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DOI: 10.1148/radiol.2471070332
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(Radiology 2008;247:49-56.)
© RSNA, 2008

Cardiac Imaging

Reperfused Myocardial Infarction: Contrast-enhanced 64-Section CT in Comparison to MR Imaging1

Koen Nieman, MD, PhD, Michael D. Shapiro, DO, Maros Ferencik, MD, PhD, Cesar H. Nomura, MD, Suhny Abbara, MD, Udo Hoffmann, MD, Herman K. Gold, MD, Ik-Kyung Jang, MD, PhD, Thomas J. Brady, MD, and Ricardo C. Cury, MD

1 From the Cardiac MRI-PET-CT Program, Department of Radiology (K.N., M.D.S., M.F., C.H.N., S.A., U.H., T.J.B., R.C.C.) and the Cardiology Division (H.K.G., I.K.J.), Massachusetts General Hospital and Harvard Medical School, 165 Cambridge St, Boston, MA 02114. Received February 17, 2007; revision requested April 26; revision received July 3; accepted August 1; final version accepted September 25. K.N. supported by the Interuniversity Cardiology Institute of the Netherlands, Utrecht, the Netherlands. Address correspondence to K.N. (e-mail: koennieman{at}hotmail.com).


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 ADVANCE IN KNOWLEDGE
 IMPLICATION FOR PATIENT CARE
 References
 
Purpose: To prospectively compare 64-section multidetector computed tomography (CT) and cardiac magnetic resonance (MR) imaging for the early assessment of myocardial enhancement and infarct size after acute reperfused myocardial infarction (MI).

Materials and Methods: The study was HIPAA compliant and was approved by the institutional review board. All participants gave written informed consent. Twenty-one patients (18 men; mean age, 60 years ± 13 [standard deviation]) were examined with 64-section multidetector CT and cardiac MR imaging 5 days or fewer after a first reperfused MI. Multidetector CT was performed during the first pass of contrast material to assess myocardial perfusion and detect microvascular obstruction (no reflow). In 15 patients, a second scan was performed 7 minutes later to assess total infarct size by using delayed hyperenhancement. Early hypoenhancement and delayed hyperenhancement were compared between multidetector CT and cardiac MR imaging with Pearson correlation coefficient and Bland-Altman analysis.

Results: Early hypoenhancement was recognized on all multidetector CT and cardiac MR images. Delayed hyperenhancement was observed with cardiac MR imaging at all examinations and with multidetector CT at 11 of 15 examinations. While signal intensity differences between hypoperfused and normal myocardium were comparable for first-pass multidetector CT and cardiac MR imaging, cardiac MR imaging had a far better contrast-to-noise ratio (CNR) for delayed acquisitions than did CT (P < .001). Hypoenhanced areas (as a percentage of left ventricular mass) at first-pass multidetector CT (11% ± 6) correlated well with those at first-pass cardiac MR imaging (7% ± 4, R2 = 0.72). Delayed-enhancement multidetector CT (13% ± 9) correlated well with delayed-enhancement cardiac MR imaging (15% ± 7, R2 = 0.55). Quantification of delayed hypoenhancement (n = 12) had very good correlation between multidetector CT (4% ± 4) and cardiac MR imaging (3% ± 2) (R2 = 0.85).

Conclusion: Early and late hypoenhancement showed good CNR and correlated well between multidetector CT and cardiac MR imaging.

© RSNA, 2008


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 ADVANCE IN KNOWLEDGE
 IMPLICATION FOR PATIENT CARE
 References
 
Early percutaneous coronary intervention has improved the prognosis of patients after myocardial infarction (MI) (1). Nevertheless, patency of the epicardial coronary artery after primary percutaneous coronary intervention does not guarantee reflow at a microvascular level or functional recovery. Knowledge about myocardial perfusion and transmural infarct size after MI has prognostic value and therapeutic consequences (2,3). The ability of cardiac magnetic resonance (MR) imaging to help assess both of these parameters is well documented, and MR imaging is often regarded as the clinical standard (4).

