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European Journal of Echocardiography Advance Access published online on August 27, 2008
European Journal of Echocardiography, doi:10.1093/ejechocard/jen227
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2008. For permissions please email: journals.permissions@oxfordjournals.org

Utility of tissue characterization in apical hypertrophic cardiomyopathy diagnosis

João Abecasis*, Raquel Dourado, Isabel Arroja, José Azevedo and Aniceto Silva

Cardiologia, Centro Hospitalar de Lisboa Ocidental, Rua Professor Reynaldo dos Santos, 2795-523 Carnaxide, Portugal

Received 16 March 2008; accepted after revision 8 August 2008.

* Corresponding author. Tel: +351914054977 (J.A.)/+351914952818 (R.D.); fax: +351214241388 E-mail address: joaoabecasis{at}hotmail.com (J.A.)/raqueldourado{at}yahoo.com (R.D.).


   Abstract
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 Abstract
Case report
 Discussion
 Supplementary data
 References
 
A 60-year-old male with previous hypertension, left ventricle hypertrophy, and coronary artery disease was referred for stress echocardiography because of exertional chest pain. The electrocardiogram revealed deep T-wave inversion in the anterolateral leads. Contrast echocardiography was notable for an apical filling defect consistent with the apical form of hypertrophic cardiomyopathy. Cardiac magnetic resonance demonstrated the ‘ace of spades’ left ventricle cavity, confirming the diagnosis. Single photon emission computed tomography showed increased apical left ventricle tracer uptake. Velocity vector imaging study depicted lower than normal absolute maximal longitudinal tissue velocities. The apical longitudinal strain was negative without base to apex gradient. There were normal longitudinal strain values in the basal and mid myocardial segments (Figure 1). Apical hypertrophic cardiomyopathy is a rare condition occasionally missed by conventional echocardiographic studies. Intravenous contrast enhancement might improve diagnosis accuracy. Newer Doppler-based techniques allowing tissue characterization may complement contrast echocardiography in its diagnosis.

Keywords: Apical hypertrophic cardiomyopathy; Velocity vector imaging; Tissue characterization


   Case report
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 Abstract
 Case report
Discussion
 Supplementary data
 References
 
A 60-year-old Caucasian male was referred for stress echocardiography because of exertional chest pain. He had past history of hypertension and coronary artery disease with left anterior descendent artery percutaneous intervention. Mild left ventricle concentric hypertrophy was documented in a previous two-dimensional (2D) transthoracic echocardiographic study.

Cardiovascular exam was unremarkable and electrocardiogram revealed deep T-wave inversion in the anterolateral leads. When performing echocardiographic stress protocol with ultrasonic contrast enhancement (Sonovue®), an apical filling defect with a spade-like configuration consistent with apical hypertrophic cardiomyopathy was revealed (Figure 1, Supplementary material online, Clip S1). The apical thickness was 24.9 mm, the ratio of apical thickness to posterior wall thickness was >1.5, and the left ventricle mass was 250.5 g/m2. The left ventricle systolic function was normal and the lateral mitral annular velocity was attenuated at 8 cm/s.


Figure 1
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  		Figure 1 (A and B) ‘Ace of spades’ configuration of the left ventricle by two-dimensional (2D) contrast echocardiography and cardiac magnetic resonance. (C) Velocity vector imaging of left ventricle with whole endocardium velocities assessment. Parametric 2D images depicting endocardium velocities. (D) Velocity and strain assessment along three endocardium samples.

 
Cardiac magnetic resonance demonstrated the ‘ace of spades’ left ventricle cavity, confirming the diagnosis of apical form of hypertrophic cardiomyopathy (Figure 1). Single photon emission computed tomography was notable for increased apical left ventricle tracer uptake without perfusion defects in the stress study (Figure 2).


Figure 2
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  		Figure 2 Single photon emission tomography showing increase apical tracer uptake.

 
Velocity vector imaging (VVI) study—Siemens Syngo US workplace, left ventricle endocardium contour—is a new tracking algorithm technique applied to DICOM format 2D images, which is independent of ultrasound beam alignment or transducer location. It uses multiple tracking techniques to determine cardiac motion, including speckle tracking, mitral annulus displacement, and blood-tissue interface. At each stage of the tracking, Fourier analysis is used and applies the constraint that the trace returns to the same location at the subsequent cardiac cycle. This provides global and regional information concerning myocardial velocities, strain, strain rate, and synchrony.

In this case, the left ventricle VVI analysis was performed in apical four-chamber view and because of endocardium restricted analysis from the available software version (1.0), only endocardial border tracing was performed. The analysis depicted lower than the normal absolute maximal longitudinal tissue velocities, as was previously known from lateral mitral annular velocity by tissue Doppler imaging (TDI). There was a normal base to apex decreased longitudinal velocity gradient (Figures 1 and 3, Supplementary material online, Clip 2).


Figure 3
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  		Figure 3 Velocity assessment along five endocardium samples with time-to–peak velocity and phase evaluation. Identical phases with no intra-left ventricle dyssynchrony are demonstrated.

 
There were normal longitudinal strain values in the basal and mid-myocardial segments, previously identified as hypertrophic segments by conventional 2D echo. However, the apical longitudinal strain was negative without base to apex gradient. When time to peak tangential velocity was assessed at six different left ventricle points, only the left apical segment was non-significantly delayed (32 s). All other segments simultaneously reached peak velocities and this could be confirmed by the <10% shift of the sinusoid of each segment (time to peak velocity curve Fourier analysis—phase) towards the average global phase (Figures 1 and 4).


Figure 4
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  		Figure 4 Three-dimensional parametric strain image with evidence of negative apical longitudinal strain.

