Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3752_Библиотеки_им_академика_М_И_Перельмана
.pdf
213
scan times have decreased, reducing the amount of contrast
material per scan [ 8 ]. Such techniques are ideal for the
assessment of patients with chest pain who also have calcifi ed coronaries, as well as the follow up of patients with
advanced heart disease post coronary artery bypass surgery
or multiple stent implantations.
Using iodine molecules as a tracer, current research has
demonstrated that by measuring the concentration in time of
the tracer in the myocardium, MDCT can determine absolute
blood fl ow in different regions of the myocardium [ 2 ].
Recent attention to patients with chest pain but no obstructive epicardial CAD (syndrome X) has demonstrated that in
Signal Density Curve (HU)
Time (seconds)
LV
Stenosed
Remote
700
600
500
400
300
200
100
0
147
10131619222528313437404346
49
a
b
Fig. 12.1 Myocardial enhancement upslope curves for the left ventricular cavity, remote and ischemic region ( a ). The usual timing of a coro-
nary CT angiogram is shown as the region between the vertical bars.
following the contrast bolus with an ROI placed at the ischemic ( fi lled
circle ) and remote ( open circle ) areas present a delta in myocardial
enhancement intensity ( b ) that can be measured, as shown inside the
dashed box ( a )
Fig. 12.2 Schematic coverage of a 256-detector as compared to a 64-detector MDCT scanner
12 Cardiovascular CT for Perfusion and Delayed Contrast Enhancement Imaging
https://t.me/medicina_free

214
a substantial proportion of these individuals microvascular
processes can be identifi ed by perfusion reserve measurements in association with traditional CAD risk factors such
as hypercholesterolemia, hypertension and smoking as well
as with diabetes [ 9 ]. The possibility of quantifying epicardial
coronary plaque while also assessing microvascular disease
during maximal vasodilatation enables coronary MDCTA –
armored with high spatial resolution – to characterize macrovascular atherosclerosis as well as microvascular dysfunction
secondary to atherosclerosis or other disease processes. The
capability of quantifying myocardial blood fl ow by contrast
enhanced MDCT represent a “quantum leap” in our ability to
assess and characterize the entire process of cardiac
atherosclerosis.
Single center studies [ 10 – 12 ] have demonstrated the
incremental diagnostic performance of MDCT stress perfusion imaging in addition to coronary CTA in assessing
fl ow- limiting stenosis. Subsequently, the CORE320 study
[ 13 ], a multicenter, international study also validated
improved diagnostic accuracy of coronary CTA plus MDCT
perfusion imaging compared to the reference standard of
invasive coronary angiography plus a corresponding perfusion defi cit on SPECT imaging. On head to head comparison, the ability of stress MDCT perfusion imaging to detect
myocardial ischemia was similar to SPECT imaging, with
better MDCT sensitivity for left main and multivessel stenoses [ 14 ]. This enhanced sensitivity is attributed to better
spatial resolution of MDCT and favorable kinetics of iodine
dye which serves as a tracer in MDCT perfusion imaging.
Previously limited to single center experience [ 10 , 15 –
17 ], current efforts are directed towards expanding this tech-
nique to different MDCT scanner systems (including 64-,
128-, 256-, and 320-slice) and across multivendor platform
using different stress agents. The ongoing multicenter, multivendor study of Regadenoson in Subjects Undergoing
Stress Myocardial Perfusion Imaging Using Multidetector
Computed Tomography Compared to Single Photon
Emission Computed Tomography [ 18 ] ( www.clinicaltrials.
gov , NCT01334918) is a step in this direction.
MDCT for Detection of Myocardial Fibrosis
and Viability
The ability to distinguish dysfunctional but viable myocardium from nonviable tissue after acute or chronic ischemia
has important implications for the therapeutic management
of patients with coronary artery disease [ 19 , 20 ]. Image-
based characterization of myocardial scar morphology can
identify those patients with hibernating myocardium who
may achieve functional systolic recovery with revascularization [ 21 ]. The assessment of myocardial viability and infarct
morphology with delayed contrast-enhanced MRI has been
well validated over the past several years and is performed
routinely at several clinical cardiac MRI centers.