First-pass imaging performed immediately after contrast material administration will show relative hypoenhancement of infarcted myocardium caused by reduced microvascular perfusion of the affected tissue (5,6). Delayed images, which are acquired within 15 minutes after contrast material administration, may demonstrate delayed hyperenhancement that corresponds to myocardial necrosis (6,7), which allows differentiation of viable from nonviable myocardium (7). Particularly, when delayed imaging is performed early after an ischemic event, hyperenhanced infarcted myocardium may contain tissue with low signal intensity in its core. Even after 15 minutes, circulating contrast medium has not yet reached the hypodense core of the infarction; this is likely the result of severe obstruction of the microvasculature.

A large volume of data supports the use of single photon emission computed tomography for infarct quantification, although accurate assessment of the transmural infarct size is limited by its modest spatial resolution (8). Expanding use of coronary multidetector computed tomography (CT) imaging in clinical practice has sparked renewed interest in nonangiographic CT applications, which include imaging of MI. With multidetector CT, different patterns of myocardial enhancement, early and late after contrast material administration, have been demonstrated in animal models with coronary occlusion (9–14) and in humans after acute MI (15–17) in a manner comparable to that of cardiac MR imaging. Combined with noninvasive coronary angiography (18,19) and assessment of ventricular function (20,21), multidetector CT evaluation of infarct size and viability could be of clinical value.

Thus, the purpose of our study was to prospectively compare 64-section CT and cardiac MR imaging for the assessment of myocardial enhancement and infarct size early after acute reperfused MI.


   MATERIALS AND METHODS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
RESULTS
 DISCUSSION
 ADVANCE IN KNOWLEDGE
 IMPLICATION FOR PATIENT CARE
 References
 
Patients
Our study was Health Insurance Portability and Accountability Act compliant, and an initial protocol without and a second protocol with delayed CT imaging were approved by our institutional review board (Partners Human Research Committee). All participants provided informed consent to either protocol in writing. Detailed explanation concerning radiation risks related to CT and risks related to MR and CT contrast media was given to each patient and was approved by the institutional review board for both protocols.

Patients who had a first acute ST-elevation MI at presentation and who were treated with percutaneous coronary intervention were prospectively considered for enrollment. Clinical heart failure (use of intravenous inotropic therapy, intraaortic balloon pump), ongoing ischemia, and relevant arrhythmia were reasons for exclusion from the study. Multidetector CT–related exclusion criteria included pregnancy, irregular heart rhythms, impaired renal function, contrast material allergy, and large volume of contrast material used during percutaneous coronary intervention (>3 mL per kilogram of body weight). Standard exclusion criteria for cardiac MR imaging were applied (metal implants, claustrophobia, etc). Twenty-one patients met these criteria and were prospectively and consecutively enrolled in the study (Table 1).


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  		Table 1. Characteristics of 21 Patients with MI

 
Cardiac MR imaging and multidetector CT were performed within 5 days after acute MI. In 18 patients, cardiac MR imaging and multidetector CT were performed on the same day; in three patients, cardiac MR imaging was performed 1 day after multidetector CT. On the basis of angiographic findings, the infarct-related coronary artery was the right coronary artery in 12, the left anterior descending artery in five, the left circumflex coronary artery in three, and the ramus intermedius in one patient. The culprit lesion resulted in complete vessel occlusion in 15, subtotal occlusion in four, and 75%–90% stenosis in two patients (Table 1). Percutaneous coronary intervention was successful, with normal postprocedural flow (Thrombolysis in Myocardial Infarction grade 3 [22]) in all but one patient.

CT Imaging Protocol
First-pass CT imaging.—Cardiac CT was performed with a 64-section multidetector system (Sensation 64; Siemens, Forchheim, Germany). Parameters were as follows: rotation time, 330 msec (temporal resolution, ≤165 msec); 32 x 0.6-mm-wide detector collimation, and double z-axis acquisition technology (Z-Sharp; Siemens) (23). In the absence of contraindications (hypotension, conduction abnormalities, obstructive airway disease), 2–5 mg of metoprolol was intravenously administered approximately 5 minutes before the scan in eight patients with a heart rate of more than 70 beats per minute. Average heart rate during the scan was 65 beats per minute ± 8 (standard deviation) (range, 51–80 beats per minute).

