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vessels. Echocardiography is the most common imaging
technique used for the initial diagnosis and management of
cardiomyopathy; however, other imaging modalities, including nuclear cardiac imaging, cardiac magnetic resonance
imaging, and cardiac computed tomography, may play an
important role depending on the underlying etiology of the
cardiomyopathy [ 2 ].
Dilated Cardiomyopathy
Dilated cardiomyopathy is characterized by ventricular
enlargement and decreased systolic function. Besides the
reconstructed CT data at specifi c diastolic (and/or systolic)
phases of the cardiac cycle for evaluation of the coronary
arteries and cardiac morphology, a multiphase data set,
which reconstructs the entire cardiac cycle at 5–10 % intervals, allows for viewing images in cinematic mode. This
multiphase reconstruction allows for assessment of left and
right ventricular systolic function in any orientation,
including all of the standard echocardiographic planes [ 3 ].
Thus, CCT can assess myocardial thickness (Video 13.1 ),
ventricular shape and volume, and global and regional
ventricular function with excellent correlation to
echocardiography and cardiac MRI [ 4 , 5 ]. Additionally,
patients with severely reduced left ventricular function are at
risk for the development of mural thrombus. Given its
inherently high contrast to noise ratio and excellent spatial
resolution, CCT can readily identify such mural thrombi.
Restrictive Cardiomyopathy
Restrictive cardiomyopathy is characterized by increased
ventricular stiffness and associated diastolic dysfunction.
Ventricular size and systolic function are usually normal, but
the atria and systemic veins (superior and inferior vena cavae,
hepatic veins, coronary sinus) are often dilated due to
increased fi lling pressures. These features are easily depicted
by CCT but are nonspecifi c. While CCT is not indicated
solely for the evaluation of possible restrictive cardiomyopathy, it is useful in differentiating it from constrictive pericarditis by excluding pericardial abnormalities. This distinction
leads to important therapeutic consequences.
Hypertrophic Cardiomyopathy
Hypertrophic cardiomyopathy is a genetic disorder of various sarcomeric proteins resulting in cardiac myocyte disarray and left ventricular hypertrophy with or without
obstruction. This most commonly involves asymmetric
septal hypertrophy, although other variants exist, including
apical and mid-ventricular hypertrophy (Fig. 13.1 ). In
patients with dynamic left ventricular outfl ow obstruction,
CCT delineates the systolic anterior motion of the anterior
mitral valve leafl et on the multiphase images. While poor
acoustic windows may limit echocardiography, CCT can
reliably identify all areas of the myocardium and provide
accurate, reproducible measurements of wall thickness.
Arrhythmogenic Right Ventricular
Cardiomyopathy (ARVC)
ARVC is an unusual cardiomyopathy characterized by
abnormal right ventricular function, fi brofatty deposition
into the right ventricular myocardium, and abnormal electrocardiographic changes, which predispose these patients
to sudden cardiac death. CCT has an advantage over echocardiography in its ability to visualize the right ventricle
and thus to evaluate right ventricular morphology and systolic function, similar to MRI. However, MRI has superior
tissue characterization capabilities and remains the modality of choice for evaluating suspected ARVC. CCT becomes
the modality of choice when metal implants or claustrophobia preclude MRI. When performing CCT in these patients,
it is important to ensure adequate opacifi cation of the right
ventricle at the time of image acquisition. This can be
achieved by either prolonging the contrast administration
by several seconds (4–6 s) or by empirically utilizing a
shorter delay time. Alternatively, placing a region of interest in the main pulmonary artery and triggering the scan at
its peak opacifi cation can consistently achieve preferential
right- sided opacifi cation. CCT can reliably characterize
right ventricular dimensions as well as focal aneurysms of
the myocardium, increased trabeculations, and/or areas of
right ventricular dysfunction, all confi rmatory fi ndings in
RV dysplasia. Importantly, CCT can also detect fatty infi ltration as areas of hypoattenuation, confi rmed by CT attenuation measurements. However, the fi nding of fat is
sensitive but not specifi c for ARVC [ 6 ]. Hence, CCT fi nd-
ings must be correlated with clinical and electro-cardiographic data to establish the diagnosis of ARVC.