The recent advent of MDCT technology has expanded its
potential for a more comprehensive evaluation of cardiovascular diseases. While hypo attenuation in the non-contrasted
scan (due to fatty degeneration of the infarcted area) or during the contrast enhanced coronary angiography scan has
been shown to demonstrate areas of previous MI, it is largely
underestimated by MDCT [ 22 , 23 ]. Delayed enhanced
MDCT (DE-MDCT) myocardial imaging can accurately
identify and characterize morphological features of acute
and healed myocardial infarction, including infarct size,
transmurality, and the presence of microvascular obstruction
and collagenous scar (Fig. 12.4 ) [ 24 , 25 ]. Infarcted myocar-
dial tissue by DE-MDCT is characterized by well-delineated
hyper-enhanced regions, whereas regions of microvascular
obstruction by MDCT are characterized by hypoenhancement on imaging early after MI [ 24 , 25 ]. Detection
of fi brosis by DE-MDCT has been validated against gold
standards such as histology and contrast enhanced MRI [ 24 ,
26 – 28 ]. In addition, recent studies [ 29 , 30 ] have also sub-
stantiated the utility of contrast enhanced MDCT in assessment of extracellular volume fraction (ECV), a measurement
of interstitial myocardial volume expansion which corresponds to diffuse myocardial fi brosis.
Introduction of delayed contrast enhanced MDCT imaging in assessment of hypertrophic cardiomyopathy has been
Fig. 12.3 Schematic
demonstration of the radiation
exposure time differences
between retrospective gating
(single heart beat) and
prospective triggering used in
wide coverage MDCT scanners
R.K. Sharma et al.
https://t.me/medicina_free

215
abc
Fig. 12.4 Typical contrast-enhanced myocardial MDCT images showing axial slices ( a ) at baseline (preinfarct) 5 min after contrast,
( b ) postinfarct during fi rst-pass contrast injection, and ( c ) postinfarct
5 min after contrast injection. the infarcted region is represented by the
subendocardial anterior hyperintense region ( arrows )
a
de
bc
Fig. 12.5 Multiplanar reconstruction of the left ventricular basal ( a ),
mid ( b ), and apical short-axis ( c ) views and horizontal ( d ) and vertical
long-axis ( e ) views show delayed hyperenhancement in the basal ante-
rior, basal to mid septal, and apical septal walls ( arrows ). A small aneu-
rysm is noted in the apical septum ( c , d ) (Reprinted from Gore R et al.
[ 41 ] with permission from Elsevier)
12 Cardiovascular CT for Perfusion and Delayed Contrast Enhancement Imaging
https://t.me/medicina_free

216
of particular interest where it has shown comparable accuracy
to delayed contrast enhanced MRI in detecting myocardial
fi brosis (Fig. 12.5 ) [ 31 – 33 ]. This has allowed comprehensive
evaluation of myocardial tissue characteristics with signifi cant bearing on the management [ 31 ], prognosis [ 34 ], and
follow-up in these patients who may not be ideal candidates
for MRI given signifi cant proportion of them have implantable cardiac defi brillator.
The mechanism of myocardial hyperenhancement and
hypo-enhancement in acutely injured myocardial territories
after iodinated contrast administration is similar to that proposed for delayed gadolinium-enhanced MRI [ 19 ]. Under
conditions of normal myocyte function, sarcolemmal membranes serve to exclude iodine from the intracellular space.
After myocyte necrosis, however, membrane dysfunction
ensues, and iodine molecules are able to penetrate the cell.
Because 75 % of the total myocardial volume is intracellular, large increases in the volume of distribution are achieved,
which results in marked hyperenhancement relative to the
non-injured myocytes. The mechanism of hyperenhance-
ab
c
Fig. 12.6 Multiplanar reconstruction images showing normal left anterior descending ( a ), left circumfl ex ( b ), and right coronary artery ( c )
R.K. Sharma et al.
https://t.me/medicina_free

217
ment of healed myocardial infarction or collagenous scar is
thought to be related to an accumulation of contrast media
in the interstitial space between collagen fi bers and thus an
increased volume of distribution compared with that of
tightly packed myocytes. The low signal intensity of microvascular obstruction regions despite restoration of normal
fl ow through the infarct-related artery is explained by the
death and subsequent cellular debris blockage of intramyocardial capillaries at the core of the damaged region. These
obstructed capillaries do not allow contrast material to fl ow
into the damaged bed, which results in a region of low signal
intensity compared with normal myocardium. In minutes to
hours, contrast material is able to penetrate this relatively
“no refl ow” region, and the necrotic myocytes that reside in
that myocardial territory then become hyperenhanced as
iodine is internalized by the cell. In weeks the microvascular
obstruction area is replaced by collagenous scar tissue and
the former dark area now become bright. Since the transmu-
rality of delayed enhancement predicts functional recovery
after revascularization [ 21 ], the better spatial resolution of
MDCT as compared to CMR may infl uence the accuracy of
viability assessment, but no study thus far has tested this
hypothesis.
Integrating All Methodologies into One
Examination
The number of scans to be performed varies for individual
patients, depending on the clinical questions to be answered.
