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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
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100
0
147
10131619222528313437404346
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a
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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
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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 [ 1012 ] 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 , 2628 ]. 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
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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)
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of particular interest where it has shown comparable accuracy to delayed contrast enhanced MRI in detecting myocardial fi brosis (Fig. 12.5 ) [ 3133 ]. 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 )
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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
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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.[ 2325 ]
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.
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© 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.
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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
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