European Journal of Echocardiography (2009) 10, iii9iii14 doi:10.

1093/ejechocard/jep157

Echocardiography in hypertrophic cardiomyopathy diagnosis, prognosis, and role in management

L.K. Williams*, M.P. Frenneaux, and R.P. Steeds
Department of Cardiology, University Hospital Birmingham, NHS Trust, Edgbaston, Birmingham B15 2TT, UK

KEYWORDS
Hypertrophic cardiomyopathy; Echocardiography

Hypertrophic cardiomyopathy (HCM) is diagnosed on the basis of left ventricular (LV) hypertrophy for which there is insufcient explanation (e.g. mild hypertension or mild aortic stenosis with marked hypertrophy). Echocardiography is an invaluable tool in the diagnosis and follow-up of patients with HCM. Echocardiographic assessment requires a comprehensive assessment in several imaging planes with careful attention to correct beam alignment in order to minimize errors in the measurement of LV wall thickness and appropriate identication of hypertrophy with an unusual distribution.

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Introduction
Hypertrophic cardiomyopathy (HCM) is diagnosed on the basis of left ventricular hypertrophy (LVH) for which there is insufcient explanation (e.g. mild hypertension or mild aortic stenosis with marked hypertrophy). In the past, HCM was considered a rare disorder associated with a poor prognosis but more recent population screening studies suggest that it is actually common (1:500 individuals).1 Echocardiography is an invaluable tool in the diagnosis and follow-up of patients with HCM. It is essential when assessing a patient with a potential diagnosis of hypertrophic cardiomyopathy to carry out a systematic study of cardiac structure and function.

Approach to the patient

Conrming the presence/absence of left ventricular hypertrophy
Although HCM is typically characterized by asymmetric septal hypertrophy (ASH), almost any myocardial segment may be involved. The following two-dimensional (2D) echocardiographic criteria are used to aid diagnosis: (i) unexplained maximal wall thickness .15 mm in any myocardial segment, or (ii) septal/posterior wall thickness ratio .1.3 in normotensive patients, or (iii) septal/posterior wall thickness ratio .1.5 in hypertensive patients.2

However, genotype positive adults (including those who die suddenly) may have normal or near normal wall thickness. This is particularly true for patients with mutations in cardiac troponin T in whom LVH is frequently modest but may also be the case in patients with mutations in cardiac myosin binding protein C in whom the development of LVH may occur relatively late in life. Screening earlier in adult life may show no abnormality in the latter and current recommendations are to repeat the assessment every 5 years if normal. Assessing the extent and severity of hypertrophy must include the measurement of maximal wall thickness in multiple segments, noting both the length of septal hypertrophy and also the presence or absence of extension into the apical segments (Figure 1). Extension of LVH to the anterolateral wall of the LV may be particularly difcult to detect. Involvement of the papillary muscles may occur, and papillary muscle abnormalities have been demonstrated in up to 59% of patients with non-obstructive HCM,3 involving either anterior displacement of the anterolateral papillary muscle or direct insertion of the papillary muscle into the mitral valve.

Assessment of the mitral valve

Systolic anterior motion (SAM) of the mitral valve was rst described as a feature of HCM in the late 1960s, and although initially thought to be diagnostic of HCM, it has now been demonstrated in many other conditions (including patients with no other evidence of cardiac disease)4 30 60% of patients with HCM demonstrate SAM, with 2550% demonstrating left ventricular outow tract obstruction (LVOTO).5 The haemodynamic consequences of SAM include prolongation of ejection time and a reduction in stroke volume. Coaptation of the mitral leaets may be disrupted resulting in mitral regurgitation. The presence of SAM is documented using M-mode echocardiography and is

* Corresponding author. Tel: 44 0121 415 8825; fax: 44 0121 414 3713.
E-mail address: l.k.williams@bham.ac.uk

Published on behalf of the European Society of Cardiology. All rights reserved. & The Author 2009. For permissions please email: journals.permissions@oxfordjournals.org.

