at rest or during exercise, is in itself an indication for mitral valve intervention in a patient with significant mitral stenosis or MR.3

Estimation of RV filling pressure or mean RA pressure is performed by evaluating inferior vena cava (IVC) size and collapsibility.25 The status of the IVC helps in guiding fluid management in critically ill patients. Additionally, dilated IVC is also helpful in diagnosis of certain cardiac disorders such as restrictive cardiomyopathy (RCM) or constrictive pericarditis. However, the IVC size and collaps-ibility are not reliable indicators of RA pressure in mechanically ventilated patients. Interrogation of hepatic vein flow pattern can be of help in such situations.25

Echocardiography also permits assessment of LV diastolic function and estimation of LV filling pres-sure. The American Society of Echocardiography has recommended a simplified integrative algo-rithm for this purpose (figure 3). From a clinical



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table 6 Common conditions resulting in overestimation or underestimation of the severity of valve lesions (other than technical errors)

Factors leading to underestimation of severity Factors leading to overestimation of severity

Mitral stenosis Underestimated by gradients ► Bradycardia ► Severe tricuspid regurgitation ► Severe tricuspid stenosis ► CHF

Underestimated by pressure half-time method ► Low left atrial compliance ► Severe aortic regurgitation ► LVH due to hypertension, aortic stenosis—variable effect due to

competing influence of raised LV filling pressure and LV relaxation impairment

Underestimated by planimetry ► Subvalvular obstruction ► CHF with reduced valve opening

Overestimated by gradients ► Tachycardia ► Significant mitral regurgitation ► High cardiac output states, for example, anaemia

Overestimated by pressure half-time method ► Impaired LV relaxation (elderly age, hypertension, aortic stenosis and

so on)

Mitral regurgitation ► Low systemic blood pressure ► Low systemic vascular resistance ► Volume depletion

► High blood pressure ► Concomitant severe aortic stenosis

Aortic stenosis Underestimated by valve gradients ► LV systolic dysfunction ► Reduced LV stroke volume due to small LV cavity size ► Increased systemic vascular resistance, increased valvulo-arterial

impedance ► Uncontrolled hypertension ► Severe mitral stenosis or mitral regurgitation

Overestimated by valve gradients ► Coexisting aortic regurgitation ► High cardiac output states, for example, anaemia ► Post-PVC assessment ► Coexisting subaortic stenosis (fixed or dynamic)

Overestimated by planimetry ► LV systolic dysfunction (pseudosevere stenosis)

Aortic regurgitation ► Low systemic blood pressure ► Low systemic vascular resistance ► Tachycardia ► LV systolic dysfunction ► Severe aortic stenosis (reduced LV compliance)

► High blood pressure ► Increased systemic vascular resistance

CHF, congestive heart failure; LV, left ventricular; LVH, left ventricular hypertrophy; PVC, premature ventricular contraction.

Figure 3 Algorithm for echocardiographic estimation of left atrial pressure and grading left ventricular diastolic function in patients with myocardial disease. Modified from: Nagueh SF, Smiseth OA, Appleton CP, et al. Recommendations for the evaluation of left ventricular diastolic function by echocardiography: An update from the American Society of Echocardiography and the European Association of Cardiovascular Imaging. J Am Soc Echocardiogr. 2016;29:277–314. A, mitral inflow late diastolic velocity; E, mitral inflow early diastolic velocity; e’, mitral annular early diastolic velocity; LA, left atrial; LAP, left atrial pressure; TR, tricuspid regurgitation.

standpoint, however, the presence of restrictive mitral inflow pattern signifying advanced LV diastolic dysfunction is the most useful. A restrictive filling pattern in patients with LV systolic dysfunc-tion is a poor prognostic marker and calls for more aggressive decongestion and further optimisation of heart failure therapies. When observed in patients with preserved LV systolic function, a restrictive LV filling pattern has considerable diagnostic value as it allows diagnosis of heart failure with preserved EF, RCM or constrictive pericarditis.

Aortic diseasesAortic dissection is one of the true cardiac emergen-cies and needs to be promptly diagnosed and treated surgically, especially when it involves the proximal segment of aorta. TTE is the initial modality used for diagnosing aortic dissection and has a sensi-tivity of 77%–80% for this purpose. TOE has much higher (≈98%) sensitivity for diagnosing ascending aortic dissection and should always be employed when the index of suspicion is high and the TTE is non-confirmatory.26 27 Once ascending aortic dissection is diagnosed, the impact of dissection on the aortic valve function, involvement of coronary ostia and the presence of pericardial effusion need to be confirmed to help determine the appropriate management strategy.

Aortic root enlargement may occur either in combination with an aortic valve disease or as an isolated entity. In such patients, accurate assessment



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Key messages

► Echocardiography has the capability to provide a large amount of cardiac structural and functional information. However, the clinical utility of echocardiography is dependent on the ability of the treating physician to extract relevant information from the echocardiography report.

► For a non-imager, the primary goal should be to recognise those echocardiography findings that directly impact clinical decision making.

► All echocardiographic findings should be viewed in relation to the overall clinical scenario. When diagnostic uncertainty persists, further evaluation using transoesophageal echocardiography, cardiac CT, MRI, nuclear imaging and so on may be needed.

► Left ventricular ejection fraction (LVEF), despite its limitations, remains the most important determinant of cardiac outcomes in a wide variety of clinical conditions and is one of the most important findings sought from the echocardiography report.

► Speckle tracking echocardiography-based global longitudinal strain measurement can help in recognising subclinical left ventricular (LV) systolic dysfunction during the early stages of the diseases when LVEF is still within the normal range. While it has therapeutic implications in patients receiving potentially cardiotoxic chemotherapy, its role in decision making in other conditions is not yet well established.

