Download Cardiac apex: Spectrum of diseases in Cardiovascular Magnetic

Cardiac apex: Spectrum of diseases in Cardiovascular
Magnetic Resonance
Poster No.:
C-1491
Congress:
ECR 2013
Type:
Educational Exhibit
Authors:
Y. Arous , A. Omri , M. Ben Gadri , H. BOUJEMAA , N. BEN
1
2
4 1
2
2
3
3
ABDALLAH ; Ariana/TN, Tunis/TN, MONTFLEURY-TUNIS, TU/
4
TN, TN
Keywords:
Congenital, Arthrography, MR, CT, Musculoskeletal bone,
Cardiovascular system, Abdomen
DOI:
10.1594/ecr2013/C-1491
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Learning objectives
To illustrate the spectrum of Left Ventricular (LV) apex diseases using Cardiovascular
Magnetic Resonance (CMR).
To show the advantages of CMR comparing to Echocardiography.
Background
Cardiovascular magnetic resonance (CMR) is established in clinical practice for the
diagnosis and management of diseases of the cardiovascular system.
Echocardiography is the first line imaging modality.
However, it is well known that the apex may be difficult to image because of poor
acoustic window or incomplete visualization of the LV apex.
CMR is an imaging modality that provides a mechanism to assess cardiac or vascular
anatomy, function, perfusion, and tissue characteristics in a highly reproducible manner
during a single examination. Images can be acquired in patients of various body habitus,
in a time-efficient fashion, without an invasive procedure or exposure to ionizing radiation
or iodinated intravenous contrast medium.
CMR can image the heart in any desired plan and provide an accurate imaging of
the LV apex.
Spectrum of LV apex diseases is wide: Infarct, thrombus, Tako Tsubo cadiomyopathy,
apical hypertrophic cardiomyopathy.
Apex can be also the site of physiologic fat deposition.
In the Military Hospital of tunis, we perform our cardiac MRI on a 3 Tesla scanner
(Siemens verio).
MR Image Acquisitions:
All MR images were electrocardiographically gated and obtained during
repeated breath-holds. Cine MR images were acquired with a steady-state freeprecession sequence. After acquiring cine MRI images on
the 2- and 4-chamber long-axis projections, we obtained shortaxis
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cine MR images that encompassed the LV from base to
apex. For the assessment of myocardial edema, T2 STIR images were
obtained. late gadolinuim enhancement images was acquired 10 min after
intravenous administration of 0.15 mmol/kg of gadolinium. A
PSIR ( phase sensitive inversion recovery) sequence was
used.
Imaging findings OR Procedure details
APICAL HYPERTROPHIC CARDIOMYOPATHY
Apical HCM is characterized as myocardial hypertrophy that predominantly involve the
apex of left ventricle (LV). Apical HCM was originally described in individuals of asian
descent but it is now being diagnosed increasignly in the western world. the reported rate
of occurance of apical HCM range from 2 to 25%.
Unlike typical HCM, apical HCM shows a predilection for middle-aged men, is rarely
associated with sudden cardiac death, is frequently complicated by hypertension and
has a relatively good prognosis.
Echocardiography has been the first line imaging modality for patient with suspected
HCM but it is well known that the apex may be difficult to image which can lead to
false negative interpretation.
CMR can image in any plane and introduction of SSFP sequences has resulted in an
improvement in blood to myocardium contrast which is ideal for accurate imaging of the
apex. CMR was found to be superior to echocardiography in detecting apical segment
hypertrophy. the consequences of missed apical HCM for a patient include unnecessary
investigations and missed treatment.
The diagnostic criterion for apical HCM is absolute apical wall thickness of more
15mm or a ratio of apical to basal LV wallthickness of 1.3.
The characteristic "spade like" configuration of the LV cavity at end diastole is well
appreciated on long axis views (fig 1 and 2).
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More subjective criteria for the diagnosis of apical HCM include obliteration of the LV
apical cavity in systole and failure to identify a normal progrssive reduction in LV
wall thickness toward apex (Fig 3 and 4).
Concomitant apical involvement of the right ventricle is also commonly seen.
Moon and al found that 10 patients with a history of ECG abnormalities and negative
findings for apical HCM on echocardiography had positive MRI findings for apical HCM
on CMR.