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Figure 2 Mid-cavity obstruction determined by colour ow mapping.

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Figure 1 Measurement of left ventricular wall thickness in multiple segments at multiple levels.

characterized by mid-systolic notching of the aortic valve and contact of the anterior mitral valve leaet/chordae with the septum. The severity of SAM can be inferred from the duration of leaet/chordal contact with the septum, being mild if contact occurs for ,10% of systole, and severe if .30% of systole. Patients with HCM may have abnormalities of the mitral valve itself, including prolapse, excessive leaet tissue, chordal elongation, elongation of the mitral leaets which coapt at the leaet body rather than the tip, anterior displacement of the mitral apparatus, and insertion of the papillary muscle directly into the anterior mitral valve leaet. Many patients have co-existing degenerative disease, and either this or a combination of inherited and acquired factors may lead to the development of signicant mitral regurgitation.6 A thorough assessment of the mitral valve should be performed in all patients, particularly if surgery is being considered, as mitral valve repair/replacement may need to be performed at the time of septal myectomy.

obstruction. The presence of mid-cavity obstruction may be associated with the formation of an apical aneurysm, and this may be associated with ventricular arrhythmias and systemic embolism.9 Most individuals with HCM do not exhibit signicant resting LVOTO but a dynamic gradient occurs in 2530% of patients, with the resulting pressure gradient being highly variable and strongly inuenced by central blood volume and contractile state. All symptomatic patients without evidence of a resting gradient should be investigated for dynamic LVOTO, either by exercise or the use of glyceryl trinitrate (GTN) and/or the Valsalva manoeuvre. Incremental symptom-limited exercise should be performed with continuous assessment of the gradient both at mid-cavity and LVOT levels for evidence of dynamic obstruction. It is important to continue monitoring the gradient into the recovery period as obstruction may occur at this time rather than at peak exercise (Figure 3). If the patient is unable to perform an adequate exercise test, the Valsalva manoeuvre or GTN may be used. Sublingual GTN is administered with the patient supine, and evidence of a gradient should be assessed 510 min later with the patient standing, as the resulting reduction in preload may unmask dynamic obstruction.

Assessment of systolic function

Systolic function is typically normal or supranormal in both obstructive and non-obstructive HCM when assessed using conventional echocardiographic indices such as M-mode, ejection fraction, or fractional shortening. Ejection fraction is typically preserved (or increased) despite an impairment of long-axis function, as demonstrated by the tissue Doppler-derived mitral annular velocities.10 Systolic dysfunction occurs in a small subset (1015%) of patients as a result of progressive impairment of systolic function, often termed end-stage or burnt-out HCM. This transformation occurs as a result of wall thinning, cavity dilation, and brosis and is associated with increased mortality (up to 11% annual risk) and risk of SCD.11 A thorough assessment of systolic function by means of a Biplane Simpsons ejection fraction and tissue Doppler image (TDI)-derived systolic velocities should be performed in the basal inferoseptal and anterolateral walls routinely in all patients at initial diagnosis and on subsequent scans.

Left ventricular outow tract obstruction

The presence of resting obstruction, dened as a peak LVOT gradient .30 mmHg, has prognostic signicance in HCM as a predictor of the risk of sudden cardiac death (SCD) and progression to heart failure.7 LVOTO arises due to narrowing of the LVOT by septal hypertrophy, anterior displacement of the mitral apparatus, and SAM. Patients with HCM exhibit a difference in LVOTO, and it has been demonstrated that a steeper LV to aortic root angle is a predictor of LVOTO, irrespective of basal septal thickness.8 The level of obstruction can be determined using colour ow mapping, which should encompass both the LVOT and the mid-cavity of the ventricle (Figure 2). Similarly, pulse-wave Doppler should be used to sequentially interrogate from the LV apex down to the LVOT in order to conrm the anatomical level of

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Figure 3 Provocable outow tract gradient with exercise in a patient with gross asymmetric septal hypertrophy and systolic anterior motion of the mitral valve.