A 20-mL test bolus consisting of contrast medium, followed by 40 mL of normal saline, was used to determine the contrast material transit time. To allow sufficient myocardial enhancement, 4 seconds were added to the measured time of peak aortic root enhancement before image acquisition. Depending on the longitudinal scan range, an intravenous bolus of 75–90 mL (mean, 83 mL ± 4) of contrast agent (iodixanol [320 mg of iodine per milliliter], Visipaque; GE Healthcare, Princeton, NJ) was administered by using a double-head power injector and was followed by 40 mL of normal saline at 4–5 mL/sec. Tube voltage was 120 kV; tube current varied between 850 and 930 mAs (mean, 871 mAs ± 29), depending on the size of the subject. Electrocardiographically gated modulation of tube current could be used in patients with a slow and stable heart rate (n = 17) to reduce radiation exposure during systole (23). The radiation dose was calculated as 11.8 mSv ± 3.4. After data acquisition, consecutive 8-mm short-axis sections throughout the left ventricle (perpendicular to the interventricular septum) were reconstructed throughout the R-R interval at steps of 6% by using retrospective electrocardiographic gating. Motion-free middiastolic images were selected for analysis.

Delayed-enhancement CT acquisition.—In the last 15 patients enrolled in the study, a second scan was performed 7 minutes after contrast material injection. To minimize radiation exposure, a wider detector collimation (24 x 1.2 mm) and lower tube output were used (100 kV, 800 mAs). The calculated radiation dose was 4.5 mSv ± 2.4. Similarly to the first scan, 8-mm short-axis images were reconstructed throughout the cardiac cycle, and the middiastolic phase was selected for further analysis.

MR Imaging Protocol
First-pass perfusion MR imaging.—Cardiac MR imaging was performed with a 1.5-T system (Twin-Speed Excite; GE Healthcare, Milwaukee, Wis) equipped with an eight-element phased-array cardiac coil and high-speed gradients (maximum amplitude, 40 mT/m; slew rate, 150 T/m/sec). A bolus injection of 0.1 mmol/kg gadopentetate dimeglumine (Magnevist; Schering, Berlin, Germany) was administered by using an infusion pump (Medrad, Indianola, Pa) at 5 mL/sec, followed by 20 mL of normal saline. First-pass images were acquired during 30 phases (50 seconds per examination) by using a hybrid gradient-echo echo-planar imaging pulse sequence. With this pulse sequence, five to eight (depending on the heart rate) short-axis sections every other heartbeat were acquired (repetition time msec/echo time msec, 6.7/1.4; echo train length, four; flip angle, 20°; matrix, 128 x 128; bandwidth, 125 kHz; field of view, 34 x 34 cm; section thickness, 8 mm; and saturation pulse, 90).

Delayed-enhancement MR imaging.—Ten minutes after the administration of a second bolus of 0.1 mmol/kg of gadopentetate dimeglumine (total, 0.2 mmol/kg), consecutive short-axis images (8-mm section thickness) were obtained by using an inversion-recovery prepared fast gradient-echo pulse sequence. Delayed-enhancement images were acquired and displayed to optimally show normal myocardium (dark) and regions of delayed-enhancement myocardium (bright) with proper selection of the inversion time. We performed multiple sequences with varying inversion times and then selected images with the most appropriate inversion time. Imaging parameters were as follows: 7.1/3.1; image matrix, 256 x 192; flip angle, 20°; inversion pulse, 180°; and inversion time, 150–300 msec.

Data Analysis
Infarct imaging.—Images were transferred to dedicated cardiac MR (Advantage WS; GE Medical Systems) and multidetector CT (Leonardo; Siemens) image processing workstations. Multidetector CT attenuation and MR signal intensity were sampled by two independent readers (K.N., 5 years of cardiac CT experience; R.C.C., 5 years of cardiac MR imaging experience) for each technique by placing separate regions of interest (approximately 50 mm2) within the areas of apparent MI (in regions of both hyperenhanced and hypoenhanced myocardium on delayed acquisitions), remote myocardium (myocardial tissue in an unaffected coronary territory), and the middle of the left ventricular cavity. The relative signal intensity contrast was calculated as the difference in MR signal intensity or CT attenuation between the infarction and normal myocardium or the left ventricular cavity, divided by the signal intensity or attenuation of the normal myocardium of the left ventricular cavity (as a percentage). The contrast-to-noise ratio (CNR) was calculated as the signal intensity difference for MR imaging or the attenuation difference for CT between infarcted and remote myocardium, divided by the standard deviation of the signal intensity or attenuation within the remote myocardium.