TAKO TSUBO CARDIOMYOPATHY (TTCM)
TTCM is a reversible CM often precipitated by a stressful event with clinical features
indistinguishables from acute myocardial infarction. This disease usually affect post
menopausal women and it is characterized by hypokinesis or akinesis in the mid and
apical segments of the LV wall in the absence of obstructive coronary lesions.
ECG changes mimic myocardial infarction. A slight increase of cardiac enzymes level
also occurs in TTCM but is lower than expected in relation to extension of the ECG and
Echocardiography findings.
CMR is an non invasive imaging method that can provide useful information for the
diagnosis of TTCM. STIR sequence shows high signal intensity in the ventricular wall
with a transmural distribution in both apical and mid segments but not related to a vascular
distribution (fig 5). this area of edema shows dysfunction with cine MRI sequences (fig
6). The contraction abnormality produces the balloning morphology that characterizes
TTCM with a severe systolic dysfonction.
Another finding suggestive of TTCM is the presence of hyperkinesis in the basal plane
of the LV (fig 7).
Delay enhancement shows typically an absence of late enhancement.
However, recent studies indicate that gadolinuim enhancement may occur in
patients with TTCM and may indicate late recovery of wall motion abnormalities.
Usually, late gadolinium enhancement disappears within 12 months.
LEFT VENTRICULAR APICAL THROMBUS
Accurate detection of LV thrombus is important as thrombus provides a substrate for
embolic events and a rationale for anticoagulation.
Echocardiography is widely accepted as the primary screening test for LV thrombus.
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Delayed enhancement CMR has been well validated as an accurate technique for
LV thrombus. In many studies, DE-CMR has yielded a 2- to 3-fold improvement
in thrombus detection versus noncontrast echo. LGE, which is typically used for
detection of myocardial fibrosis or scar, can be used for improved differentiation of
enhancing cardiac masses from nonenhancing bland thrombus. It has also the ability to
distinguish a cardiac tumor from thrombus.
Weinsaft and al demonstrate that Patients who derived incremental benefit from delayed
enhancement CMR had lower LVEF than those in whom noncontrast echo alone
accurately assessed thrombus. LV function can be useful for guiding imaging
strategies for thrombus. they also demonstrate that Thrombi detected by DE-CMR but
not by contrast echo are typically mural in shape or small in volume.
In our experience the most frequently missed apical thrombus in echocardiography are
small in volume (fig 8) or occurs in patients with idiopathic dilated cardiomyopathy (fig 9).
In case of idiopathic dilated cardiomyopathy, hypertrabeculation of the LV can mask
apical thrombus in echocardiography.
MYOCARDIAL INFRACTION
Late gadolinium enhancment CMR can be used for identifying the extent and location
of myocardial necrosis in individuals suspected of having or possessing chronic or
acute ischemic heart disease. Typically, delyaed enahncement is subendocardial and/
or transmural.
CMR has a crucial role for the diagnosis of myocardial infarction in patient with a
normal coronarography.
PHYSIOLOGIC FAT DEPOSITION
Physiologic fat deposition can mimic pathologic condition and diseaeses particulary
healed myocardial infarction. Fat in healed myocardial infarction is usually easily
distinguished from physiologic fat because of its characteristic subendocardial location,
which corresponds to the distribution of a coronary artery. However, when a small
amount of fat is identified in the LV apex, it may be difficult to differentiate
physiologic fat from fat deposition secondary to a small myocardial infarct. In
this case, CMR is crucial (fig 13, 14 and 15). it shows fat deposition with no delay
enhancement and no motion abnormalities of LV apex.
Images for this section:
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Fig. 1: 55 years old patient with an acute coronary syndrom and a normal
coronarography. The echcocardiography shows an akinetic LV apex. A CMR was
performed. the cine image in vertical long axis view shows a "spade like" configuration
of the LV cavity at end diastole.
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Fig. 2: 57 years old patient with a suspected apical CMH on echocardiography. CMR
shows a "spade like" configuration of the LV cavity.
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Fig. 3: Same patient as in figure 2: SSFP cine image on short axis view shows obliteration
of the LV apical cavity in systole.
