Heart Sci J 2020; 1(3): 4-9
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Heart Science Journal
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Review Article

Multimodality Cardiovascular Imaging of Hypertrophic
Cardiomyopathy: A Review Article
Veny Kurniawati1, 2* , Ardian Rizal3 , Mohammad Saifur Rohman2,3, Novi Kurnianingsih3,
Anna Fuji Rahimah3
Department of Cardiology and Vascular Medicine, Prof Dr Sulianti Saroso Infectious Disease Hospital, Jakarta, Indonesia
Brawijaya Cardiovascular Research Center, Department of Cardiology and Vascular Medicine, Faculty of Medicine, Universitas Brawijaya, Malang, Indonesia.
3
Department of Cardiology and Vascular Medicine, Faculty of Medicine, Universitas Brawijaya, Malang, Indonesia.
1
2

ARTI C LE I NFO

AB STR A C T

Keywords:
Hypertrophic Cardiomyopathy;
Cardiovascular Imaging;
Echocardiography;
CMR;
CCT

The most common genetic cardiomyopathy, HCM, has a prevalence of about 0.2%. It is inheritance pattern with
the autosomal dominant transmission. The natural history is benign but adverse outcomes can happen in some
patients including sudden cardiac death, symptoms due to dynamic obstruction of the outflow tract of the left
ventricular (LVOT), abnormal diastolic filling, atrial fibrillation, and dysfunction of systolic LV.
Imaging modalities can be used to evaluate the structure and function of the heart, the dynamic obstruction and
its severity, mitral valve abnormalities, regurgitation of the mitral valve, and also myocardial ischemia and
fibrosis. Echocardiography is the first imaging modality for cardiac structure evaluation. CMR is recommended
when echocardiographic images are not adequate in patients with high suspicion for HCM. In the case of
contraindication to CMR, patients with ICDs or pacemakers, Cardiac CT is recommended. Imaging can be used to
screening, preclinical diagnosis and treatment guidance in a patient with HCM.

Important microscopic features of this disorder are the occurrence of
extensive myocardial hypertrophy, myofiber disarray and fibrosis.3

1. Introduction

Hypertrophic cardiomyopathy (HCM) is the genetic cardiomyopathy that can be divided into two categories, hypertrophic
obstructive cardiomyopathy (HOCM) and hypertrophic non-obstructive
cardiomyopathy (HNCM). Prevalence of HCM is 1:500 in the general
population. It is an autosomal dominant disease caused by over 1,400
mutations in at least 11 genes encoding proteins of the cardiac
sarcomere.1 Although the majority of patients with HCM is asymptomatic, subset remains at risk for having sudden death. The rate of mortality of HCM in the general population ranges <1% until 3-6% in tertiary
referral centres.2
HCM management is based on an understanding of its anatomy and
pathophysiology. It is highly dependent on accurate non-invasive
examination. A careful examination to see the presence of other
structural heart diseases by imaging is crucial to do a systematic evaluation of the structure and function of the heart in terms of proper patient
selection for further therapy.

3. Epidemiology

Prevalence of HCM vary between 1:500 (0.2%) and 1:3,000
(0.03%) in studies at North America, Europe, Asia and Africa.3 In the
2015 prevalence study in Germany, HCM occurred in 4,000 of
5,490,810 patients (0.07%; 1: 1,372). The prevalence of HCM increasing with age from 7.4/100,000 people at the age of 0-9 years to
298.7/100,000 people in patients aged >80 years. Men have a higher
prevalence, especially in patients >30 years of age.4
4. Pathogenesis and Pathophysiology

The pathogenesis of HCM is due to the presence of mutated
genes responsible for producing sarcomere complex proteins including
heavy-chain beta myosin protein, troponin, and myosin-binding protein
C, which will result in impaired contraction of heart muscle.5
The pathophysiology of HCM can be divided into:

2. Definition
HCM is cardiomyopathy marked by global or asymmetric
cardiac hypertrophy, that is not caused by chronic overpressure

(1) Echocardiography

*Corresponding author at: Brawijaya Cardiovascular Research Center, Department of Cardiology and Vascular Medicine, Faculty of Medicine,
Universitas Brawijaya, Malang, Indonesia
E-mail address: veny_kurniawati@yahoo.com (V. Kurniawati).
https://doi.org/10.21776/ub.hsj.2020.001.03.2
Received 9 September 2020; Received in revised form 12 September 2020; Accepted 24 September 2020
Available online 21 October 2020