For a comprehensive cardiac evaluation, in the future four
consecutive scans should be performed, with acceptable
radiation dose. The fi rst one would be a low dose prospectively unenhanced calcium score scan (<1 mSv) [ 35 ], the
second one also prospectively gated and contrasted for the
acquisition of coronary angiography and morphology
(approximately 1–4 mSv) [ 36 ], the third would be the stress
perfusion study during maximum vasodilation, which could
be performed as a “static” perfusion acquisition, i.e. one
acquisition at peak contrast opacifi cation of the myocardium
(approximately 1–4 mSv); or alternatively as a “dynamic”
perfusion acquisition, i.e. several low dose prospective
acquisitions representing the contrast passage through the
heart (approximately 3–7 mSv) (Fig. 12.6 and 12.7 , Videos
12.1 , 12.2 , 12.3 , and 12.4 ).[ 16 ] Static perfusion has been
more validated and can be performed in scanners with 4 cm
coverage or more, but dynamic perfusion might improve
accuracy, by allowing construction of contrast wash in curves
in the myocardium. For that, one would need a scanner with
at least 8 cm coverage, multiple “shots” are acquired during
contrast administration and at least a large portion of the
myocardium needs to be imaged at each “shot”. Finally, a
low dose prospectively triggered delayed enhancement scan
would be performed 5–10 min after the stress study
(1–3 mSv) [ 36 ]. The fi nal result would be calcium score,
coronary anatomy, morphology, stress perfusion and viability in a “one stop shop” scan that lasts around 20 min.
(Fig. 12.8 ) shows a timeline for a comprehensive cardiac
evaluation. Employing dose reduction techniques [ 37 ] like
Fig. 12.7 Multiplanar reconstruction image showing obstructive
coronary artery stenosis of left anterior descending artery ( a )
Calcium score scan
1-2mSv
Helical stress perfusion
scan (7-9 mSv)
Start adenosine
infusion
3–4 min 3–4 min
End adenosine
Prospectively
triggered scan
with contrast for
coronary anatomy
(3–4 mSv)
Prospectively triggered
no contrast delayed
enhancement scan
(3–4 mSv)
Time approximately 20 minutes
Fig. 12.8 Proposed timeline for a
comprehensive MDCT scan
12 Cardiovascular CT for Perfusion and Delayed Contrast Enhancement Imaging
https://t.me/medicina_free

218
limiting scan length, prospective scan acquisition, post processing methods such as iterative reconstruction and fi ltered
back projection [ 38 ], and availability of next generation
scanners with faster gantry rotation time and wide volume
coverage could result in substantial reduction in the amount
of radiation exposure, allowing one to acquire enhanced
information at the cost of less than 10 mSv of radiation.
Clinical Pearls DE
1. The optimal contrast dose to be used for DE images is
still not defi ned, but studies in humans [ 23 , 25 ] showed
that the usual amount used for a 16-detector coronary
CTA (120–140 ml) provide good enhancement and
could be as low as 80–90 ml using advanced scanner
system.[ 31 ]
2. For optimal contrast between the infarcted and the remote
regions, the delayed enhanced scan should be done
between 5 and 10 min after contrast injection.[ 24 ]
3. Most of the studies done so far reconstructed the images
in end-diastole for DE analysis.
4. The delayed enhancement pattern is important to differentiate between ischemic and non-ischemic etiologies,
the earlier being found as a wave front from the endocardium to the pericardium. Non-ischemic cardiomyopathies can also result in myocardial scar that appears on
DE images, but those tend to be patchy and do not follow
the endocardium-to-epicardium pattern seen in ischemic
cardiomyopathy.[ 39 ]
5 Molecular size of the iodinated contrast material may
affect the uptake of the tissue by that agent. Two trials
used a smaller molecule with high iodine concentration
(iomeprol) [ 23 , 25 ] while another one used a larger mol-
ecule with a lower iodine concentration (iodixanol).[ 24 ]
It is still unclear which one is the best, if any, or whether
other factors (such as ionic polarization) are important.
6. DE imaging by MDCT can be obtained both in patients
with an acute MI as well as patients that had infarcts more
than 6 months prior to imaging.[ 23 – 25 ]
7. Microvascular obstruction can be imaged in the early
phase after MI, and it is gradually replaced by fi brous tissue that appears bright on the DE images 2–4 weeks after
the MI.[ 40 ]
Clinical Pearls Ischemia
1. MDCT myocardial perfusion is shown to have incremental diagnostic accuracy in identifying or excluding hemodynamically signifi cant stenosis.