Left Ventricular Noncompaction
Left ventricular noncompaction is a cardiomyopathy characterized by a 2-layered myocardium: a thin compacted layer
and a thick noncompacted layer. The ratio of noncompacted to
compacted myocardium has been reported to be greater than
or equal to 2.3:1 by cardiac MRI in cases of non-compaction
[ 7 ]. The hypertrabeculations of the noncompacted myocar-
dium, as well as thrombi that may form within the recesses,
are easily delineated with CCT due to its favorable contrast-tonoise ratio (Fig. 13.2 ). Left ventricular noncompaction fre-
quently manifests itself as a dilated cardiomyopathy with
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Fig. 13.1 The most common form of hypertrophic cardiomyopathy
manifests as asymmetric septal hypertrophy with or without obstruction. This three-chamber view in end-diastole ( a ) demonstrates abnor-
mal thickening of the mid-and basal interventricular septum. The
short-axis view in end-diastole ( b ) demonstrates normal mitral valve
morphology and opening. In systole, the three-chamber view ( c ) dem-
onstrates systolic anterior motion of the anterior mitral valve leafl et
( arrow ) causing a gradient across the left ventricular outfl ow tract. This
is consistent with hypertrophic obstructive cardiomyopathy. The shortaxis view in systole ( d ) also demonstrates systolic anterior motion of
the mitral valve as well as incomplete coaptation of the leafl ets ( arrow ),
causing mitral regurgitation. In the apical form of hypertrophic cardio-
myopathy, muscle thickening occurs predominantly at the apex of the
left ventricle, as can be seen in end-diastolic images in the four- and
two-chamber views ( e , f ). The corresponding end-systolic images dem-
onstrate complete obliteration of the left ventricular apex ( g , h ). When
the left ventricular hypertrophy primarily affects the mid- ventricular
level, there can be mid-cavitary obliteration with an associated gradient
at the level of obstruction. End-diastolic images in the short-axis ( i ),
two-chamber ( j ), and four-chamber ( k ) views, and the 3-D volume-
rendered image ( l ) demonstrate prominent thickening at the mid-ven-
tricular level. The corresponding end-systolic images
( m – p ) demonstrate complete obliteration of the mid-cavity and early
apical outpouching
a
d
g
jkl
hi
ef
bc
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m
op
n
Fig. 13.1 (continued)
reduced left ventricular function, which can also be assessed
by CCT. Clinically, noncompaction is associated with both
heart failure and sudden death.
Myocardial Infl ammation (Myocarditis)
on CT Scan
Acute myocarditis is a relatively uncommon disease but may
well be under diagnosed. CCT can be helpful in the diagnosis of myocarditis. With the typical history of chest pain and
elevated serum troponin-I level in young patients, myocarditis on CCT will show normal epicardial coronary arteries.
Due to edema of the myocardium, CCT may also show low
attenuation at ventricular wall and interventricular septum
[ 8 ], which can be confi rmed with Cardiac MR as increased
signal on T2-weighted imaging. There may also be delayed
myocardial enhancement on contrast-enhanced CCT images
in acute myocarditis [ 9 ]. The morphologic features of the
enhancement are similar to the myocardial enhancement of
myocarditis with gadolinium contrast on CMR, and different
from the enhancement patterns seen in patients with myocardial infarction [ 9 ]. On CMR there is a subepicardial delayed
contrast enhancement (DCE) pattern typical of acute myocarditis in comparison to an ischemic DCE pattern, which is
transmural or subendocardial [ 10 ].
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CT Imaging of Pericardial Disease
Pericardial diseases represent an important cause of morbidity and mortality in patients with cardiovascular disease and
constitute a spectrum ranging from benign to malignant
causes. Pericardial diseases can present clinically as acute
pericarditis, pericardial effusion, cardiac tamponade, and
constrictive pericarditis. Patients can subsequently develop
chronic or recurrent pericarditis. Structural abnormalities
including congenitally absent pericardium and pericardial
cysts are usually asymptomatic and are uncommon.
Advances in multimodality noninvasive cardiac imaging
have enhanced its role in the management of patients with
suspected pericardial disease. Structural and functional
information obtained from echocardiography and the anatomic detail provided by cardiac computed tomography and
magnetic resonance have led to growing interest in the complementary use of these techniques. Management of the
patient with suspected pericardial disease requires expertise
with the key imaging modalities and the ability to choose the
appropriate imaging tests for each patient.