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Heart Sci J 2020; 1(3): 4-9

shows a decrease in strain on HCM (Figure 2).16

Two-dimensional (2D) echocardiographic criteria diagnosis
of HCM:7-9
• Maximal thickness of LV wall >15 mm in any segment myocardial,
measured by echocardiography, CMR or computed tomography CT),
which cannot be explained only by changing loading conditions, or
• >12-15 mm in relatives,
• ≥2 SD greater than the normal body-surface in pediatric patients
• The thickness ratio of septal and posterior wall > 1.3 in normotensive
patients, or > 1.5 in hypertensive patients
The distribution of hypertrophy can occur in various forms,
locations, and includes the right ventricle. In patients suspected as
HCM, all LV segments from the base to the apical must be examined, to
ensure the thickness of the wall (Figure 1).3,7,8

Figure 1. (A) Apical 4C position, LVH with diffuse massive hypertrophy;
(B) short-axis view, at the level of PMs; (C) ASH in long-axis view (D)
Apical 4C view with apical wall thickness 15 mm. (E) Ace of spade
configuration in apical HCM (F) LV cavity opacification with contrast.8

Figure 2. The global LV strain was reduced by 7% in patients with HCM
(left). Radial strains were significantly reduced in six segments
(right).14

One of an atypical form of HCM is apical HCM/ApHCM, also
known as Yamaguchi syndrome, presenting exertional chest pain and
dyspnea mimicking acute coronary syndrome.10,11 ApHCM is marked by
giant negative T-waves on precordial lead ECG but no ST-T changes
and spade-like configuration of LV cavity in end-diastole on echocardiogram.12,13 Predominant LVH in the LV apex wall with ≥ 15mm
thickness. Typically, there is no LVOT obstruction in ApHCM, from
SAM and no mitral regurgitation. However, it can coincide with
obstruction of the midventricular wall and LV cavity obliteration
(MVOCO), and formation of an apical aneurysm.13

Diastolic abnormalities in HCM can be assessed with Dopler
echocardiography. A study showed in HCM patients, an association
between impaired severe LV relaxation and a significant decrease in
annular velocities. The size of the LA provides prognostic information
on HCM. The increase of LA size is multifactorial, with significant
contributions from the severity of mitral regurgitation, the occurrence
of diastolic dysfunction, and the possibility of atrial myopathy.7

There are three forms of ApHCM: (1) “pure”, isolated apical
hypertrophy; (2) “mixed”, both apical and septal hypertrophy with the
apex thickest; and (3) “relative” ApHCM, an early ApHCM phenotype
that can be detected by CMR.13

LVOT obstruction is defined as an increase of gradient of the
LVOT ≥30 mmHg at rest or during the physiological provocations such
as the manoeuvre of Valsalva, standing and exercise. Gradients ≥50
mmHg is the threshold at which LVOT obstruction becomes hemodynamically important. In the dynamic obstructive HCM, there is an
appearance of a late-peaking dagger-shaped (Figure 3).16 Administering
amylnitrite, upright exercise, or the manoeuvre of Valsalva in symptomatic patients with gradients at rest <30 mm Hg should be pursued to
provoke hemodynamic obstruction. It is essential to exclude that
obstruction is not associated with SAM, such as obstruction of LV mid
cavity, membrane sub-aortic abnormality of the mitral valve, especially
when considering interventions to reduce the LVOT obstruction.3

Transthoracic Echocardiography (TTE) with contrast agent
should be considered in patients with suspicion of apical HCM, to
determine the extent of hypertrophy, diagnosing apical aneurysm and
clots.14,15 Echocardiography 3D can accurately calculate the LV mass
with adequate image quality and experienced operators.14
Left ventricle EF is generally normal in patients with HCM.
LV systolic dysfunction in HCM, referred to as "dilated or progressive
phase of HCM", "end-stage HCM", "burnt-out HCM", with EF <50% and
only occur in a small proportion of patients (2% - 5%).9.14