2. Adenosine is the drug most often tested for stress perfusion in MDCT, due to its short onset and offset, safety
profi le and proved effi cacy in diverging blood from ischemic to non-ischemic territories. Utility of regadenoson is
currently being explored.[ 18 ]
3. Since adenosine usually increases heart rate, aggressive
beta-blockade should be pursued. Adequate hydration
prior to the scan may potentially blunt the refl ex increase
in heart rate from the adenosine infusion.
4. Nitroglycerin should not be given concomitantly to adenosine, since it can reverse the ischemic effects of the latter, as well as decrease blood pressure and increase heart
rate even further.
5. The visual contouring of the underperfused myocardial
areas is the method currently being applied in addition to
the semi-automated software. However, the best threshold for quantitatively discriminating ischemia from
remote myocardium is still not defi ned.
6. The problem of balanced ischemia will potentially be
solved with wide coverage MDCT scanners by allowing
absolute quantifi cation of myocardial blood fl ow.
7. Whether stress perfusion scans will be recommended to
everyone or just selected patient populations (such as the
ones with high calcium scores) is still under
investigation.
References
1. Lerman LO, Siripornpitak S, Maffei NL, Sheedy 2nd PF, Ritman
EL. Measurement of in vivo myocardial microcirculatory function
with electron beam CT. J Comput Assist Tomogr. 1999;23:390–8.
2. George RT, Jerosch-Herold M, Silva C, Kitagawa K, Bluemke DA,
Lima JA, Lardo AC. Quantifi cation of myocardial perfusion using
dynamic 64-detector computed tomography. Invest Radiol.
2007;42:815–22.
3. Smith Jr SC, Feldman TE, Hirshfeld Jr JW, Jacobs AK, Kern MJ,
King SB, Morrison DA, O'Neil WW, Schaff HV, Whitlow PL,
Williams DO, Antman EM, Adams CD, Anderson JL, Faxon DP,
Fuster V, Halperin JL, Hiratzka LF, Hunt SA, Nishimura R, Ornato
JP, Page RL, Riegel B. ACC/AHA/SCAI 2005 guideline update for
percutaneous coronary intervention: a report of the American
College of Cardiology/American Heart Association Task Force on
Practice Guidelines (ACC/AHA/SCAI Writing Committee to
Update 2001 Guidelines for Percutaneous Coronary Intervention.
Circulation. 2006;113:166–286.
4. van Werkhoven JM, Schuijf JD, Gaemperli O, Jukema JW, Boersma
E, Wijns W, Stolzmann P, Alkadhi H, Valenta I, Stokkel MP, Kroft
LJ, de Roos A, Pundziute G, Scholte A, van der Wall EE, Kaufmann
PA, Bax JJ. Prognostic value of multislice computed tomography
and gated single-photon emission computed tomography in patients
with suspected coronary artery disease. J Am Coll Cardiol.
2009;53:623–32.
5. Rodes-Cabau J, Candell-Riera J, Angel J, de Leon G, Pereztol O,
Castell-Conesa J, Soto A, Anivarro I, Aguade S, Vazquez M,
Domingo E, Tardif JC, Soler-Soler J. Relation of myocardial perfusion defects and nonsignifi cant coronary lesions by angiography
with insights from intravascular ultrasound and coronary pressure
measurements. Am J Cardiol. 2005;96:1621–6.
6. Ragosta M, Bishop AH, Lipson LC, Watson DD, Gimple LW,
Sarembock IJ, Powers ER. Comparison between angiography and
R.K. Sharma et al.
https://t.me/medicina_free

219
fractional fl ow reserve versus single-photon emission computed
tomographic myocardial perfusion imaging for determining lesion
signifi cance in patients with multivessel coronary disease. Am
J Cardiol. 2007;99:896–902.
7. Schuijf JD, Wijns W, Jukema JW, Atsma DE, de Roos A, Lamb HJ,
Stokkel MP, Dibbets-Schneider P, Decramer I, De Bondt P, van der
Wall EE, Vanhoenacker PK, Bax JJ. Relationship between noninvasive coronary angiography with multi-slice computed tomography
and myocardial perfusion imaging. J Am Coll Cardiol.
2006;48:2508–14.
8. Hein PA, May J, Rogalla P, Butler C, Hamm B, Lembcke
A. Feasibility of contrast material volume reduction in coronary
artery imaging using 320-slice volume CT. Eur Radiol.
2010;20:1337–43.
9. Buchthal SD, den Hollander JA, Merz CN, Rogers WJ, Pepine CJ,
Reichek N, Sharaf BL, Reis S, Kelsey SF, Pohost GM. Abnormal
myocardial phosphorus-31 nuclear magnetic resonance spectroscopy in women with chest pain but normal coronary angiograms. N
Engl J Med. 2000;342:829–35.