Total infarct size.—Four independent observers blinded to the clinical history evaluated the total size of the perfusion defect or infarct (as a percentage of the total left ventricular myocardial mass) on both early and late phase images. Two observers (K.N., 5 years of cardiac CT experience; M.D.S., 2 years of cardiac CT experience) evaluated all CT data, with at least 4 weeks between assessment of the first-pass CT images and assessment of delayed-enhancement CT images. Two observers (R.C.C.; C.H.N., 2 years of cardiac MR imaging experience) evaluated all MR data, with at least 4 weeks between assessment of the first-pass MR images and assessment of delayed-enhancement MR images.

Areas of hypoenhancement on early phase first-pass CT and first-pass MR images and areas of hyperenhancement (including central hypoenhancement) on delayed acquisitions were measured by using manual planimetry on workstations (ADW, version 4.0, GE Healthcare; Leonardo, Siemens) and by using software (MASS Analysis, Medis, Leiden, the Netherlands for ADW workstation; HeartView and Argus, Siemens for Leonardo workstation). First-pass CT images were assessed by using predefined image display settings: window width, 150 HU; window level, 100 HU. For delayed-enhancement CT, the window was set equal to the attenuation value of the normal remote myocardium, and the width was set at 100 HU.

Statistical Analysis
Continuous variables are presented as means ± standard deviations. Differences in MR signal intensity and CT attenuation and CNR were compared by using a Student t test. Infarct sizes found by using different acquisition methods and/or modalities (average of measurements by two readers) were compared by using the Pearson correlation coefficient and Bland-Altman analysis. Interobserver reproducibility was reported by using the Pearson correlation coefficient (Intercooled STATA, version 6.0; Stata, College Station, Tex). P values less than .05 were considered to indicate significant differences.


   RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
DISCUSSION
 ADVANCE IN KNOWLEDGE
 IMPLICATION FOR PATIENT CARE
 References
 
First-Pass Imaging
Regions of relative hypoenhancement were clearly identified on both first-pass CT and MR images in all patients (Fig 1). On first-pass CT images, sufficient signal intensity contrast was achieved between infarcted and remote myocardium (55.3%) and between infarcted myocardium and the left ventricular cavity (87.1%) (Table 2). For first-pass MR images, these respective signal intensity differences were similar (47.1% and 67.3%). CNR for differentiating hypoenhanced from normal myocardium was better for first-pass MR images than for first-pass CT images (P < .001).


Figure 1A
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  		Figure 1a: MR and CT images of MI of anterolateral wall (arrows). (a) During first pass of contrast material at MR imaging (MRFP), MI appears as area of decreased signal intensity. Late acquisition at (b) cardiac MR imaging (MRDE) shows hyperenhanced myocardium around central area of hypoenhanced myocardium. (c) Infarct at first-pass perfusion CT (CTFP) appears as area of lower attenuation. Late acquisition at (d) multidetector CT (CTDE) shows hyperenhanced myocardium around central area of hypoenhanced myocardium.

 

Figure 1B
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  		Figure 1b: MR and CT images of MI of anterolateral wall (arrows). (a) During first pass of contrast material at MR imaging (MRFP), MI appears as area of decreased signal intensity. Late acquisition at (b) cardiac MR imaging (MRDE) shows hyperenhanced myocardium around central area of hypoenhanced myocardium. (c) Infarct at first-pass perfusion CT (CTFP) appears as area of lower attenuation. Late acquisition at (d) multidetector CT (CTDE) shows hyperenhanced myocardium around central area of hypoenhanced myocardium.

 

Figure 1C
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  		Figure 1c: MR and CT images of MI of anterolateral wall (arrows). (a) During first pass of contrast material at MR imaging (MRFP), MI appears as area of decreased signal intensity. Late acquisition at (b) cardiac MR imaging (MRDE) shows hyperenhanced myocardium around central area of hypoenhanced myocardium. (c) Infarct at first-pass perfusion CT (CTFP) appears as area of lower attenuation. Late acquisition at (d) multidetector CT (CTDE) shows hyperenhanced myocardium around central area of hypoenhanced myocardium.

 

Figure 1D
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  		Figure 1d: MR and CT images of MI of anterolateral wall (arrows). (a) During first pass of contrast material at MR imaging (MRFP), MI appears as area of decreased signal intensity. Late acquisition at (b) cardiac MR imaging (MRDE) shows hyperenhanced myocardium around central area of hypoenhanced myocardium. (c) Infarct at first-pass perfusion CT (CTFP) appears as area of lower attenuation. Late acquisition at (d) multidetector CT (CTDE) shows hyperenhanced myocardium around central area of hypoenhanced myocardium.