Abnormalities of the apparatus of the mitral valve include
hypertrophied papillary muscles, which causes an anterior shift of
papillary muscles and mitral valve elongation. It causes the valve tends
to be pushed into the LVOT forming systolic anterior motion (SAM), as
a characteristic of obstructive HCM.17 SAM will cause turbulent flow,
seen as a mosaic pattern with colour Doppler that can cause uncoaptation of the mitral leaflet, and led to the mitral regurgitation (Figure 4).14

Subclinical LV systolic dysfunction can be assessed by the
velocity of myocardial movement in the systolic and diastolic phases.
Decreased systolic velocity (Sa) and initial phase diastolic velocity (Ea
or e’) can occur before the significant onset of hypertrophy. Imaging to
determine the strain rate is useful distinguishing non-obstructive HCM
from hypertensive LV hypertrophy. Speckle-tracking echocardiography
(STE) assess myocardial motion directly through 2D images which

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Heart Sci J 2020; 1(3): 4-9

(N)-labeled ammonia or 15-oxygen (O)-labeled water, evaluation of
perfusion in the transmural (subepicardial and subendocardial) can be
performed.18
In normal coronary arteries, the study PET myocardial
perfusion has shown that there is significantly reduced the augmentation of blood flow in the subendocardial region by vasodilatation (eg.,
Dipyridamole), despite the resting myocardial blood flow, in
millilitres/gram/minute, probably the same with the normal control.18

Figure 3. Continuous-wave Doppler (CW), concave contours, peak
velocity of LVOT (4.5 m/sec) (left) and a top speed signal mitral
regurgitation (6.3 m / sec) (right). Identification of these contours can
be useful to distinguish high CW jet of the dynamic obstruction of LVOT
and mitral regurgitation from aortic valve stenosis.14

Figure 5. Evaluation of myocardial ischemia in HCM using 201Thallium
SPECT.
(A, B) shows severe asymmetric septal hypertrophy at short-axis and 4C
position. Multidetector CT shows no atherosclerosis of the LAD (C), LCx
(D), and RCA (E). Stress-induced perfusion defects in the septum and
inferior wall, and transient LV dilatation at short-axis slices of 201Tl
SPECT (F), which normalize at rest (G). It suggest extensive subendocardial ischemia, without obstructive major epicardial coronary
arteries.18

Figure 4. SAM M-mode recording and contact septal mitral leaflet
(arrow) (left). 2D echocardiography view of SAM (arrow) (right).
Color Doppler showed a high speed across the LVOT in a mosaic
pattern and eccentric mitral regurgitation jet.14
(2) Nuclear Imaging
Assessing the systolic and diastolic function of the LV in HCM
patients can be performed with nuclear imaging techniques. It is also
used to assess myocardial ischemia (microvascular dysfunction using
positron emission tomography or PET).18
• SPECT (Single Photon Emission Computed Tomography)
In the absence of epicardial coronary artery stenosis,
ischemia in patients with HCM can be caused by disease of the small
blood vessels intramural, massive hypertrophy, and abnormal microcirculation which causes myocardial blood flow is inadequate, especially
if myocardial oxygen demand increased such as the presence of LV
hypertrophy and obstruction of the outflow tract.18

Figure 6. Rest (A) and Stress (B) perfusion mapping in ApHCM.13

(3) Cardiovascular Magnetic Resonance (CMR)
Tomographic imaging technique with a high-resolution 3D,
CMR gives a sharp contrast between the myocardium and blood pool. It
has emerged as an imaging technique to characterize the morphological of HCM. The imaging choice when the diagnosis of HCM still
unclear after echocardiography. Contrast-enhanced CMR with late-gadolinium enhancement (LGE) can identify areas of scarring or myocardial fibrosis.19

SPECT perfusion imaging using 201 Tl or 99m Tc sestamibi
or tetrofosmin, may show fixed defects or reversible perfusion or mix
defects. Stress-induced reversible perfusion defects reflect ischemia of
myocardium and are frequently observed in patients with good LV
function (Figure 5).18
The perfusion map of ApHCM showed ‘solar polar” on
SPECT. Bright apical spot surrounded by a circumferential ring of
decreasing counts (Figure 6).13

Imaging CMR produces multiple slices of myocardial thin
(thickness 7 mm) on the short axis view provides coverage tomography
entire myocardium and the measurement of wall thickness accuracy
and volume and ventricular mass (Figure 7).20

• Positron Emission Tomography (Positron Emission Tomography /
PET)