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Fig. 4: Same patient as in figure 2 and 3: SSFP cine sequence on horizantal long axis
view shows an absence of the normal progrssive reduction in LV wall thickness toward
the apex.
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Fig. 5: T2 STIR sequence on apical short axis view in 83 years old woman in acute
state of Takotsubo cardiomyopathy. Transmural edema is observed in apical plane of left
ventricle. intensity. Areas with edema show wall motion abnormalities in cine MRI.
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Fig. 6: Cine MR image on short axis view (from same patient as in Fig 5) shows severe
hypokinesis in the area of edema
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Fig. 7: Cine MR image on basal short axis view (same patient as in Fig.7) shows
hyperkinesis of the LV wall.
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Fig. 8: PSIR sequence on vertical long axis view in a 65 years old patient shows a small
apical thrombus. No thrombus seen on echocardiography.
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Fig. 9: PSIR sequence in horizantal long axis view in a 40 years old patient with
a idiopathic dilated cardiomyopathy shows a 25mm apical thrombus not seen on
echocardiography;
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Fig. 10: STIR sequence on vertical long axis view in 68 years old woman with an
acute coronary syndrom with a normal coronarography and echocardiography shows
hypersignal (edema) of 17 segment .
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Fig. 11: PSIR sequence on vertical long axis view (same patient as in fig 10) shows
transmural late enhancement of the LV apex: Myocardial infarction.
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Fig. 12: SSFP cine sequence on vertical long axis view (same patient as in fig 10 and
11) shows an akinetic LV apex.
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Fig. 13: ECG gated CT scan in a 45 years old man shows subendocardial fat deposition
at the LV apex
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Fig. 14: T1 sequence on vertical long axis view shows high signal intensity areas in the
apex and the basal wall.
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Fig. 15: T1 with fat saturation confirms the fat deposition (same patient as in figure 13
and 14). the absence of delayed enhancement and motion abnormalities confirm the
physiologic fat deposition.
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Conclusion
CMR provide an accurate imaging of the LV apex.
LV apex diseases are numerous.
the LV apex may not assessed well with echocardiography and can lead ta false negative
interpretation
In apical HCM, CMR is strongly recommanded as the optimal imaging modality.
CMR is crucial in coronary acute syndrom with a normal coronarography particulary in
apex lesions ( small apex infarct, Tako Tsubo cardiomyopathy).
CMR is also an accurate technique for LV thrombus detection.
References
1. Hansen MW, Merchant N. MRI of hypertrophic cardiomyopathy: Part I; MRI
appearances: AJR 2007;189:1335-43.
2. ACCF/ACR/AHA/NASCI/SCMR 2010 Expert Consensus Document on
Cardiovascular Magnetic Resonance: A Report of the American College of Cardiology
Foundation Task Force on Expert Consensus Documents. JACC; 55:2614-62.
3. Moon JCC, Fisher NG, McKenna WJ, Pennell DJ. Detection of apical hypertrophic
cardiomyopathy by cardiovascular magnetic resonance in patients with nondiagnostic
echocardiography. Heart 2004;90:645-649.
4. Teraoka K, Kiuchi S, Takada N, Hirano M, Yamashina A. Images incardiovascular
medicine: No delayed enhancement on contrast magnetic
resonance imaging with Takotsubo cardiomyopathy. Circulation 2005;111: e261 - e262.
5. Nakamori S, Matsuoka K, Onishi K et al. Prevalence and Signal Characteristics of
Late Gadolinium Enhancement on Contrast-Enhanced Magnetic Resonance Imaging in
Patients With Takotsubo Cardiomyopathy.
Circ J 2012; 76: 914-21.
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6. JW Weinsaft, RJ Kim, MRoss et al.Enhanced Anatomic Imaging as Compared to
Contrast-Enhanced Tissue Characterization for Detection of Left Ventricular Thrombus.
J Am Coll Cardiol Img 2009;2:969-79.
7. F Kimura, Y Matsuo, T Nakajima et al. Myocardial Fat at Cardiac Imaging: How
Can We Differentiate Pathologic from Physiologic Fatty Infiltration? RadioGraphics 2010;
30:1587-1602
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