Anatomy of Pericardium and CT Scan
The pericardium is a double-layered membrane normally
measuring <2 mm in thickness that forms a sac which surrounds the heart and the origins of the great vessels (Fig. 13.3 )
[ 11 ]. It is made of two sacs in one. The outer sac is the fi brous
pericardium and inner sac is the double-layered serous pericardium. Layers of serous pericardium are divided by the
pericardial space , which usually only contains 15–50 mL of
serous fl uid. They have quite different structures—the
fi brous pericardium is a tough connective tissue continuous
with and bound to the central tendon of the diaphragm, the
roots of the great vessels, the pretracheal layer of the deep
cervical fascia and the sternum via the superior sterno-pericardiac ligaments (to manubrium) and inferior sterno-pericardiac ligaments (to xiphoid process). The serous
pericardium is composed of a single layer of fl attened cells
forming a closed sac and in turn also forms two continuous
layers. The visceral serous pericardium (or epicardium) covers heart and great vessels. The parietal serous pericardium
lines the fi brous pericardium and is inseparable from it.
abc
de f
Fig. 13.2 The morphological hallmark of left ventricular noncompaction is the presence of hypertrabeculations. These hypertrabeculations are
often most prominent toward the left ventricular apex. End-diastolic
images in the two-( a ), three-( b ), and four-chamber ( c ) views demonstrate
these characteristically prominent trabeculations that form the noncompacted layer ( white arrows ). End-diastolic images in the short-axis view
at the base ( d ), mid-ventricular ( e ), and apical levels ( f ) again demon-
strate these hypertrabeculations, most prominently at the apex
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The serous pericardium is invaginated by the heart and
great vessels to form two sinuses: the oblique sinus is
formed by the indentations of the superior and inferior vena
cavae and the four pulmonary veins (blind-ending) and thus
sits posterior to the left atrium where it may be mistaken for
an esophageal mass or bronchogenic cyst. The transverse
sinus lies between the aorta and pulmonary artery anteriorly
and the atria posteriorly, surrounding the ascending aorta. It
includes several recesses (superior aortic recess, inferior aortic recess, pulmonic recesses and post caval recess) that may
be mistaken for dissection or lymphadenopathy [ 12 ]. These
recesses are important when evaluating for pericardial metastatic disease in oncology patients.
While echocardiography is conventionally used for the
evaluation of pericardial diseases, CCT offers a number of
distinct advantages. CCT provides a larger imaging fi eld
allowing assessment of concomitant pathology. In addition,
CCT offers a superior soft tissue contrast, and thus characterization of specifi c pericardial processes is sometimes possible. CCT is exquisitely sensitive to the detection of calcium
and thus can be useful in identifying pericardial calcifi cation,
a fi nding that can be associated with constrictive pericarditis
(Fig. 13.4 ). One of the limitations of CCT in evaluating the
pericardium, however, is its occasional diffi culty in differentiating pericardial fl uid from a thickened pericardium.
With CCT, the normal pericardium (Video 13.2 ) is best
imaged in systole and appears as a line of average thickness
of 1.3–2.5 mm (almost always <4 mm). CCT delineates the
pericardium as a well-defi ned, linear structure that is easily
detectable in both contrast and noncontrast-enhanced examinations because of its visibility against the low attenuation of
the surrounding fat. Visualization of the pericardium varies
with location and is sometimes diffi cult at the lateral, posterior, and inferior left ventricular walls because of a paucity of
pericardial fat in these locations.
I n fl ammation of Pericardium on CT Scan
To evaluate for pericardial infl ammation, a noncontrast CT
can be performed prior to the contrast-enhanced CT.