The number and papillary muscle mass were also increased in HCM. In
addition, a small portion of patients with HCM have a focal LV

PET has a higher spatial resolution than SPECT that allows
quantification of myocardial blood flow. Using tracers of 13-nitrogen

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Heart Sci J 2020; 1(3): 4-9

LV hypertrophy (with normal LV mass) but showed significant papillary
muscle hypertrophy.21

T1 mapping in CMR further can help differentiation of HCM
from the infiltrative cardiomyopathies, as they show sign and symptom
of HCM with an increased wall thickness (Figure 10).19. Screening of
first-degree relatives should begin at adolescence. Repeat evaluation
every 12–18 months, and every five years until the fourth decade of
life.19

Sequences CMR using contrast LGE can detect areas of
abnormal myocardium.22 LGE area can be measured and quantified as
a percentage of the total mass of the LV (Figure 8).14 In ApHCM, LGE
patterns are usually apical and subendocardial patterns which are rare
in other variants of HCM, without coronary artery disease (Figure 9).13

Figure 7. Upper: CMR short-axis images demonstrating massive LV
hypertrophy with wall thickness of 31 mm. Lower: 4C and long axis
view.19

Figure 10. CMR for differentiation of etiology of LV hypertrophy19. A)
Pre-contrast CMR image of patients 64 yo with septum wall thickness of
18 mm and lateral wall thickness of 14 mm, B) Post-contrast image of
patients, confirmed amyloidosis from cardiac biopsy, demonstrates
epicardial LGE in septum (arrows) and global subendocardial LGE
concern for amyloidosis, C) Pre-contrast images of patients 44 yo, with
septum wall thickness of 16 mm and 13 mm in lateral wall, D) Post-contrast image of patients, confirmed genetic testing that revealed
mutation of galactosidase alpha gene, demonstrates basal inferolateral
LGE (arrows) leading to concern for Fabry`s Disease. E) Pre-contrast
images of patients 21 yo, maximum wall thickness of 32 mm in septum,
F) Post-contrast image of patients, confirmed genetic testing that
revealed mutation of lysosomal-associated membrane protein 2 gene,
demonstrates transmural LGE at anterior and lateral wall and mid-myocardial LGE in the septum, leading to concern for Danon Disease.19

Figure 8. Contrast-enhanced CMR with LGE in HCM. (A) Female 58
years old asymptomatic transmural LGE vast area in the basal anterior
septum and anterior wall. (B) Area LGE diffuse and midmyocardial
patchy in the area of the ventricular septum in men aged 21 years. (C)
LGE limited to the insertion area RV free wall to the anterior and
posterior ventricular septum. 14

(4) Cardiac Computed Tomography (CCT)
CCT can be used to assess the anatomy of the heart in the
presence of inadequate echocardiographic images and has a contraindication to CMR such as on pacemakers or ICD, claustrophobia, or when
the patient can not hold their breath for a long time.14,22,23 Technique 3D
tomographic imaging provides excellent spatial and temporal resolution. Display in thin slices of 0.4 mm from the short axis and long-axis
view, CCT provides complete coverage of the entire myocardium
tomography.14,24
High resolution with a contrast gives a clear picture of the
myocardium, with the separation of white and grey (the myocardium)
(Figure 11).14
CCT can be used to evaluate the 3D shape, size, and
movement of the annulus of the mitral, SAM in multiphase images and
also evaluate the annular calcification.25 Evaluation of the coronary
arteries identifying the presence of the stenotic lesion, as well as
identify the presence of myocardial bridging. This technique should be
considered in patients complaining of chest pain who have a medium to
high probability of CAD.14

Figure 9. Giant precordial negative T wave and CMR of apical hypertrophy in relative ApHCM.13

CCT can determine the length of the coronary arteries and
myocardial LV, provide a clear picture of the relation of both. This
information can be helpful in surgical myectomy procedure. Planning

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Heart Sci J 2020; 1(3): 4-9

Planning alcohol septal ablation procedure and evaluation of post
procedures in HCM.14,26

approved the final draft and are responsible for the content and similarity index of the manuscript.

