Published online before print August 9, 2007, 10.1148/radiol.2443061397
(Radiology 2007;244:736-744.)
© RSNA, 2007
Is Functional Improvement after Myocardial Infarction Predicted with Myocardial Enhancement Patterns at Multidetector CT?1
Jonathan Lessick, MD, DSc,
Robert Dragu, MD,
Diab Mutlak, MD,
Shmuel Rispler, MD, DSc,
Rafael Beyar, MD, DSc,
Diana Litmanovich, MD,
Ahuva Engel, MD,
Yoram Agmon, MD,
Michael Kapeliovich, MD,
Haim Hammerman, MD, and
Eduard Ghersin, MD
1 From the Departments of Cardiology (J.L., R.D., D.M., S.R., R.B., Y.A., M.K., H.H.) and Medical Imaging (D.L., A.E., E.G.), Rambam Health Care Campus, Haaliya St, Haifa 31096, Israel; and Technion-Israel Institute of Technology, Haifa, Israel (J.L., R.B., Y.A., H.H., A.E., E.G.). Received August 12, 2006; revision requested October 17; revision received November 14; accepted December 20; final version accepted January 15, 2007.
Address correspondence to J.L. (e-mail: jlessick{at}rambam.health.gov.il).
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ABSTRACT
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Purpose: To prospectively evaluate the sensitivity of myocardial early perfusion defects (EDs) and late enhancement (LE) at multidetector computed tomography (CT) following acute myocardial infarction (AMI) to predict segment myocardial dysfunction and myocardial functional recovery (MFR), by using echocardiography as the reference standard.
Materials and Methods: Institutional review board approval and informed consent were obtained. Twenty-six patients (25 men, one woman; mean age, 53 years ± 9 [standard deviation]), underwent baseline multidetector CT, coronary angiography, and echocardiography within a week of AMI and a follow-up echocardiography at 3 months. ED, LE, and late hypoattenuation were compared with regional left ventricular function and MFR. A logistic regression model and generalized estimating equation analysis were applied to estimate the predictive effect of ED and LE. Differences between groups were evaluated by using nonpaired Student t tests.
Results: All EDs and LE corresponded with AMI location determined by using angiography and echocardiography. For occluded arteries (n = 5), no relationship was found between the presence of ED or LE and MFR. For patent arteries (n = 21), presence of LE had a respective sensitivity and specificity of 73% and 85% for predicting follow-up segment dysfunction, compared with 57% and 90% for ED. In abnormal baseline segments, nonrecovery was clearly related to the presence and size of segment defect area for both ED (odds ratio: 1.95 [95% confidence interval: 0.9, 4.1] per square centimeter) and LE (odds ratio: 1.85 [95% confidence interval: 1.2, 2.9] per square centimeter). Segments that recovered had significantly lower prevalence of ED and LE, and if present, were significantly smaller than in segments remaining abnormal (P < .05).
Conclusion: The presence and size of ED and LE at multidetector CT is closely related to follow-up segment myocardial dysfunction and MFR.
© RSNA, 2007
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INTRODUCTION
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Multidetector computed tomography (CT) is mainly used to evaluate coronary arteries (1), while evaluation of the myocardium is performed less often. Several studies (2–10) have shown the inherent potential of evaluating myocardial enhancement in the presence of acute myocardial infarction (AMI). Three types of abnormal myocardial enhancement patterns have been described: (a) hypoenhanced regions on the initial scan and (b) hyperenhanced and (c) hypoenhanced regions on late scans obtained 5–15 minutes after contrast material injection. These patterns have been described by using gadolinium-enhanced magnetic resonance (MR) imaging, and the absence of late enhancement (LE) at MR has been verified as strongly predictive of myocardial viability (11–13). Nonetheless, no study regarding the ability of multidetector CT enhancement patterns to help predict myocardial functional recovery (MFR) has been published, to our knowledge. Thus, the purpose of our study was to prospectively evaluate the sensitivity of myocardial early perfusion defects (EDs and LE at multidetector CT following AMI to predict segment myocardial dysfunction and MFR, by using echocardiography as the reference standard.