10. Cury RC, Magalhaes TA, Borges AC, Shiozaki AA, Lemos PA,
Junior JS, Meneghetti JC, Rochitte CE. Dipyridamole stress and
rest myocardial perfusion by 64-detector row computed tomography in patients with suspected coronary artery disease. Am
J Cardiol. 2010;106:310–5.
11. George RT, Arbab-Zadeh A, Miller JM, Vavere AL, Bengel FM,
Lardo AC, Lima JA. Computed tomography myocardial perfusion imaging with 320-row detector computed tomography
accurately detects myocardial ischemia in patients with
obstructive coronary artery disease. Circ Cardiovasc Imaging.
2012;5:333–40.
12. Rief M, Zimmermann E, Stenzel F, Martus P, Stangl K, Greupner J,
Knebel F, Kranz A, Schlattmann P, Laule M, Dewey M. Computed
tomography angiography and myocardial computed tomography
perfusion in patients with coronary stents: prospective intraindividual comparison with conventional coronary angiography. J Am
Coll Cardiol. 2013;62:1476–85.
13. Rochitte CE, George RT, Chen MY, Arbab-Zadeh A, Dewey M,
Miller JM, Niinuma H, Yoshioka K, Kitagawa K, Nakamori S,
Laham R, Vavere AL, Cerci RJ, Mehra VC, Nomura C, Kofoed KF,
Jinzaki M, Kuribayashi S, de Roos A, Laule M, Tan SY, Hoe J, Paul
N, Rybicki FJ, Brinker JA, Arai AE, Cox C, Clouse ME, Di Carli
MF, Lima JA. Computed tomography angiography and perfusion to
assess coronary artery stenosis causing perfusion defects by single
photon emission computed tomography: the CORE320 study. Eur
Heart J. 2014;35:1120–30.
14. George RT, Mehra VC, Chen MY, Kitagawa K, Arbab-Zadeh A,
Miller JM, Matheson MB, Vavere AL, Kofoed KF, Rochitte CE,
Dewey M, Yaw TS, Niinuma H, Brenner W, Cox C, Clouse ME,
Lima JA, Di Carli M. Myocardial CT perfusion imaging and
SPECT for the diagnosis of coronary artery disease: a Head-toHead comparison from the CORE320 multicenter diagnostic performance study. Radiology. 2014;272:407–16.
15. Rocha-Filho JA, Blankstein R, Shturman LD, Bezerra HG, Okada
DR, Rogers IS, Ghoshhajra B, Hoffmann U, Feuchtner G, Mamuya
WS, Brady TJ, Cury RC. Incremental value of adenosine-induced
stress myocardial perfusion imaging with dual-source CT at cardiac
CT angiography. Radiology. 2010;254:410–9.
16. George RT, Arbab-Zadeh A, Miller JM, Kitagawa K, Chang HJ,
Bluemke DA, Becker L, Yousuf O, Texter J, Lardo AC, Lima
JA. Adenosine stress 64- and 256-row detector computed tomography angiography and perfusion imaging: a pilot study evaluating
the transmural extent of perfusion abnormalities to predict atherosclerosis causing myocardial ischemia. Circ Cardiovasc Imaging.
2009;2:174–82.
17. Blankstein R, Shturman LD, Rogers IS, Rocha-Filho JA, Okada
DR, Sarwar A, Soni AV, Bezerra H, Ghoshhajra BB, Petranovic M,
Loureiro R, Feuchtner G, Gewirtz H, Hoffmann U, Mamuya WS,
Brady TJ, Cury RC. Adenosine-induced stress myocardial perfusion imaging using dual-source cardiac computed tomography.
J Am Coll Cardiol. 2009;54:1072–84.
18. Cury RC, Kitt TM, Feaheny K, Akin J, George RT. Regadenosonstress myocardial CT perfusion and single-photon emission CT:
rationale, design, and acquisition methods of a prospective, multicenter, multivendor comparison. J Cardiovasc Comput Tomogr.
2014;8:2–12.
19. Wu KC, Lima JA. Noninvasive imaging of myocardial viability: current techniques and future developments. Circ Res. 2003;93:1146–58.
20. Pagley PR, Beller GA, Watson DD, Gimple LW, Ragosta
M. Improved outcome after coronary bypass surgery in patients
with ischemic cardiomyopathy and residual myocardial viability.
Circulation. 1997;96:793–800.
21. Kim RJ, Wu E, Rafael A, Chen EL, Parker MA, Simonetti O,
Klocke FJ, Bonow RO, Judd RM. The use of contrast-enhanced
magnetic resonance imaging to identify reversible myocardial dysfunction. N Engl J Med. 2000;343:1445–53.