CCT has inferior temporal resolution and soft tissue characterization comparing with CMR. A 64-channel computed tomography
scanner has a mean of 6.7 ± 2.07 mSv radiation exposure compared
with CMR.22

5.7. Acknowledgements
We thank to Brawijaya Cardiovascular Research Center.
6. References

1. Rowin EJ and Maron MS. The role of cardiac MRI in the diagnosis
and risk stratification of hypertrophic cardiomyopathy. Arrhythmia
& Electrophysiology Review 2016;5(3):197-202
2. Noureldin RA, Liu S, Nacif MS, Judge DP, Halushka MK, et al. The
diagnosis of hypertrophic cardiomyopathy by cardiovascular
magnetic resonance. Journal of Cardiovascular Magentic
Resonance 2012; 14:17
3. Elliot PM, Anastasakis A, Borger MA, Borggrefe M, Cecchi F, et al.
Guidelines on diagnosis and management of hypertrophic cardiomyopathy. European Heart Journal 2014; 35:2733-2779

Figure 11. Patients with asymmetric septal hypertrophy has been
undergoing implantation of a pacemaker, so that CMR imaging is not
possible. The lines and the measurement refers to the wall thickness of
the septum and lateral wall. Short-axis cardiac CT showed asimetris
myocardial hypertrophy, anterior septum (19.6 mm) and inferolateral
wall (5.4 mm).14

4. Husser D, Ueberham L, Jacob J, Heuer D, Riedel-Heller S, et al.
Prevalence of clinically apparent hypertrophic cardiomyopathy in
Germany-An analyses over 5 million patients. Plos One
2018,13(5):e0196612
5. Kumar, Abbas, Fausto, Aster, Robbins and Cotran. Pathologic basis
of disease. 8ed. Philadelphia: Saunders;2010

4. Conclusion

Imaging in hypertrophic cardiomyopathy (HCM) plays an
important role. It can provide solutions to clinical needs, ranging from
diagnosis, prognosis, risk stratification, anatomic and functional
evaluation to the detection of ischemia, monitoring of treatment
modalities, family screening and diagnosis of preclinical to differential
diagnosis.

6. Lilly LS. Patophysiology of heart disease. 5ed. Philadelphia: Lippincott William&Wilkins;2011
7. Parato VM, Antoncecchi V, Sozzi F, Marazia S, Zito A, et al.
Echocardiographic diagnosis of the different phenotypes of
hypertrophic
cardiomyopathy.
Cardiovascular
ultrasound
2016;14(30):1-12

The multimodality imaging approach, including echocardiography, cardiac magnetic resonance (CMR), computed tomography
(CT) of the heart and cardiac nuclear imaging is recommended in the
assessment of patients with HCM. Selection examination techniques
should be used based on knowledge about the advantages of the
technique are offered. Each modality should be chosen in rational in
order to give a clear answer to a clinical problem by considering the
availability, benefits, risks, and costs.

8. Cardim N, Galderisi M, Edvardsen T, Plein S, Popescu BA, et al.
Role of multimodality cardiac imaging in the management of
patients with hypertrophic cardiomyopathy: an expert consensusof
the EuropeanAssociation of Cardiovascular Imaging endorsed by
Saudi Heart Association. European Heart Journal Cardiovascular
Imaging 2015, 1-35
9. Williams LK, Frenneaux MP and Steeds RP. Echocardiography in
hypertrophic cardiomyopathy diagnosis, prognosis and role in
management. European Heart Journal of Echocardiography
2009;10:iii9-iii14

5. Declarations
5.1. Ethics Approval and Consent to participate
Not applicable.

10. Ki-Woon Kang. Apical Hypertrophic CardiomyopathyPresenting
Mimicking Acute Coronary Syndrome at an Advanced Age.
Emergency Medicine 2014;4:3

5.2. Consent for publication
Not applicable.

11. Camelia C Diaconu, Nicoleta Dumitru, Ana G Fruntelata, Smarandita L, Daniela. Apical Hypertrophic Cardiomyopathy: The Ace of
Spades as the Disease Card. Acta Cardiol Sin 2015;31:83-86

5.3. Availability of data and materials
Data used in our study were presented in the main text.
5.4. Competing interests
Not applicable.