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MATERIALS AND METHODS
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Study Group
We included 30 consecutive patients with first AMI who met our criteria and underwent multidetector CT between November 2002 and March 2004. Exclusion criteria included old infarction, renal failure, iodine allergy, and arrhythmia. After excluding four patients who did not complete the study protocol, 26 patients (25 men, one woman; mean age ± standard deviation, 53 years ± 9) remained (Fig 1). The presence of typical clinical symptoms, echocardiographic changes, and elevated creatine phosphokinase or troponin level established a clinical diagnosis of AMI. Helsinki committee approval and informed consent (including explanation of radiation exposure) were obtained.
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Figure 1: Flowchart of study design. Main parameters (dotted box) appear below each event (solid box), evaluated with median time (± interquartile range) from AMI to the left. Echo = echocardiography.
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Multidetector CT and Interpretation
Gated multidetector CT angiography was performed by using a 16-section scanner (Brilliance; Philips Medical Systems, Cleveland, Ohio) with collimation, 16 x 0.75 mm; voltage, 120–140 kV; current, 400–600 mAs; typical effective dose, 10.5 mSv; relative pitch, 0.2–0.3; rotation time, 0.42 second; and section width, 1 mm. Routine premedication with ß-blockers was not employed. Mean heart rate was 71 beats per minute ± 13. A 120–130 mL dose of nonionic iodinated contrast material (370 mg iodine per milliliter, Ultravist; Schering, Berlin, Germany) was injected at a rate of 4 mL/sec by using a power injector (EnVision CT; MedRAD, Indianola, Pa). Scans were performed during a single breath hold lasting 20–30 seconds. Cone-beam corrected reconstructions (14), by using an adaptive multisegment reconstruction algorithm, were performed at 0%, 40%–50%, and 70%–80% of the R-R interval.
A second scan without additional contrast material administration was performed 6 minutes after the initial scan, with collimation, 16 x 1.5 mm; voltage, 120 kVp; current, 250–350 mAs; and section width, 2 mm. Dose modulation at 70% of the R-R interval was implemented to reduce tube current by 80% during the remainder of the heart cycle, resulting in a 50% or smaller reduction in radiation dose for the delayed scan, giving an average effective dose of 2.9 mSv (range, 2.1–3.7 mSv).
Reformation, processing, and assessment of the presence and characteristics of ED, LE, and late hypoattenuation were independently performed by an attending radiologist (E.G., with 1 year experience in cardiac CT) and an attending cardiologist (J.L., with 6 years experience in cardiac CT) by using an Extended Brilliance Workspace (Philips Medical Systems, Cleveland, Ohio). Initially, horizontal and vertical long-axis reformations of the left ventricle were produced and manually corrected by using automatic calculation of the left ventricular (LV) long axis from the LV apex through the center of mass of the LV blood pool. Short-axis reformations were then reconstructed for each phase, at six equidistant levels along the long axis, from approximately 0.5–1 cm above the apex to the level that the LV outflow tract started appearing, giving two apical, two mid-LV, and two basal sections, each approximately 10–13 mm wide, depending on long axis length. This approach was used to ensure that the entire myocardial volume would be analyzed.
Each of the six short-axis sections (one pair each at the basal, mid-, and apical LV regions) was divided into either four (apical) or six (mid-LV and basal) circumferential sectors. For calculation purposes, the results for each pair of adjacent sections were combined, creating the equivalent of 16 myocardial segments, thus paralleling the American Heart Association 17-segment model (15), while omitting the most apical segment. Regions of interest of approximately 25 mm2 were drawn over the normal myocardium of a mid-LV section to obtain reference CT numbers for that study. A region of interest involving the interventricular septum was chosen unless obvious septal hypoattenuation was present, in which case the anterior or lateral walls were used.
The CT window level was adjusted so that the center of the scale corresponded to 20 HU below the myocardial reference value when evaluating early ED and late hypoattenuation and to 20 HU above the reference value when evaluating LE. This approach was chosen to define a visual threshold approximately 2 standard deviations above or below the mean of normal myocardium, and for hyper- and hypoenhancement, respectively.
The window width was made as narrow as possible (50–80 HU) to emphasize the threshold between normal and abnormal myocardium and still allow the surrounding anatomy to be visualized. By using careful visual inspection, both investigators, each blinded to the location of the AMI and to results of other diagnostic studies, independently sought regions of hypo- or hyperattenuation. By using the phase where the defect was best defined, the defect was digitally traced to obtain measurements for defect area per segment and mean Hounsfield units.