Enhancement of the pericardium after contrast administration is indicative of pericardial infl ammation, and may be
seen in cases of pericarditis. The current reference standard for the noninvasive evaluation of pericardial constriction is cardiac MRI. The characteristic anatomic changes
associated with constrictive pericardial disease (elongated
and narrow RV, enlargement of the right atrium and inferior cava, and pericardial thickening) are clearly identifi ed
with both MRI and CCT. However, since patients with true
constrictive pericarditis typically present with orthopnea,
it is often diffi cult for them to lie fl at in the MRI scanner
for up to 1 h. CCT may offer another option for evaluating
constrictive pericarditis, with short examination times representing one of its major advantages. The excellent spatial resolution of CCT allows for accurate measurement of
ab
Fig. 13.3 Due to its excellent spatial resolution, cardiac CT can image
the pericardium, which is normally <2 mm thick. These short-axis ( a )
and four-chamber ( b ) views demonstrate the normal, thin pericardium
( white arrowheads ). The pericardium is often best visualized over the
right side of the heart, as the more abundant epicardial fat located there
provides good tissue contrast
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228
pericardial thickness. A pericardial thickness >4 mm is
considered pathological and, in the appropriate clinical
context, is suggestive of pericardial constriction [ 13 , 14 ].
However, it is important to note that neither pericardial
calcifi cation nor thickening is diagnostic of constrictive
pericarditis. Besides these morphological characteristics,
the demonstration of an early diastolic septal bounce on
the multiphase cine images is suggestive of constrictive
physiology [ 15 ].
The normal pericardium is a double-layered membrane
that is <2 mm thick. A pericardial thickness >4 mm is considered pathological. Pericardial thickening may be found in
the absence of constriction (e.g., acute pericariditis, uremia,
collagen vascular diseases). Enhancement of the pericardium, indicative of pericardial infl ammation, may be found
in cases of pericarditis. Pericardial infl ammation can be evaluated by performing CCT with and without contrast. The
infl amed pericardium will demonstrate a signifi cant increase
in CT attenuation after contrast administration.
Congenital Absence of Pericardium
Rare individuals demonstrate a congenital absence of the
pericardium. While this can present as a complete absence of
pericardial tissue, most cases demonstrate only partial pericardial defects, typically on the left side (Fig. 13.5a ). Clues
on CCT that suggest this diagnosis are rotation of the heart to
the left, interposition of lung tissue in the aortopulmonary
window, and bulging of the left atrial appendage through the
pericardial defect. Infrequently, the left atrial appendage can
be incarcerated in the defect requiring surgical enlargement
or closure.
Pericardial Effusion on CT Scan
Echocardiography remains the modality of choice for the initial evaluation of pericardial effusion (Fig. 13.5b ). However,
several fi ndings make further evaluation with CCT useful,
such as a loculated effusion, hemorrhagic effusion, or equivocal fi ndings on echocardiography. Pericardial effusions may
be characterized with CCT by measuring their CT attenuation.
A CT attenuation close to water (e.g., 0 Hounsfi eld Units, HU)
suggests a simple pericardial effusion. If the CT attenuation is
greater than that of water, the effusion may represent hemorrhage, purulence, or a malignant/cellular process.
Pericardial Masses
Pericardial masses include cysts and neoplasms. Pericardial
cysts are congenital and are usually found at the right costophrenic angle [ 16 ]. They tend to be asymptomatic
smooth-walled simple cysts that do not enhance after contrast administration (Fig. 13.5c ). However, sometimes
pericardial cyst can present on left side and can compress
the left atrium with clinical symptoms of dyspnea [ 17 ].
With regard to neoplasms, metastases are far more common than primary pericardial tumors. Neighboring structures, such as the lung and breast, are most commonly the
source of metastatic disease to the pericardium. Other
fi ndings associated with metastatic disease include pericardial effusion and an irregularly thickened pericardium
[ 18 ]. Primary neoplasms of the pericardium occur infre-
quently and may be benign (fi broma, teratoma, lipoma,
hemangioma) or malignant (mesothelioma, lymphoma,
sarcoma, and liposarcoma) [ 19 ].
ab
Fig. 13.4 Cardiac CT is exquisitely sensitive for the detection of calcium. In this case of pericardial constriction, the patient was found to
have a thickened, heavily calcifi ed pericardium ( white arrowheads ) as
noted on the short-axis view ( a ) and 3-D volume-rendered image ( b ).