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Assessment of diastolic function

The reduction in chamber compliance and increase in chamber stiffness secondary to increased LV mass and myocardial brosis play a role in diastolic dysfunction. Doppler echocardiography allows accurate assessment of diastolic function in HCM, and mostly demonstrates impaired relaxation regardless of symptoms or the presence of LVOT obstruction.12 Conventional Doppler parameters such as the E wave deceleration time and the E/A ratio on transmitral ow do not correlate well with left ventricular enddiastolic pressure (LVEDP) in HCM.13 Similarly, pulmonary venous velocities appear to be less useful in HCM. The E/Ea ratio (using the TDI-derived Ea velocity from the lateral mitral annulus) provides a more accurate estimate of lling pressures,14 although the correlation is only modest in HCM when compared with other patient populations.15 In one study, up to 25% of patients with an E/Ea ratio .15 had an invasively measured left atrial pressure ,15 mmHg.16 Colour ow propagation velocity has also proved useful in HCM and can be derived from colour M-mode through the mitral valve by adjusting the Nyquist limit until a distinct colour border is obtained and then measuring the slope of its most linear component. The E wave/propagation velocity ratio also demonstrates a good correlation with invasively measured pressures and may prove useful in this patient group.17 The use of TDI in the assessment of diastolic function becomes problematic, particularly as patients get older. It is worthwhile noting that if left atrial size is normal, then left atrial pressure and LVEDP are very likely to be normal, making a diagnosis of phenotypic HCM less likely.18

not demonstrate overt hypertrophy.20 The early-diastolic mitral annular velocity (Ea) is a preload-independent marker of diastolic function and is reduced in HCM patients compared with age-matched controls, with the degree of attenuation related to the magnitude of hypertrophy.21 TDI velocities are particularly useful in the diagnosis of subclinical disease in patients with a known mutation (genotype positive)22 and in the screening of family members of affected individuals. TDI may also help in the differentiation of various conditions resulting in LVH, with demonstrable differences in TDI velocities between conditions of physiological hypertrophy (athletes heart) and pathological hypertrophy [hypertensive heart disease (HHD)].23 TDI has a role in determining prognosis, as a mitral annular systolic velocity ,4 cm/s is an independent predictor of death or hospitalization for worsening heart failure.24 One-dimensional strain and strain rate imaging Rather than measuring myocardial motion relative to the transducer, strain assesses myocardial motion relative to the adjacent myocardium and is unaffected by translational cardiac motion and tethering.25 Strain is a measure of myocardial deformation, whereas strain rate measures the local rate of deformation. HCM patients demonstrate signicant reductions in strain in the septal segments (particularly the mid-septal segment), which correlate with the septal/ posterior wall ratio.26 Longitudinal deformation abnormalities are often focal or subsegmental in HCM and may be underestimated if careful spatial mapping is not used. Two-dimensional speckle tracking Utilizing greyscale imaging, this technique allows spatial and temporal tracking of longitudinal, circumferential (representing systolic shortening), and radial (representing systolic thickening) myocardial deformation and the calculation of strain. Its ability to provide angle-independent measures of LV strain is advantageous. Studies in patients with HCM have demonstrated a reduction in longitudinal strain, an increase in circumferential strain, and normal systolic twist or torsion,27 but a reduction in untwisting in diastole.28 Three-dimensional echocardiography Three-dimensional echocardiography (3D-E) can help in aiding diagnosis, assessing systolic function, and

Evolving echocardiographic techniques

Tissue Doppler imaging TDI has become relatively standard in most tertiary centres managing patients with cardiomyopathies. By measuring high-amplitude, low-velocity signals, it allows real-time quantication of both radial and longitudinal myocardial motion.19 Systolic and diastolic myocardial velocities are recorded by placing a pulsed TDI sample volume within the ventricular myocardium immediately adjacent to either the medial or lateral mitral valve annulus. Systolic velocities are attenuated in HCM despite a preserved or supranormal ejection fraction, even in myocardial segments which do