Segment defect area was divided by segment defect length (Fig 2) to derive mean segment defect thickness. The defect thickness percentage was derived by dividing the mean segment defect thickness by the absolute wall thickness, as measured from the endocardium to the epicardium at the center of each segment. For the late study, two tracings were performed, one for the entire defect, including both the hyperenhanced and hypoattenuating regions, and one for the hypoattenuating core. Whole defect mass per patient was calculated by summing all segment defect areas and multiplying the total by section thickness and then by 1.05 (myocardial specific gravity) (16). For each defect, a relative enhancement ratio was derived by dividing the mean, in Hounsfield units, of the defect by that of the normal reference myocardium to normalize for interpatient variability (Fig 3).
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Figure 2a: Multidetector CT images demonstrate how study is analyzed. For (a) early and (b) late images (6 minutes), six contrast-enhanced LV short-axis sections are reformatted. The images show anterior infarction manifesting as ED on a and as LE on b (arrowheads). For each of 16 segments, the hypoattenuated and hyperenhanced regions are planimetered and their area, length, and mean CT number are recorded. Mean wall thickness is calculated as area divided by length. Areas are summed and multiplied by section thickness to derive defect mass.
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Figure 2b: Multidetector CT images demonstrate how study is analyzed. For (a) early and (b) late images (6 minutes), six contrast-enhanced LV short-axis sections are reformatted. The images show anterior infarction manifesting as ED on a and as LE on b (arrowheads). For each of 16 segments, the hypoattenuated and hyperenhanced regions are planimetered and their area, length, and mean CT number are recorded. Mean wall thickness is calculated as area divided by length. Areas are summed and multiplied by section thickness to derive defect mass.
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Figure 3: Multidetector CT images show enhancement defects on contrast-enhanced LV short-axis CT reformations. Top left: Early posterolateral wall hypoenhanced transmural perfusion defect (arrows). Top right: Same region after 6 minutes shows persistent late defect (arrows) surrounded by a hyperenhanced zone. Bottom left: Early posterolateral wall hypoenhanced transmural perfusion defect (arrows). Bottom right: Same region after 6 minutes shows no late defect. Large subendocardial hyperenhanced zone is visible.
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In three of 26 patients who did not undergo invasive coronary angiography, coronary artery evaluation was performed by using multidetector CT. These three had heart rates of 58, 70, and 88 beats per minute during the scan. Two attending radiologists (E.G., D.L.) evaluated multidetector CT images by consensus. Multidetector CT images were reformatted by using curved multiplanar reformats through the coronary vessel lumen, and percentage of stenosis was measured by using electronic calipers. Stenoses were classified as mild (<50%), moderate (50%–90%), or subtotal (>90%).
Reference Standard Echocardiography
Each patient underwent early and follow-up (3 months) echocardiography (Fig 1), with either Sequoia (Acuson, Mountain View, Calif) or Vivid-3 (GE Healthcare, Milwaukee, Wis) equipment, that were recorded on S-VHS videotape. The early echocardiography was performed within 2 days (interquartile range, 1–3 days) of multidetector CT imaging. To evaluate regional LV function, short-axis sections were recorded at the mitral valve, papillary muscle, and apical levels, as were apical four-chamber, two-chamber, and long-axis views. An attending cardiologist (D.M., with 20 years experience in echocardiography) scored each examination in a blinded fashion by using the same 16-segment model as that of multidetector CT. Each segment was scored as follows: 1 = normal, 2 = hypokinetic, or 3 = akinetic and/or dyskinetic. The same investigator scored the tapes from all examinations and examined the baseline and follow-up examinations of each patient simultaneously to optimize the detection of temporal changes in segment function.
MFR was defined as a segment with abnormal function at baseline and normal function at follow-up echocardiography.