 

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  		Table 2. CT Attenuation and MR Signal Intensity on Early and Late Acquisitions

 
The volume of hypoenhanced myocardium, as a percentage of the total left ventricular volume, was 11% ± 6 (range, 2%–25%) at first-pass CT imaging (n = 21), compared with 7% ± 4 (1%–15%) at first-pass MR imaging. Despite good correlation (R2 = 0.72), a significantly larger perfusion defect was measured at first-pass CT than at first-pass MR imaging (mean difference, 4% ± 3) (P < .001) (Fig 1).

Delayed Imaging
Hyperenhanced myocardium was identified at delayed-enhancement MR imaging in all patients. For delayed-enhancement CT, three studies were considered nonassessable because of excessive image noise (n = 2) and streak artifacts (n = 1) speculated to be caused by attenuation of the x-ray through the liver. In the 12 assessable studies, hyperenhancement was detected in 11 patients; there were regions of hypoenhancement within these hyperenhanced areas in eight patients (Fig 1). In one patient, delayed-enhancement CT images showed hypoenhanced myocardium without hyperenhancement.

The signal intensity difference between hyperenhanced and remote myocardium was significantly higher for delayed-enhancement MR imaging than for delayed-enhancement CT: 272.7% versus 29.3% (Table 2, Fig 2). The signal intensity difference between hypoenhanced and remote myocardium at delayed-enhancement MR imaging was 23.6%, compared with 36.9% at delayed-enhancement CT. Delayed-enhancement MR images had a far better CNR than delayed-enhancement CT images (P < .001) (Fig 3).


Figure 2
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  		Figure 2: First-pass CT (CTFP) and delayed CT (CTDE) images during diastole and delayed MR images (MRDE) during systole at corresponding short-axis levels from the base toward the apex in a patient with transmural inferior wall infarction (arrows). While hypoenhanced myocardium is visible on all first-pass CT levels, infarct size appears underestimated in comparison to that on delayed-enhancement CT and MR images. Despite showing apparently similar infarct size, delayed-enhancement CT images have more noise, and contrast between infarcted and normal myocardium is modest in comparison to that on delayed-enhancement MR images. At the basal level, central area of hypoenhancement within area of hyperenhancement is present on delayed-enhancement CT and MR images.

 

Figure 3
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  		Figure 3: Graph shows comparable CNRs for first-pass CT (CTFP) and MR (MRFP) imaging. CNR is nearly four times better for delayed-enhancement MR imaging (MRDE) than for delayed-enhancement CT (CTDE).

 
For the delayed acquisitions, the amount of hyperenhanced myocardium (including hypoenhanced microvascular obstruction) at delayed-enhancement CT imaging (n = 12) was 13% ± 9 (range, 1%–29%), which was similar to that at delayed-enhancement MR imaging (15% ± 7; range, 1%–28%), with a mean difference of –2% ± 6 (P = .37) and good correlation between delayed-enhancement CT and delayed-enhancement MR imaging (R2 = 0.55) (Fig 4).


Figure 4A
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  		Figure 4a: Graphs of (a–c) correlation and (d–f) Bland-Altman analysis for comparison of (a, b) total infarct size (as percentage of left ventricular [LV] myocardial mass) between early phase CT (CTFP) and MR (MRFP) imaging, (c, d) infarct size on delayed CT (CTDE) and MR (MRDE) images, and (e, f) delayed hypoenhancement (microvascular obstruction) on delayed CT and MR images.

 

Figure 4B
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  		Figure 4b: Graphs of (a–c) correlation and (d–f) Bland-Altman analysis for comparison of (a, b) total infarct size (as percentage of left ventricular [LV] myocardial mass) between early phase CT (CTFP) and MR (MRFP) imaging, (c, d) infarct size on delayed CT (CTDE) and MR (MRDE) images, and (e, f) delayed hypoenhancement (microvascular obstruction) on delayed CT and MR images.