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understanding the mechanics of SAM and LVOTO in HCM. 3D-E can provide volumetric data for accurate assessment of systolic function and has been shown to correlate well with magnetic resonance imaging for the assessment of LV volumes, ejection fraction, and LV mass. 3D-E also provides more information about the distribution of hypertrophy within the LV myocardium than 2D echocardiography. A novel 3D-E derived mass dispersion index (MDI) has been used in differentiation of HCM from other forms of LVH.29 The MDI equates to the average of the standard deviations of the segmental mass volumes. The authors demonstrated that the MDI was signicantly greater in patients with HCM than those with hypertension or athletes heart, reecting the asymmetric nature of the hypertrophy. Assessment of intraventricular dyssynchrony Inter- and intraventricular dyssynchrony are relatively common in HCM despite the absence of bundle branch block on the surface ECG. The degree of dyssynchrony appears to correlate with the degree of septal hypertrophy and the presence of LVOTO.30 A signicant increase in LV dyssynchrony is seen in HCM patients compared with controls and patients with HHD, with no signicant differences in dyssynchrony in those HCM patients with ASH vs. those with apical HCM.31

Table 1 Risk factors for sudden death in HCM* Major Possible in individual patients

Prior aborted cardiac Atrial brillation arrest (VF) Spontaneous sustained VT Myocardial ischaemia The presence of Left ventricular outow tract non-sustained VT on 48 h obstruction ambulatory ECG monitoring A history of at least one Specic high-risk mutations sudden cardiac death in (troponin T and I) a relative aged ,45 years Unexplained syncope Intense physical exertion Maximum wall thickness .30 mm Abnormal blood pressure response during exercise

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*Adapted from the ACC/ESC Expert Consensus Document on Hypertrophic Cardiomyopathy. The italic text indicates which risk factors for sudden death are identiable with echocardiography.

Risk stratication and selection of implantable cardioverter debrillator therapy

In most patients, the natural history of HCM is benign. However, the incidence of SCD can range from 1% in the community to 24% in tertiary referral centre populations. Identication of patients at risk for SCD is vital as effective treatment in the form of an implantable cardioverter debrillator is available. A single risk factor carries an annual SCD risk of 1%, whereas two or more risk factors carry an annual risk of 36%. Echocardiography plays an important role in risk stratication, based mainly on the assessment of maximal wall thickness and the presence or absence of LVOTO (Table 1).

Role in treatment (alcohol septal ablation)

Septal alcohol ablation for the relief of symptomatic medically refractory obstructive HCM was rst introduced in 1994 and is effective in reducing symptoms, outow tract gradients, and SAM.32 Myocardial contrast echocardiography allows identication of the target septal branch and avoids alcohol injection into the papillary muscle or LV free wall. Prior to alcohol injection, 12 mL of contrast medium is administered under colour and 2D imaging (Figure 4A). Injection into an optimal septal branch will result in complete coverage of the echo-contrast marked septal area and the colour Doppler-estimated area of maximal ow acceleration, as well as the area of contact of the anterior mitral valve leaet. Alcohol should not be injected when myocardial contrast echocardiography fails to identify a target branch or reveals opacication of any cardiac structure other than the target septal area. Post-ablation images often demonstrate a scalloped appearance due to remodelling (Figure 4B).

Figure 4 Myocardial contrast echocardiography during alcohol septal ablation (A). Remodelling of the left ventricular after alcohol septal ablation resulting in a scalloped appearance of the interventricular septum (B).