Invasive Coronary Angiography
Invasive coronary angiography was performed by using standard techniques in 23 of 26 patients. Images were acquired in optimal projection angles at 25 frames per second and were digitally recorded on a Coroskop Top system (Siemens Medical Solutions). A 4th-year cardiology resident (R.D.), under the supervision of an experienced interventional cardiologist (R.B.) and blinded to multidetector CT results, quantitated all stenoses by using electronic calipers. Thrombolysis in myocardial infarction flow grade (17) was also recorded.
Statistical Analysis
Comparisons between groups were made by using the nonpaired Student t test. Comparisons between different types of defects were made by using the paired t test. A comparison of the frequency of defects in different groups was made by using the 
2 test. Multiple logistic regression analysis was used to calculate the odds ratios of ED and LE to predict follow-up segment dysfunction and MFR. The effect of intrapatient correlation was estimated by using generalized estimating equations.
Areas under receiver operating characteristic curves were calculated to assess the predictive value of various measures of defect size. Interobserver variability of ED and LE mass was analyzed by using Bland-Altman analysis and Pearson correlation. A P value of less than .05 was considered to indicate statistically significant difference. All results are expressed as mean ± standard deviation unless specified otherwise. Statistical analysis was performed by using the GB-Stat (version 6.5; GB-Stat, Silver Spring, Md) and the SAS/STAT (version 8; SAS, Cary, NC) software packages.
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RESULTS
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Patient Characteristics and Angiographic Data
Patient characteristics are summarized in Table 1. Eleven patients underwent successful culprit-lesion percutaneous coronary intervention before multidetector CT (median, 4 days; interquartile range, 3–4.5 days) and before echocardiography (median, 2 days; interquartile range, 1–3.5 days); 10 had patent infarct-related arteries with residual stenoses of more than 50%, but thrombolysis in AMI grade 3 flow (normal flow distal to the stenosis); and five had occluded infarct-related vessels with thrombolysis in AMI grade 0 flow (no flow distal to the stenosis). Two of the latter had good collateral flow.
Patients were divided into two groups according to coronary artery patency: Group 1 consisted of 21 patients with patent arteries and was further subdivided into group 1A with 11 patients who underwent successful angioplasty and group 1B with 10 patients with residual stenoses. Group 2 consisted of five patients with occluded infarct arteries and thrombolysis in AMI grade 0 flow. The three patients whose coronary arteries were evaluated by using multidetector CT all had moderately stenotic but clearly patent arteries and were thus placed in group 1B.
Enhancement Patterns
Seventy-seven percent (20 of 26) of patients demonstrated ED, and 77% (20 of 26) had LE; of the latter, 12 of 20 also had late hypoattenuation at the core of the LE region (all 12 also had ED in the same segments) (Table 2, Fig 3). Three patients (12%) demonstrated neither ED nor LE, and two of these had normal baseline LV function. The third had substantial baseline dysfunction, with full recovery at follow-up. Three of 20 patients with ED did not have LE and three of 20 patients with LE did not have ED. All EDs and LE occurred in the determined infarct territory determined at angiography and echocardiography and were associated with regional dysfunction at baseline echocardiography in all studies except one.
Relation of CT Enhancement Patterns to Regional Function on the Basis of Segment
Analysis was performed separately for patients with patent (group 1, n = 21) and occluded (group 2, n = 5) arteries, with most subsequent analysis referring to the former.
In group 1, 71 of 336 (21%) segments had ED and 96 of 336 (29%) segments had LE. Of those, 24 of 96 (25%) had a late hypoattenuation at their core. One hundred fifteen of 336 (34%) segments had ED and/or LE, of which 52 had both, 44 had LE only, and 19 had ED only (Table 3, 4). The presence of an ED in a particular segment had a respective sensitivity, specificity, positive predictive value, negative predictive value, and accuracy of 57% (46 of 81), 90% (230 of 255), 65% (46 of 71), 87% (230 of 265), and 82% (276 of 336) to predict follow-up segment dysfunction, while the presence of LE gave values of 73% (59 of 81), 85% (218 of 255), 61% (59 of 96), 90% (218 of 240), and 82% (277 of 336). Segments with both ED and LE had a high specificity (94%), positive predictive value (75%), and negative predictive value (85%) at the expense of a low sensitivity (48%) for predicting follow-up dysfunction. Of those segments with a late hypoattenuation, 23 of 24 (96%) had follow-up dysfunction.