The volume rendered image demonstrates circumferential pericardial
calcifi cation at the base
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Pericardial Fat Assessment with CT Scan
Recent studies have shown that increased pericardial fat is
strongly associated with increased coronary artery calcium,
coronary plaque burden and major adverse cardiovascular
events (MACE) [ 20 , 21 ]. These fi ndings suggest that peri-
cardial fat may play a role in causing coronary atherosclerosis [ 22 – 26 ]. Due to distinct attenuation values of fat on CT,
fat can be readily measured around the heart with cardiac
CT, both with and without contrast [ 27 ]. Cardiac CT, with
its high spatial resolution, allows accurate measurement of
epicardial and thoracic fat distances and volumes (Fig. 13.6 ).
Volumetric quantifi cation of epicardial fat and thoracic fat
require the following steps: demarcation of the heart boundaries on CT images, and tracing of the inner thoracic cavity
and pericardium, which can be manual [ 21 , 28 ] or semi-
automated [ 20 ]. The superior most slice is typically chosen
at the bifurcation of the pulmonary artery. The anatomic
landmark for the inferior limit of the heart is typically the
most inferior slice of the myocardium [ 26 ] or the most infe-
rior slice with the posterior descending artery [ 29 ]. With
semi-automated measurement, pericardial fat contours are
generated by spline interpolation through several control
points, which are placed manually on the visceral pericardium [ 30 ], and the inner thoracic cavity is segmented auto-
matically [ 31 ]. CT uses standard fat attenuation values to
defi ne fat attenuation; for non-contrast CT typically an
attenuation range of (−30, −190) Hounsfi eld Units is used.
Fat voxels within this attenuation range within the visceral
pericardium are classifi ed as epicardial fat, and within the
inner thoracic cavity classifi ed as thoracic fat.
Comparison to Other Imaging Modalities
Generally cardiac computed tomography is superior to
echocardiography and cardiac MRI because of its superior and ultrasensitive resolution and excellent fi eld of
view. Echocardiography is good for a quick assessment of
pericardium but it does not give the detail of pericardial
disease as clearly as CT/MRI. Cardiac MRI is limited in
use because of high cost and time duration of the scan that
make it less suitable for emergent pericardial conditions
such as cardiac tamponade. Table 13.1 [ 32 , 33 ] compares
pericardial disorder assessment with CCT, echocardiography and CMR. Table 13.2 [ 34 – 90 ] compares myocardial
disorder assessment with these imaging modalities.
a b c
Fig. 13.5 Partial absence of the pericardium ( a ). In this example, nor-
mal pericardium is found over the right ventricular free wall ( white
arrowheads ), but there is absence of the pericardium over the right ventricular apex and left ventricle ( black arrowheads ). Pericardial effu-
sions ( asterisks ) are often found in the context of pericarditis ( b ). In this
case, the pericardium also enhanced after administration of iodinated
contrast ( white arrowheads ), suggesting pericardial infl ammation.
Pericardial cysts ( asterisk ) are benign fl uid-fi lled pericardial masses,
typically found at the right cardio-phrenic angle ( c )
Fig. 13.6 Axial view of heart with normal pericardium on Revolution
CT calcium scan ( yellow arrowhead )
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Table 13.1 Pericardial disorders assessment with cardiac imaging modalities
Pericardial condition Defi nition CT angiographic diagnostic fi nding Echocardiographic diagnostic fi nding MRI diagnostic fi nding
Pericarditis Pericarditis is an
infl ammation of the
pericardium.
Normal pericardial thickness is
less than 4 mm and is usually
1–2 mm
Pericardial thickening/
enhancement (the most accurate
single parameter for pericarditis,
with sensitivity of 54–59 % and
specifi city of 91–96 %) [ 32 ].
Only helpful if a pericardial effusion is present
with pericarditis.
Can determine whether the effusion is limiting
the fi lling of the heart (i.e., causing cardiac
tamponade).
Most sensitive method for the diagnosis of acute
pericarditis is delayed enhancement of the
pericardium on cardiac MR (CMR) [ 33 ].
On CMR, the pericardium normally appears
black because of its low water content;
However, in patients with pericarditis, enhanced
gadolinium uptake in the infl amed pericardium
is present on delayed images
Cardiac Tamponade Cardiac Tamponade is a
clinical syndrome caused
by the accumulation of
fl uid in the pericardial
space, resulting in reduced
ventricular fi lling and
subsequent hemodynamic
compromise. The
condition is a medical
emergency, the
complications of which
include pulmonary edema,
shock, and death.