► In patients with significant valve lesions, it is important to look for additional echocardiographic characteristics that help in planning management strategy. These include valve morphology (ie, aetiology of valve dysfunction and suitability for repair), LV systolic function, intracardiac haemodynamics, coexisting valvular and non-valvular pathologies and so on.

► Presence of significant LV diastolic dysfunction (especially restrictive pattern) is a bad prognostic marker. In patients with LV systolic dysfunction, it indicates the need for more aggressive decongestion and further optimisation of heart failure therapies, whereas in patients with preserved LV systolic function, it has considerable diagnostic value (diagnosis of heart failure with preserved EF, restrictive cardiomyopathy and so on).

of aortic root and ascending aorta dimensions is essential for defining the need for aortic root/ascending aorta surgery. Aortic dimensions by echo-cardiography are measured using the leading edge-to-leading edge approach, which results in larger measurements compared with the inner edge-to-inner edge approach on CT (average difference 2 mm).28 Furthermore, a difference of up to 3 mm can occur due to test–retest variation alone, regard-less of the imaging modality. Therefore, when performing serial assessment, changes <3 mm should be viewed with caution.

PericardiumPericardial effusion, with or without tamponade, and constrictive pericarditis are the two most commonly encountered pericardial diseases.

In patients with pericardial effusion, the pres-ence of right atrial/right ventricular diastolic collapse, significant respiratory variation in mitral and tricuspid inflow velocities and dilated non-col-lapsing IVC suggest underlying tamponade. The size of the pericardial collection itself is not much helpful as even apparently mild effusions can also produce tamponade if they accumulate rapidly. Nonetheless, the size and the location of the pericardial collection are important for plan-ning pericardiocentesis. Needle pericardiocentesis

is difficult and is associated with a greater risk of complications when pericardial effusion is small or when it is confined posterior to the left ventricle.

In patients with suspected constrictive pericar-ditis, pericardial thickening and calcification may be difficult to discern on echocardiography, and it is usually the haemodynamic features that lead to the diagnosis. The haemodynamic features sugges-tive of constriction include evidence of exagger-ated ventricular interdependence (interventricular septal bounce, shift in septal position with respi-ration, significant respiratory variation in mitral and tricuspid inflow velocities), preserved mitral annular early diastolic velocity despite evidence of elevated filling pressure and dilated non-col-lapsing IVC.29 Since RCM also presents with normal-sized ventricles with elevated filling pressures, there is always a diagnostic dilemma between these two conditions. Unlike constric-tive pericarditis, RCM is characterised by marked impairment of mitral annular velocities and the lack of the features suggestive of exaggerated ventricular interdependence.29 In addition, strain imaging can also be helpful in making this distinc-tion. The finding of preserved longitudinal strain favours a diagnosis of constrictive pericarditis, but converse is not true as reduced longitudinal strain may occur in both these conditions.30

Other abnormalitiesDuring echocardiography, numerous other findings are encountered, which may be coincidental or may be the primary indication for performing the study. The interpretation of these findings would depend on the nature of the abnormality found and the overall clinical scenario.

For example, asymmetrical septal hypertrophy (ASH) usually suggests a diagnosis of hypertro-phic cardiomyopathy (HCM) but may also occur in patients with AS, hypertension and so on. Conversely, patients with HCM may present with concentric LV hypertrophy also. When ASH is present, the extent of septal hypertrophy and the presence and severity of the LV outflow obstruction and MR need to be assessed to decide about the need for and the choice of the intervention (alcohol septal ablation or surgical myomectomy, with or without concomitant mitral valve repair or replace-ment). Additionally, a septal thickness of >30 mm also indicates high risk for sudden cardiac death and the potential need for an ICD.31

In case of intracardiac masses, although the defin-itive diagnosis requires histopathological confirma-tion, the clinical setting and the echocardiographic features themselves often provide useful clues.32 For example, in a patient with rheumatic mitral stenosis and AF, an LA or LA appendage mass is likely to be a thrombus, whereas a pedunculated mass attached to the interatrial septum is most likely to be a myxoma. Similarly, an LV apical mass in a patient with previous apical infarct is most likely to be a thrombus. If a cardiac mass is attached to



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cMe credits for education in heart

Education in Heart articles are accredited for CME by various providers. To answer the accompanying multiple choice questions (MCQs) and obtain your credits, click on the ‘Take the Test’ link on the online version of the article. The MCQs are hosted on BMJ Learning. All users must complete a one-time registration on BMJ Learning and subsequently log in on every visit using their username and password to access modules and their CME record. Accreditation is only valid for 2 years from the date of publication. Printable CME certificates are available to users that achieve the minimum pass mark.

one of the valve leaflets, the aetiological possibili-ties would include a vegetation (infective or non-in-fective), benign Lambl’s excrescence or papillary fibroelastoma.

competing interests None declared.

provenance and peer review Commissioned; externally peer reviewed.

author note References which include a * are considered to be a key reference.

© Article author(s) (or their employer(s) unless otherwise stated in the text of the article) 2017. All rights reserved. No commercial use is permitted unless otherwise expressly granted.

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26 Hiratzka LF, Bakris GL, Beckman JA, et al. ACCF/AHA/aats/acr/asa/sca/scai/sir/sts/svm guidelines for the diagnosis and management of patients with thoracic aortic disease. A report of the American college of Cardiology foundation/American heart association task force on practice guidelines, American association for thoracic surgery, American college of radiology, American stroke association, Society of cardiovascular anesthesiologists, Society for cardiovascular angiography and interventions, Society of interventional radiology, Society of thoracic surgeons,and Society for vascular medicine. J Am Coll Cardiol 2010;2010:e27–129.



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how to interpret an echocardiography report (for the non

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