12. Weiliang Huang, Lina Guan, Liwen Liu, Yuming Mu. Apical Hypertrophic Cardiomyopathy with Apical Endomyocardial fibrosis and
calcification. Medicine 2019,98:27

5.5. Funding source
Not applicable.

13. Rebecca KH, Kristtopher , James M, Augusto, Saidi A et al.Apical
Hypertrophic Cardiomyopathy: The Variant LessKnown, Journal
American Heart Association 2020:9

5.6. Authors contributions
Idea/concept: VK. Design: VK. Control/supervision: AR, MSR, NK, AFR.
Data collection/processing: VK. Extraction/Analysis/interpretation: VK.
Literature review: AR, MSR, NK, AFR. Writing the article: VK. Critical
review: AR, MSR, NK, AFR. All authors have critically reviewed and

14. Nagueh SF, Bierig MS, Budoff MJ, Desai M, Dilsizian V, et al.
Clinical Recommendations for Multimodality Cardiovascular
Imaging of Patients with Hypertrophic Cardiomyopathy. JAmSoc
Echocardiografi 2011;04: 473-98
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V. Kurniawati, et al.

Heart Sci J 2020; 1(3): 4-9

15. Mulvagh SL, Rakowski H, Vannan MA, Abdelmoneim SS, Becher H,
Bierig SM, et al. American Society of Echocardiography consensus
statement on the clinical applications of ultrasonic contrast agents
in echocardiography. J Am Soc Echocardiogr 2008;21:1179-201
16. Afonso LC, Bernal J, Bax JJ, Abraham TP. Echocardiography in
hypertrophic cardiomyopathy. J Am Coll Cardiol cardovascular
imaging 2008;1(6): 787-800.
17. Sherrid MV, Wever-Pinzon O, Shah A, Chaudhry FA. Reflections of
inflections in hypertrophic cardiomyopathy. J Am Coll Cardiol
2009;54: 212-9.
18. Delgado B and Bax JJ. Clinical topic: Nuclear imaging in hypertrophic cardiomyopathy. J Nucl Cardiol 2014; 1071-3581
19. Rowin EJ and Maron MS. The role of cardiac MRI in the diagnosis
and risk stratification of hypertrophic cardiomyopathy. Arrhythmia
& Electrophysiology Review 2016;5(3):197-202
20. Maron MS, Maron BJ, Harrigan C, Buros J, Gibson CM, Olivotto I,
et al. Hypertrophic cardiomyopathy phenotype revisited after 50
years with cardiovascular magnetic resonance. J Am Coll Cardiol
2009;54: 220-8
21. Noureldin RA, Liu S, Nacif MS, Judge DP, Halushka MK, et al. The
diagnosis of hypertrophic cardiomyopathy by cardiovascular
magnetic resonance. Journal of Cardiovascular Magentic
Resonance 2012; 14:17
22. Rubinshtein R, Glockner JF, Ommen SR, Araoz PA, Ackerman MJ,
Sorajja P, et al. Characteristics and clinical significance of late
gadolinium enhancement by contrast-enhanced magnetic
resonance imaging in patients with hypertrophic cardiomyopathy.
Circ Heart Fail 2009;3: 51-8
23. Oliveira DC, Boldrini F, Santos AA, Nacif MS. Cardiac magnetic
resonance and computed tomography in hypertrophic cardiomyopathy: an update. Sociadade brasileira de cardiologia
2016;107(2):163-172.
24. Gopal A, Mao SS, Karlsberg D, Young E, Waggoner J, Ahmadi N, et
al. Radiation reduction with prospective ECG-triggering acquisition
using 64-multidetector computed tomographic angiography. Int J
Cardiovasc Imaging 2009;25:405-16
25. Mark DB, Berman DS, Budoff MJ, Carr JJ, Gerber TC, Hecht HS, et
al. ACCF/ACR/AHA/NASCI/SAIP/SCAI/SCCT 2010 expert consensus document on coronary computed tomographic angiography: a
report of the American College of Cardiology Foundation Task
Force on Expert Consensus Documents. J Am Coll Cardiol
2010;55:2663-99.
26. Alkadhi H, Desbiolles L, Stolzmann P, Leschka S, Scheffel H, Plass
A, et al. Mitral annular shape, size, and motion in normals and in
patients with cardiomyopathy: evaluation with computed tomography. Invest Radiol 2009;44:218-25.
27. Okayama S, Uemura S, Soeda T, Horii M, Saito Y. Role of cardiac
computed tomography in planning and evaluating percutaneous
transluminal septal myocardial ablation for hypertrophic obstructive cardiomyopathy. J Cardiovasc Comput Tomogr 2010;4:62-5

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