Enlargement of the SVC and IVC
Periportal lymphedema
Refl ux of contrast material within
the IVC and azygos vein, and
enlargement of hepatic and renal
veins.
Flattened heart sign.
Compression of the coronary sinus.
Angulation or bowing of
interventricular septum.
RV diameters are reduced.
Early diastolic collapse of RV
RA free-wall collapse during late diastole. RA
isovolumic contraction is prolonged to occupy
one third of the cardiac cycle.
LA free-wall compression in patients with fl uid
posterior to the left atrium. LV free-wall may
exhibit paradoxical movement
SVC & IVC may show congestion (unless
patient is relatively volume depleted)
IVC is usually greater than 2.2 cm in diameter
with less than 50 % inspiratory compression
Exaggerated inspiratory effects, especially with
pulsus paradoxus, may include RV expansion,
interventricular septum shift to the left, and LV
compression
Mitral changes, with reduced D-E amplitude or
E-F slope and delayed mitral opening time
Aortic valve with premature closure
Echocardiographic stroke volume diminished
RV epicardial notching during isovolumic
contraction
Coarse vibrations of LV posterior wall.
Pseudohypertrophy or apparent wall thickening
due to compression
CMR has a limited role in the setting of cardiac
tamponade owing to the emergent and
life- threatening nature of this condition.
CMR fi ndings with other imaging modalities
include; swinging heart and paradoxical septal
bounce seen on short-or long-axis cine MR
images.
CMR imaging can help differentiate the nature
of the pericardial effusion (transudative,
exudative, and or hemorrhagic) in addition to
the effects on cardiac functioning and diastolic
fi lling.
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Constrictive
Pericarditis
Constrictive pericarditis is
a reduction in the
elasticity, or stiffening, of
the pericardium, a
sack-like covering that
surrounds the heart,
resulting in impaired
fi lling of the heart with
blood.
Diffuse thickening of anterior
pericardium upto the vascular root
best seen on multiplanar
reformats.
Size of all 4-heart chambers
should be within the normal range.
-IVC is dilated to more than
double the size of aortic diameter.
Poor opacifi cation of liver
parenchyma due to congestion and
no contrast enhancement in the
portal vein.
No progression of the contrast-
agent bolus through the vascular
system, and evidence of
signifi cant systolic dysfunction
should be absent
Cardiac echograms show normal contraction
and systolic function.
Special procedures, including an assessment of
Doppler velocities across the mitral and
tricuspid valves during inspiration and
expiration, are needed to demonstrate
ventricular interdependence.
Newer echocardiographic procedures, such as
the evaluation of the early diastolic Doppler
myocardial velocity gradients at the posterior
wall, echocardiographic TDI, and color M mode
fl ow propagation, have been reported to
enhance the differentiation between CP and
restrictive cardiomyopathy
Cardiac MRI can detect constrictive physiology.
MRI allows precise measurement pericardial
thickness; the ideal views for measuring
pericardial thickness are short axis views
Measure chamber sizes at successive 50-msec
delays after the R wave and to determine
whether or not a fi lling plateau is present.
Assess volumetric fl ow and regurgitant fl ow to
the pulmonary veins and the hepatic vein.
Fast imaging with deep respiration help to
establish whether fi lling is concordant or
discordant. CP restriction creates discordance
with reduced left ventricular fi lling, which
corresponds to increased right ventricular
fi lling.
MRI shows reversed curvature of the
intraventricular septum.
MRI does not depict pericardial calcifi cations.
Pericardial effusion Pericardial effusion is an
abnormal accumulation of
fl uid in the pericardial
cavity. Because of the
limited amount of space in
the pericardial cavity, fl uid
accumulation leads to an
increased intrapericardial
pressure which can
negatively affect heart
function
Differentiation of the pericardial
line from the myocardium is
enabled by the presence of a small
amount of epicardial and
pericardial fat. This fat may be
visible on CT scans.
CT demonstrates the superior
recesses of the pericardium
extending over the ascending aorta
and lateral to the main pulmonary
artery. These recesses may be
distended in the presence of a
pericardial effusion.
Attenuation of the effusion on CT
may be helpful in suggesting the
etiology.