22. Sanz J, Weeks D, Nikolaou K, Sirol M, Rius T, Rajagopalan S,
Dellegrottaglie S, Strobeck J, Fuster V, Poon M. Detection of
healed myocardial infarction with multidetector-row computed
tomography and comparison with cardiac magnetic resonance
delayed hyperenhancement. Am J Cardiol. 2006;98:149–55.
23. Mahnken AH, Koos R, Katoh M, Wildberger JE, Spuentrup E,
Buecker A, Gunther RW, Kuhl HP. Assessment of myocardial viability in reperfused acute myocardial infarction using 16-slice computed tomography in comparison to magnetic resonance imaging.
J Am Coll Cardiol. 2005;45:2042–7.
24. Lardo AC, Cordeiro MA, Silva C, Amado LC, George RT,
Saliaris AP, Schuleri KH, Fernandes VR, Zviman M, Nazarian S,
Halperin HR, Wu KC, Hare JM, Lima JA. Contrast-enhanced
multidetector computed tomography viability imaging after
myocardial infarction: characterization of myocyte death,
microvascular obstruction, and chronic scar. Circulation.
2006;113:394–404.
25. Gerber BL, Belge B, Legros GJ, Lim P, Poncelet A, Pasquet A,
Gisellu G, Coche E, Vanoverschelde JL. Characterization of acute
and chronic myocardial infarcts by multidetector computed tomography: comparison with contrast-enhanced magnetic resonance.
Circulation. 2006;113:823–33.
26. Bauer RW, Kerl JM, Fischer N, Burkhard T, Larson MC, Ackermann
H, Vogl TJ. Dual-energy CT for the assessment of chronic myocardial infarction in patients with chronic coronary artery disease: comparison with 3-T MRI. AJR Am J Roentgenol. 2010;195:639–46.
27. Schuleri KH, Centola M, George RT, Amado LC, Evers KS,
Kitagawa K, Vavere AL, Evers R, Hare JM, Cox C, McVeigh ER,
Lima JA, Lardo AC. Characterization of peri-infarct zone heterogeneity by contrast-enhanced multidetector computed tomography: a
comparison with magnetic resonance imaging. J Am Coll Cardiol.
2009;53:1699–707.
28. Senra T, Shiozaki AA, Salemi VM, Rochitte CE. Delayed enhancement by multidetector computed tomography in endomyocardial
fi brosis. Eur Heart J. 2008;29:347.
29. Nacif MS, Kawel N, Lee JJ, Chen X, Yao J, Zavodni A, Sibley CT,
Lima JA, Liu S, Bluemke DA. Interstitial myocardial fi brosis
assessed as extracellular volume fraction with low-radiation-dose
cardiac CT. Radiology. 2012;264:876–83.
30. Nacif MS, Liu Y, Yao J, Liu S, Sibley CT, Summers RM, Bluemke
DA. 3D left ventricular extracellular volume fraction by
low- radiation dose cardiac CT: assessment of interstitial myocardial fi brosis. J Cardiovasc Comput Tomogr. 2013;7:51–7.
31. Zhao L, Ma X, Delano MC, Jiang T, Zhang C, Liu Y, Zhang
Z. Assessment of myocardial fi brosis and coronary arteries in
hypertrophic cardiomyopathy using combined arterial and delayed
12 Cardiovascular CT for Perfusion and Delayed Contrast Enhancement Imaging
https://t.me/medicina_free

220
enhanced CT: comparison with MR and coronary angiography. Eur
Radiol. 2013;23:1034–43.
32. Langer C, Lutz M, Eden M, Ludde M, Hohnhorst M, Gierloff C,
Both M, Burchert W, Faber L, Horstkotte D, Frey N, Prinz
C. Hypertrophic cardiomyopathy in cardiac CT: a validation study
on the detection of intramyocardial fi brosis in consecutive patients.
Int J Cardiovasc Imaging. 2014;30:659–67.
33. Berliner JI, Kino A, Carr JC, Bonow RO, Choudhury L. Cardiac
computed tomographic imaging to evaluate myocardial scarring/
fi brosis in patients with hypertrophic cardiomyopathy: a comparison with cardiac magnetic resonance imaging. Int J Cardiovasc
Imaging. 2013;29:191–7.
34. Shiozaki AA, Senra T, Arteaga E, Martinelli Filho M, Pita CG,
Avila LF, Parga Filho JR, Mady C, Kalil-Filho R, Bluemke DA,
Rochitte CE. Myocardial fi brosis detected by cardiac CT predicts
ventricular fi brillation/ventricular tachycardia events in patients
with hypertrophic cardiomyopathy. J Cardiovasc Comput Tomogr.
2013;7:173–81.