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Table 4. Contingency Table: Presence or Absence of Combined LE versus Normal or Abnormal Segment Function for Group 1
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Both the presence and the size of a defect (Fig 4) were related to the probability of having segment dysfunction. The probability of follow-up regional dysfunction for ED increased from 50% for segments in the smallest tertile (ED area, 0.1–0.4 cm2) to 91% for segments in the largest tertile (ED area, 1.0–2.9 cm2), while the likelihood for combined LE increased from 41% for segments in the smallest tertile (LE area, 0.2–0.6 cm2) to 88% for segments in the largest tertile (LE area, 1.5–4.1 cm2).
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Figure 4a: Graphs show percentage of segments with segment dysfunction at baseline and follow-up and probability of MFR according to (a) ED size, (b) combined LE size ("both" refers to presence of both ED and LE), (c) presence or absence of ED and coronary artery status, and (d) presence or absence of LE and coronary artery status. Abn = abnormal.
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Figure 4b: Graphs show percentage of segments with segment dysfunction at baseline and follow-up and probability of MFR according to (a) ED size, (b) combined LE size ("both" refers to presence of both ED and LE), (c) presence or absence of ED and coronary artery status, and (d) presence or absence of LE and coronary artery status. Abn = abnormal.
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Figure 4c: Graphs show percentage of segments with segment dysfunction at baseline and follow-up and probability of MFR according to (a) ED size, (b) combined LE size ("both" refers to presence of both ED and LE), (c) presence or absence of ED and coronary artery status, and (d) presence or absence of LE and coronary artery status. Abn = abnormal.
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Figure 4d: Graphs show percentage of segments with segment dysfunction at baseline and follow-up and probability of MFR according to (a) ED size, (b) combined LE size ("both" refers to presence of both ED and LE), (c) presence or absence of ED and coronary artery status, and (d) presence or absence of LE and coronary artery status. Abn = abnormal.
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For comparison, an average segment has an area of approximately 3 cm2. For group 2, a similar but weaker relationship was found (Fig 4c, 4d). Logistic regression analysis revealed both LE and ED to be significant independent predictors of segment dysfunction (Table 5). Intrapatient correlation was estimated to be negligible (r = 0.003) by using generalized estimating equation analysis, justifying the assumption that all segments can be analyzed independently.
Relation of CT Enhancement Patterns to MFR on the Basis of Segment
For group 1, the probability of an abnormal segment at baseline achieving normal function at follow-up was 36% for a segment with no ED and 43% for a segment with no LE, compared with 12% for a segment with ED (P = .004) and 15% for a segment with LE (P = .002). This relationship (Fig 4) was strongly size-dependent, meaning that segments in the largest tertile had a 91% and 88% likelihood of not recovering from ED and LE, respectively. The prediction of MFR could further be improved by taking into account various combinations of ED or LE. Segments with neither type of defect had a 55% chance of recovery, compared with 18% for a segment with only one type of defect and 12% for segments with both types.
The presence of late hypoattenuation was associated with 0% MFR; however, only 23 of 75 (31%) of nonviable segments had a late hypoattenuation. Comparing group 1A (after percutaneous coronary intervention) with group 1B (no percutaneous coronary intervention) showed group 1A to have a higher prevalence of segments with MFR (31% vs 13%, P = .044). In comparison, for group 2, the relationship between ED and/or LE and MFR was diametrically opposed (Fig 4c, 4d). Regarding segments with and without MFR (Table 6), those with MFR had smaller defects as defined by area and length, and to a lesser extent by absolute and percentage of defect thickness. Enhancement ratios did not differ significantly.
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Table 6. Analysis of ED and LE according to Echocardiographic Baseline and Follow-up Segment Function for Group 1
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A logistic regression model including percutaneous coronary intervention, ED, and LE showed that only early LE has a statistically significant predictive value (Table 5). After removing percutaneous coronary intervention from the model, ED had borderline significance (P = .046). Also, in this model, intrapatient correlation was estimated to be small (r = 0.163) by using generalized estimating equation analysis, justifying the assumption that all relevant segments can be analyzed independently.