Echo-free space: (1) posterior to LV (small-to-
moderate effusion); (2) posterior and anterior
(moderate-to-large effusion); (3) behind left
atrium large-to-very large effusion and/or
anterior adhesion.
Diminished mobility of posterior pericardium-
to- lung interface.
Enhanced RV wall mobility unmasked in
presence of anterior fl uid
Swinging heart (large effusions, usually
tamponade): (1) RV and LV walls move in
synchrony; (2) periodicity 1:1 or 2:1 (one or
two swings per cardiac cycle); (3) 2:1 swing is
characteristic of cardiac Tamponade; (4)
pseudoparadoxic motion of LV posterior wall;
(5) mitral and/or tricuspid pseudoprolapse; (6)
mitral systolic anterior motion; (7) alternating
mitral E-F slope and aortic opening excursion;
(8) aortic valve exhibiting midsystolic closure;
(9) pulmonic valve with midsystolic notch
Hemopericardium with blood clots identifi able
by echocardiography
Inspiratory decrease in LV ejection time (with
effusion
On spin-echo images, the pericardial effusion or
portions of it may appear as a signal void (dark)
sac because of moving fl uid in the pericardial
cavity. In gradient-echo sequences, effusions are
hyperintense.
Hemorrhagic effusions have the opposite
appearance; they have high signal intensity on
T1-weighted spin echo images and low intensity
on gradient echo images.
Depict pericardial recesses, mediastinal fat, and
other similar anatomic structures within the
pericardial sac.
Dark-blood (double inversion recovery) imaging
can measure pericardial thickness accurately.
Fat-sensitive imaging (based on chemical shift
or on T1 values) can discern pericardial fat from
other materials.
Dynamic MRI can identify constrictive disease
(failure to expand for the last 6/20 frames of
diastole).
MRI can also assess for adhesions by placing
demagnetization stripes to observe for
translational motion at the pericardium, and it
can assess for restrictive disease by strain
mapping.
CT computed tomography, MRI magnetic resonance imaging, CMR cardiac MR, SVC superior vena cava, IVC inferior vena cava, RV right ventricle, LV left ventricle, RA right atrium, LA left
atrium, CP Contrictive Pericarditis, TDI tissue Doppler imaging
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Table 13.2 Myocardial disorder assessment with cardiac imaging modalities
Myocardial
condition Defi nition
CT Angiographic
diagnostic fi nding
Echocardiographic diagnostic
fi nding MRI diagnostic fi nding
Dilated
cardiomyopathy
Dilated
cardiomyopathy is
a condition in
which the
ventricular
chambers show
increased systolic
and diastolic
volume and a low
Ejection Fraction
(<40 %) [ 1 , 34 ].
Gated CT scanning is
an accurate means of
evaluating cardiac
function, especially
with the use of
ultrafast CT scanning
and 50-millisecond
image acquisition.
Only 1 short
breath-hold period is
required, and
defi nition of the
endocardial margins is
excellent, allowing a
degree of automation
for defi ning the
ventricular volumes.
Increased in left
ventricular enddiastolic and
end-systolic volume.
Left ventricular wall
thinning.
Decrease ejection
fraction.
Left ventricular spherical
dilatation.
Normal or reduced wall thickness.
Poor systolic wall thickening, and/
or reduced inward endocardial
systolic motion.
All of the systolic indices are
reduced, including left ventricular
fractional shortening, fractional
area change, and ejection fraction.
Four chamber cardiac enlargement
is often present.
On M-mode, additional features
related to systolic dysfunction are
increased separation of the mitral
leafl et E point from the septum,
poor mitral valve opening, poor
aortic valve opening and early
closure from a reduced stroke
volume, and poor systolic aortic
root motion.
Doppler has been used in dilated
cardiomyopathy to measure
decreased stroke volume
MRI and magnetic resonance
angiography (MRA) are the most
accurate methods for assessing cardiac
anatomy or function. MRI/MRA is
used when echocardiography is
inadequate, as this study is often not
used because of its relatively high cost
and limited availability, as well as
contraindications if ferromagnetic
metallic foreign bodies are present in
the patient.
M.A. Latif and K. Nasir
https://t.me/medicina_free
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