35. Detrano R, Guerci AD, Carr JJ, Bild DE, Burke G, Folsom AR, Liu
K, Shea S, Szklo M, Bluemke DA, O'Leary DH, Tracy R, Watson
K, Wong ND, Kronmal RA. Coronary calcium as a predictor of
coronary events in four racial or ethnic groups. N Engl J Med.
2008;358:1336–45.
36. Chang HJ, George RT, Schuleri KH, Evers K, Kitagawa K, Lima
JA, Lardo AC. Prospective electrocardiogram-gated delayed
enhanced multidetector computed tomography accurately quantifi es infarct size and reduces radiation exposure. JACC Card
Imaging. 2009;2:412–20.
37. Halliburton SS, Abbara S, Chen MY, Gentry R, Mahesh M, Raff
GL, Shaw LJ, Hausleiter J. SCCT guidelines on radiation dose and
dose-optimization strategies in cardiovascular CT. J Cardiovasc
Comput Tomogr. 2011;5:198–224.
38. Chen MY, Steigner ML, Leung SW, Kumamaru KK, Schultz K,
Mather RT, Arai AE, Rybicki FJ. Simulated 50 % radiation dose
reduction in coronary CT angiography using adaptive iterative dose
reduction in three-dimensions (AIDR3D). Int J Cardiovasc
Imaging. 2013;29:1167–75.
39. Gottlieb I, Macedo R, Bluemke DA, Lima JA. Magnetic resonance
imaging in the evaluation of non-ischemic cardiomyopathies: current applications and future perspectives. Heart Fail Rev.
2006;11:313–23.
40. Wu KC, Kim RJ, Bluemke DA, Rochitte CE, Zerhouni EA, Becker
LC, Lima JA. Quantifi cation and time course of microvascular
obstruction by contrast-enhanced echocardiography and magnetic
resonance imaging following acute myocardial infarction and
reperfusion. J Am Coll Cardiol. 1998;32:1756–64.
41. Gore R, Abraham T, George RT. CT characterization of myocardial
substrate in hypertrophic cardiomyopathy. J Cardiovasc Comput
Tomogr. 2014;8(22):166–9.
R.K. Sharma et al.
https://t.me/medicina_free

221
© Springer International Publishing 2016
M.J. Budoff, J.S. Shinbane (eds.), Cardiac CT Imaging: Diagnosis of Cardiovascular Disease,
DOI 10.1007/978-3-319-28219-0_13
Cardiovascular CT for Assessment
of Pericardial/Myocardial Disease
Processes
Muhammad Aamir Latif and Khurram Nasir
Abstract
Pericardial and myocardial diseases represent an important cause of morbidity and mortality.
Although echocardiography remains the initial standard diagnostic tool for identifying
these diseases it has limited detail for the morphological and functional analysis of the
pericardium and myocardium. Cardiac CT (CCT) and MR (CMR) are the primary modalities
of choice when comprehensive functional assessment of the heart is required. These imaging
techniques provide advanced information on anatomy and cardiac function to optimize
diagnosis and treatment. However, as CMR is relatively more costly and time consuming, it
is often only used when diagnosis is not clear. Due to the volumetric nature of image
acquisition, cardiac CT provides an accurate and reproducible method for assessing both
myocardial and pericardial morphology and function. The excellent spatial resolution and
contrast to noise ratio of CT allows for the detection of mural thrombi in patients with
severely reduced left ventricular function. CCT can easily help identify pericardial diseases
such as infl ammation, effusion, pericardial cyst, benign or malignant masses, as well as
pericardial calcifi cation in the case of constrictive pericarditis. CCT is also profi cient in
diagnosing the functional assessment of the heart. As most of cardiomyopathies have
functional compromise, CCT is best suited for cardiomyopathies in terms of functional
analysis. With the advancement of CT technology, radiation exposure is minimal, and with
continued improvement in post-processing software, it is able to produce a variety of highquality images in multiple reformats with historically low radiation and contrast dose. The
new General Electric (GE) Revolution CT scanner has made it possible to image the heart
with abnormal rate and rhythm without compromising image quality. It is especially useful
for patients who have contraindications to beta-blockers or who have atrial fi brillation.
M. A. Latif , MD
Department of Medicine , Center for Healthcare Advancement and
Outcomes, Baptist Health South Florida , 6262 Sunset Dr. Suite
200 , Miami , FL 33143 , USA
e-mail: draamirlatif@gmail.com; muhammadl@baptisthealth.net
K. Nasir , MD, MPH (
*)
Department of Medicine , Center for Healthcare Advancement and
Outcomes, Baptist Health South Florida , 1691 Michigan Avenue
Suite 500 , Miami Beach , FL 33139 , USA
e-mail: khurramn@baptisthealth.net; knasir1@jhmi.edu
Electronic supplementary material The online version of this
chapter (doi: 10.1007/978-3-319-28219-0_13 ) contains supplemen-
tary material, which is available to authorized users.