 

Figure 4C
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  		Figure 4c: Graphs of (a–c) correlation and (d–f) Bland-Altman analysis for comparison of (a, b) total infarct size (as percentage of left ventricular [LV] myocardial mass) between early phase CT (CTFP) and MR (MRFP) imaging, (c, d) infarct size on delayed CT (CTDE) and MR (MRDE) images, and (e, f) delayed hypoenhancement (microvascular obstruction) on delayed CT and MR images.

 

Figure 4D
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  		Figure 4d: Graphs of (a–c) correlation and (d–f) Bland-Altman analysis for comparison of (a, b) total infarct size (as percentage of left ventricular [LV] myocardial mass) between early phase CT (CTFP) and MR (MRFP) imaging, (c, d) infarct size on delayed CT (CTDE) and MR (MRDE) images, and (e, f) delayed hypoenhancement (microvascular obstruction) on delayed CT and MR images.

 

Figure 4E
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  		Figure 4e: Graphs of (a–c) correlation and (d–f) Bland-Altman analysis for comparison of (a, b) total infarct size (as percentage of left ventricular [LV] myocardial mass) between early phase CT (CTFP) and MR (MRFP) imaging, (c, d) infarct size on delayed CT (CTDE) and MR (MRDE) images, and (e, f) delayed hypoenhancement (microvascular obstruction) on delayed CT and MR images.

 

Figure 4F
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  		Figure 4f: Graphs of (a–c) correlation and (d–f) Bland-Altman analysis for comparison of (a, b) total infarct size (as percentage of left ventricular [LV] myocardial mass) between early phase CT (CTFP) and MR (MRFP) imaging, (c, d) infarct size on delayed CT (CTDE) and MR (MRDE) images, and (e, f) delayed hypoenhancement (microvascular obstruction) on delayed CT and MR images.

 
Ten patients had hypoenhancement within the hyperenhanced infarction on both delayed-enhancement CT and delayed-enhancement MR images. When we compared the relative size of delayed hypoenhancement on delayed-enhancement CT (4% ± 4) and delayed-enhancement MR (3% ± 2) images, very good correlation (R2 = 0.85) could be demonstrated, with a mean difference of 1% ± 2 (P = .10) (Fig 4).

The interobserver agreement ({kappa}) for delayed-enhancement CT (0.96) was better than that for first-pass CT (0.72). The interobserver variability for first-pass MR and delayed-enhancement MR imaging was comparable: 0.87 and 0.96, respectively. Assessment of late hypoenhancement showed very good interobserver agreement at CT (0.99) as well as at MR imaging (0.93).


   DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
ADVANCE IN KNOWLEDGE
 IMPLICATION FOR PATIENT CARE
 References
 
In our study we found that early hypoattenuation can be clearly differentiated from normal myocardium. Given the good attenuation difference between infarcted and normal myocardium, the lower CNR at first-pass CT may in part be the result of the higher spatial resolution of CT. Without the ability to null the signal from remote myocardium, delayed imaging at CT has significantly lower CNR than MR imaging, confirming earlier observations (17).

Contrary to earlier observations by Gerber et al (17), we found larger regions of hypoperfusion at first-pass CT than at first-pass MR imaging. Late myocardial enhancement could be demonstrated in the majority of patients. Infarct size at delayed-enhancement CT and delayed-enhancement MR imaging correlated well in assessable studies, which confirms earlier comparisons between multidetector CT and cardiac MR imaging (16,17). While Mahnken et al (16) found comparable per-section infarct size, Gerber and colleagues found a small but significant overestimation of the relative total infarct size at CT (16,17).

Although delayed hypoenhancement has been observed at CT shortly after MI, to our knowledge, ours is the first quantitative comparison with cardiac MR imaging. In our study, delayed-enhancement CT and delayed-enhancement MR imaging showed very good correlation for assessment of late hypoenhancement, which may be an important parameter for prediction of adverse functional recovery and long-term prognosis after acute MI (15).

Comprehensive use of cardiac CT, including coronary angiography, ventricular function, and infarct imaging, could provide a variety of relevant information after MI. After primary percutaneous coronary intervention, CT can demonstrate decreased or absent myocardial perfusion (no reflow) and help assess transmural infarct size to predict ventricular remodeling and contractile recovery. In addition to these parameters, CT could be useful in assessing angiographic patency of the culprit lesion after thrombolysis, as well as additional coronary artery disease, and potentially help avoid invasive diagnostic studies and intervention. The objective of our study was infarct imaging. Although not part of our study, the early phase CT data set can be used for evaluation of the coronary arteries and left ventricular function.