Pitfalls in diagnosis
The diagnosis of HCM is challenging, and diagnosis can only be 100% reliable when a gene mutation is identied. Echocardiographic assessment requires a comprehensive assessment in several imaging planes with careful attention to correct beam alignment in order to minimize errors in the

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measurement of LV wall thickness and appropriate identication of hypertrophy with an unusual distribution. Over detection (false-positive diagnosis of hypertrophic cardiomyopathy) The presence of LVH or ASH is over diagnosed when an oblique section of the LV is measured, particularly when the parasternal long-axis view is off-axis. Similarly, the presence of a right ventricular moderator band or an LV tendon may result in overestimation of septal thickness. The presence of a sigmoid septum in an elderly patient, which may be associated with the presence of SAM, is often inaccurately reported as ASH. Potential misdiagnosis may occur in hypertensive patients who have had an inferior myocardial infarction. In this setting, the septal/posterior wall ratio may exceed 1.5 simply because the septum is mildly hypertrophied and the posterior wall is thinned as a result of the prior infarct. Other forms of hypertrophy may mimic HCM and are described later. The presence of SAM is not pathognomonic of HCM, and the incidental nding of an outow tact gradient is not specic and may occur with other causes of hypertrophy, in hyperdynamic states, or in hypovolaemia (particularly common in dialysis patients). Under detection (false-negative diagnosis of hypertrophic cardiomyopathy) Although ASH is the classic phenotype, hypertrophy may be concentric, eccentric, or apical in distribution. Distal or apical hypertrophy is best estimated on sequential shortaxis examination and can be overlooked on apical views. However, a foreshortened apical view may give a falsepositive nding as a result of an oblique cut. Wall thickness may be entirely normal, particularly in children and adolescents, in patients with specic gene mutations, and in endstage HCM with a dilated LV.

Athletes heart In athletes, LVH often mimics disease states, and the distinction of physiological vs. pathological hypertrophy has important consequences for young adults who participate in strenuous physical activity. HCM patients have impaired systolic and diastolic function on TDI analysis, whereas athletes typically demonstrate normal or supranormal TDI velocities. Other differentiating features include LV cavity dilation in athletes heart, and the presence of LA enlargement and abnormal diastolic function in HCM. The differential diagnosis can be particularly difcult in Afro-Caribbean athletes in whom LVH tends to be more marked and the ECG can be very abnormal (Sharma JACC paper). Cardiac amyloid Although LVH is common in cardiac amyloid, several other characteristic echocardiographic features may help to distinguish this condition from HCM, including thickened LV walls and interatrial septum, increased myocardial echogenicity, thickening of the valve leaets, and the presence of a pericardial effusion. Fabrys disease Fabrys disease is thought to account for 610% of cases of phenotypic non-obstructive HCM, particularly in men. It is particularly difcult to distinguish Fabrys disease from HCM with echocardiography alone, and the diagnosis is often suspected based on history, clinical examination, and the involvement of other organ systems.

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Conclusion
HCM is diagnosed on the basis of LVH for which there is no or insufcient explanation. Echocardiography is an invaluable tool in the diagnosis and follow-up of patients with HCM. The diagnosis of HCM using is challenging, and diagnosis can only be 100% reliable when a gene mutation is identied. In cases of unexplained LVH, accurate diagnosis of the underlying cause is inherently difcult and conditions such as HCM and hypertension may coexist. No single echocardiographic parameter is ideal, and history and clinical examination play a vital role.
Conict of interest: none declared.

Differential diagnosis
In cases of unexplained LVH, accurate diagnosis of the underlying cause is inherently difcult and conditions such as HCM and hypertension may coexist. No single echocardiographic parameter is ideal, and history and clinical examination play a vital role. However, several echocardiographic clues may help in differential diagnosis. Hypertensive heart disease This presents by far the greatest challenge on echocardiography, with considerable overlap between the two conditions. In addition, the coexistence of both disorders is not uncommon, making the diagnosis of HCM in this setting difcult. SAM is a recognized but uncommon nding in patients with HHD and is more notable in those with severe untreated hypertension. Hypertensive patients with LVH and evidence of SAM tend to have smaller LV cavity dimensions than those without. SAM occurs later in systole in HHD, occurring at the end of systole.33 Basal septal hypertrophy in HHD may result in dynamic LVOTO as well, so is not pathognomonic for either condition. Systolic velocities are similarly reduced in both HCM and HHD but early-diastolic velocities tend to be lower in HCM, with a greater degree of impairment of diastolic function.23

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