1 3
https://t.me/medicina_free

222
Keywords
Pericardial • Myocardial • Computed Tomography • Cardiomyopathies • Dilated
Cardiomyopathy • Restrictive Cardiomyopathy • Takotsubo Cardiomyopathy •
Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC)
Introduction
The twenty fi rst century has already seen extensive research
to benefi t human civilization. Theories and concepts previously considered imaginary and magical are now being
implemented in a practical way with the help of technology.
Cardiac CT is one such technology. It started as an imaging
machine to augment x-ray radiography and give detailed
three-dimensional images of the body’s internal organs.
Cardiac CT use for heart images has received great attention
worldwide because previously it was hard to image a continuously moving structure in the body. Cardiac CT is able to
freeze the image in each phases of the cardiac cycle and with
high temporal and spatial resolution give a detailed anatomical and physiological picture of the heart. Although the current primary clinical use of contrast-enhanced cardiac
computed tomography (CCT) remains the exclusion of coronary artery disease in low to intermediate risk symptomatic
patients, this modality also offers a unique opportunity to
assess both the pericardium and myocardium. Given the
associated contrast and radiation exposure, CCT presently
serves as an adjunct to echocardiography and cardiac MRI
for this purpose. However, CCT provides superb delineation
of the pericardium and can precisely localize lesions as well
as aid in their characterization. Further, CCT can effectively
evaluate morphology and function in various myocardial diseases, including the various cardiomyopathies. The volumetric nature of image acquisition with CCT provides an
accurate and reproducible method for quantifying ventricular mass, volumes, and function. This chapter will discuss
the application of CCT in the assessment of various myocardial and pericardial disease processes.
Cardiac CT Advancement
Due to the volumetric nature of image acquisition, cardiac
CT provides an accurate and reproducible method for assessing both myocardial and pericardial morphology and function. The excellent spatial resolution and contrast to noise
ratio of CT allows for the detection of mural thrombi in
patients with severely reduced left ventricular function.
While echocardiography remains the primary noninvasive
imaging modality for evaluation of the myocardium and
pericardium, CCT serves as a valuable tool for further evaluation due to its inherently superb spatial resolution and soft
tissue contrast. With further improvements in CCT technol-
ogy, including refi nements in temporal resolution and dramatic reductions in radiation exposure, CCT may play a
larger role in the evaluation of patients with known or suspected diseases of the myocardium and pericardium. The
main concern of cardiac CT is radiation exposure. With
recent advancement in technology, radiation exposure has
been minimized. Newer CT protocols have been developed
to do selective gating images that lower the dose delivered
during non-diagnostic portions of the cardiac cycle. Most
recently the General Electric Revolution CT scanner has the
ability to even further reduce the radiation dose by selective
retrospective imaging. Previously for gating purposes, it was
required to use either retrospective or prospective gating
synchronized with the patient ECG monitor. The newer
scanners no longer require a decision for which mode (retrospective or prospective) to be used but rather the focus is
primarily on when to image within the cardiac cycle according to the ECG strip as interpreted by the scanner. This has
further reduced radiation exposure. Technological advancement has also overcome the dependence on low heart rate,
beat-to-beat variability and their relation to image quality.
Now excellent image quality can be obtained with heart rates
ranging from 70 to 90 bpm by using newer CT protocols.
The Revolution CT scanner has robust, high performance
cardiac imaging based on three points of excellence: tempo-
ral resolution (0.28 s gantry rotation, intelligent motion
correction), spatial resolution and whole organ coverage
(160 mm detector). With these improvements the cardiac CT
exam provides the best possible overall picture of the heart,
including the pericardium and myocardium. The cinematic
mode is a feature of cardiac CT software to provide functional global assessment of the myocardium. These imaging
modalities can also play an important role in prognosis, as
well as direct treatment and further management.
CT Imaging of Myocardial Disease
Myocardial diseases or cardiomyopathies can be classifi ed
based on their origin, anatomy, physiology, histopathology
or genetics. The World Health Organization (WHO) defi nes
the cardiomyopathies as diseases of myocardial tissue associated with cardiac dysfunction and subdivides them mainly
into four categories: dilated, restrictive, hypertrophic, and
arrhythmogenic right ventricular cardiomyopathy (ARVC)
[ 1 ]. Non-invasive imaging can determine whether abnormal-
ities are present in the myocardium, valves, pericardium, or
M.A. Latif and K. Nasir
https://t.me/medicina_free
Соседние файлы в папке Библиотека им академика М.И. Перельмана