Early and late CT or MR imaging after contrast material enhancement provide very different information. Early hypoenhancement is caused by absent or delayed myocardial perfusion (slow wash-in), speculated to be caused by obstruction of the microvasculature. Results of previous experimental (4,7,24) and clinical (25) studies have demonstrated that regions with early hypoenhancement reflect the part of the MI (1–4) with obstructed microvascular perfusion. Delayed hyperenhancement is considered the result of slow washout of contrast medium from the infarcted myocardium due to myocyte damage and enlargement of the extracellular space.

Although delayed images display myocardial necrosis (6,7), some investigators have speculated that hyperenhanced myocardium includes injured, but not permanently damaged, tissue with the potential to recover (7,25–27). Although the amount of irreversibly injured myocardium is underestimated, early hypoenhancement is a stronger negative predictor of functional recovery than total infarct size at delayed enhancement (6,28–30), even when reperfusion of the epicardial vessels can be achieved. Assessment of early hypoenhancement at CT may provide sufficient information to predict functional recovery, similar to nuclear imaging or echocardiography (31–33). Considering the need for additional exposure to radiation (and contrast medium), it remains undecided whether total infarct size at delayed-enhancement CT provides additional predictive value over early myocardial perfusion imaging after reperfused MI.

Scar fibrosis will also show delayed enhancement on MR and CT images, although its size decreases and the central area of hypoenhancement generally disappears (17,34). Both acute and chronic MI show relative hypoperfusion during injection of contrast material, which makes differentiation based on early myocardial enhancement difficult. Very low attenuation, which may be the result of fatty replacement of scar tissue, has been demonstrated at CT in chronic MI (35).

Our study had limitations. Contrary to MR imaging, CT involves radiation and injection of potentially nephrotoxic contrast media. In our study, we used a relatively low dose of contrast medium and reduced radiation exposure during the delayed acquisition. On the basis of the results in animals, which were obtained with a higher relative radiation dose, as well as a (up to five times) higher weight-adjusted dose of contrast medium, better infarct imaging should be possible with more liberal use of contrast medium and radiation (14). Use of a lower tube voltage could improve the differentiation of infarcted myocardium as demonstrated in animals, at the expense of increased image noise (36). In humans, lower tube voltage might necessitate a higher tube current (in milliamperes) to compensate for this. Use of prospective triggering, rather than retrospective gating, could further reduce radiation exposure. Whether modifications of the scan protocol, in terms of tube voltage, acquisition timing, and so forth, could improve delayed-enhancement CT infarct imaging needs to be evaluated.

In conclusion, contrast material–enhanced CT can help visualize infarcted myocardium during early and delayed imaging. Multidetector CT allows imaging of early and late myocardial hypoenhancement after reperfused MI, with good correlation with MR imaging, although imaging of delayed hyperenhancement at multidetector CT has inferior CNRs. Nevertheless, in assessable studies, delayed hyperenhancement at CT did correlate well with that at MR imaging. Further research is needed to improve delayed-enhancement CT imaging and establish the role of cardiac CT after MI in clinical practice.


   ADVANCE IN KNOWLEDGE
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 ADVANCE IN KNOWLEDGE
IMPLICATION FOR PATIENT CARE
 References
 


   IMPLICATION FOR PATIENT CARE
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 ADVANCE IN KNOWLEDGE
 IMPLICATION FOR PATIENT CARE
References
 


   FOOTNOTES
 

Abbreviations: CNR = contrast-to-noise ratio • MI = myocardial infarction

Author contributions: Guarantors of integrity of entire study, K.N., R.C.C.; study concepts/study design or data acquisition or data analysis/interpretation, all authors; manuscript drafting or manuscript revision for important intellectual content, all authors; manuscript final version approval, all authors; literature research, K.N., M.D.S., M.F., I.K.J., T.J.B., R.C.C.; clinical studies, K.N., M.D.S., M.F., C.H.N., S.A., U.H., H.K.G., I.K.J., R.C.C.; statistical analysis, K.N., M.F., R.C.C.; and manuscript editing, all authors

Authors stated no financial relationship to disclose.


   References
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 ADVANCE IN KNOWLEDGE
 IMPLICATION FOR PATIENT CARE
 References
 

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