 

   Discussion
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 Abstract
 Case report
 Discussion
Supplementary data
 References
 
The apical form of hypertrophic cardiomyopathy is a rare condition initially described in Japanese population. Giant negative T waves in precordial leads are common electrocardiographic findings raising diagnosis suspicion. This condition can be missed by regular echocardiography, and traditionally definitive diagnosis has been made by left ventriculography demonstrating a spade-like appearance.1,2 Magnetic resonance imaging has also been used to establish the diagnosis obviating the need for invasive procedures.3

Echocardiographic image enhancement with an intravenous contrast agent has been shown to improve diagnosis accuracy. Endocardial-blood interface may be better visualized and delineation of the apical border permits regional myocardial thickness measurement.

Newer Doppler-based techniques allowing tissue characterization and preclinical myocardial dysfunction evaluation may also improve diagnosis assessment.4–7 Tissue Doppler imaging provides information concerning regional basal and mid left ventricle segments behaviour. However and because of insonation angle dependency, left ventricular apex remains inaccessible to TDI study. Two-dimensional strain techniques, both by speckle tracking imaging and by VVI analysis, assess deformation by multiple tracking techniques (‘myocardial feature tracking’) being unique for left ventricle apical study.

Hypertrophic cardiomyopathy is classically associated with myocardial relaxation and filling abnormalities despite normal left ventricle ejection fraction.5 Regional systolic function may also be impaired in preclinical states and this could be evaluated by 2D strain imaging.

In spite of recently reported paradoxical longitudinal strain in the apical segments of apical hypertrophic cardiomyopathy patients studied by speckle tracking imaging 2D strain,8 we could not confirm this abnormality. However, when VVI tissue characterization was performed, we found abnormal regional velocities and deformation parameters, particularly concerning base to apex longitudinal strain gradient. As previously reported, this could be related to the abnormal tissue hypertrophy extending beyond the more evident apical hypertrophic segments.

Conventional echocardiographic techniques can misdiagnose apical hypertrophic cardiomyopathy. Apical endocardial border may even remain inadequately defined with second harmonic imaging, and contrast enhancement could obviate this fact permitting accurate thickness measurement. Left ventricle apex tissue characterization cannot be made by TDI albeit 2D strain by VVI might have a potential role in this assessment.

In spite of this, VVI needs further clinical validation, particularly regarding comparison with 2D strain analysis by similar techniques such as that provided by speckle tracking. It should also be noted that this software vectorial analysis was restricted to endocardial border assessment. In this case, the endo-epicardic myocardial deformation gradient9 could not be evaluated and this might be related to different speckle tracking findings in other case reports.

Multiple echocardiographic modalities might be useful in apical hypertrophic cardiomyopathy diagnosis. Newer 2D tissue characterization techniques appear to complement routine and contrast echo derived diagnostic information, probably obviating the need for other, possible more expensive and invasive, imaging studies.


   Supplementary data
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 Discussion
 Supplementary data
References
 
Supplementary data are available at European Journal of Echocardiography online.


   References
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 Abstract
 Case report
 Discussion
 Supplementary data
 References
 

  1. Moukarbel GV, Alam SE, Abchee AB. Contrast-enhanced echocardiography for the diagnosis of apical hypertrophic cardiomyopathy. Echocardiography (2005) 22:831–3.[CrossRef][Medline]
  2. Ward RP, Weinert L, Spencer KT, Furlong KT, Bednarz J, DeCara J, et al. Quantitative diagnosis of apical cardiomyopathy using contrast echocardiography. J Am Soc Echocardiogr (2002) 15:316–22.[CrossRef][Web of Science][Medline]
  3. Moon JC, Fisher NG, McKenna WJ, Pennell DJ. Detection of apical hypertrophic cardiomyopathy by cardiovascular magnetic resonance in patients with non-diagnostic echocardiography. Heart (2004) 90:645–9.[Abstract/Free Full Text]
  4. Serri K, Reant P, Lafitte M, Berhouet M, Bouffos V, Roudaut R, et al. Global and regional myocardial function quantification by two-dimensional strain: application in hypertrophic cardiomyopathy. J Am Coll Cardiol (2006) 47:1175–81.[Abstract/Free Full Text]
  5. Yang H, Sun JP, Lever HM, Popovic ZB, Drinko JK, Greenberg NL, et al. Use of strain imaging in detecting segmental dysfunction in patients with hypertrophic cardiomyopathy. J Am Soc Echocardiogr (2003) 16:233–9.[CrossRef][Web of Science][Medline]
  6. Amundsen BH, Helle-Valle T, Edvardsen T, Torp H, Crosby J, Lyseggen E, et al. Noninvasive myocardial strain measurement by speckle tracking echocardiography: validation against sonomicrometry and tagged magnetic resonance imaging. J Am Coll Cardiol (2006) 47:789–93.[Abstract/Free Full Text]
  7. Sutherland GR, Di Salvo G, Claus P, D'hooge J, Bijnens B. Strain and strain rate imaging: a new clinical approach to quantifying regional myocardial function. J Am Soc Echocardiogr (2004) 17:788–802.[CrossRef][Web of Science][Medline]
  8. Reddy M, Thatai D, Bernal J, Afonso L. Apical hypertrophic cardiomyopathy: potential utility of strain imaging in diagnosis. Eur J Echocardiogr (2008) 9:560–2.[Abstract/Free Full Text]
  9. Hashimoto I, Li X, Hejmadi Bhat A, Jones M, Zetts AD, Sahn DJ. Myocardial strain rate is a superior method for evaluation of left ventricular subendocardial function compared with tissue Doppler imaging. J Am Coll Cardiol (2003) 42:1574–83.[Abstract/Free Full Text]

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This Article
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