The area under receiver operating characteristic curves for LE was approximately equivalent for defect area (mean ± standard deviation, 0.76 ± 0.05), length (0.75 ± 0.05), and percentage of thickness (0.75 ± 0.05) and was superior to the same parameters for ED (0.68–0.70). A model including both LE area and ED area improved the predictive ability (0.80 ± 0.05).
Interobserver Variability
There was 89.9% (374 of 416) concurrence concerning the presence or absence of an ED in any segment, and LE concurrence was 90.1% (173 of 192 segments). Bland-Altman analysis of the interobserver agreement for ED mass (n = 26) demonstrated a difference of 0.8 g ± 3.9 between the observers (J.L., 7.7 g ± 6.6 vs E.G., 6.9 g ± 6.5). For LE (n = 12), a difference of 1.0 g ± 4.5 was found (E.G., 13.3 g ± 8.5 vs J.L., 12.3 g ± 8.5). The Pearson correlation coefficient between the observers was r = 0.86 for LE mass and r = 0.83 for ED mass.
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DISCUSSION
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Our results show a strong association between the presence and size of ED and LE and follow-up segmental dysfunction, and a clear relationship between the presence and size of ED and/or LE and the absence of MFR for patent coronaries only.
Animal studies have shown early hypoattenuation to be a measure of low reflow regions (18), which may result from abnormal flow at the level of either the epicardial artery and/or the myocardial capillaries. Flow obstruction at the capillary level may be a result of tissue edema (19), necrosis, microembolism, or vasoconstriction. Late hyperenhancement has been shown to be a marker of necrotic tissue (18,19). Cell destruction together with capillary membrane damage results in accumulation of contrast agent in the expanded extracellular space.
Thus, it is not surprising that hypoattenuation and hyperenhancement have independent prognostic significance regarding infarct size and myocardial viability and that their pathophysiologic significance depends on coronary artery patency. Late hypoattenuation is thought to be a measure of no reflow at the infarct core (4,7,8,20). Indeed, the presence of late hypoattenuation was associated with a lack of MFR; however, it provided little additional prognostic value, since it was almost always associated with the presence of both ED and LE.
The absence of either ED or LE in a particular segment predicts normal function at follow-up, but even segments without any defect had only a 55% chance of recovering, which is much less than that predicted with MR (20). This may be related to the inferior contrast and temporal resolution of multidetector CT relative to MR, resulting in some small regions of LE being missed. Also, the use of a more sensitive quantitative technique to evaluate LV function, such as strain imaging by means of MR or echocardiography may more accurately identify segments with subtler forms of functional recovery (20). MR studies of LE have generally shown a strong relationship between defect thickness and MFR (11–13), while our study has shown defect area to be marginally better than either absolute or relative percentage of defect thickness.
Even though the number of patients is small, there is a clear differentiation between occluded and patent arteries regarding the relationship between the presence of enhancement patterns and MFR. This is not unexpected with regard to ED, since occluded arteries would likely result in capillary derecruitment to maintain normal tissue perfusion pressure gradients in tissue supplied by primitive collateral flow (21). Later on, maturation of the collateral circulation would allow MFR to occur. In reperfused patent arteries, on the other hand, ED is a sign of no or slow reflow, which has been associated with permanent tissue damage (22).
The ability to predict MFR could be especially important as an ancillary finding in patients after AMI undergoing thrombolytic therapy and multidetector CT for coronary artery evaluation or patients with acute ischemia with suspected myocardial stunning.
There were limitations to this study. The small study population with potential selection bias is an important limitation. There was a mean period of 3–4 days between the AMI and the multidetector CT and baseline echocardiography. During this period, a certain amount of regional function may already have improved and enhancement patterns may have changed. On the other hand, the ideal time to measure the relationship between no reflow and myocardial necrosis is at least 48 hours following reperfusion, since the no-reflow zone may change dynamically over the initial period. Comparing segments by using two different modalities would have some degree of misregistration and may account for the imperfect association between the presence of defects and regional function in certain segments.
In summary, this study has demonstrated a strong relationship, on a segment level, between the presence and size of ED and LE and the degree of follow-up regional dysfunction after AMI. Also, the probability of MFR is significantly inversely related to the presence and size of both ED and LE. Further studies are required to evaluate the clinical value of these preliminary findings in larger patient populations.
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ADVANCES IN KNOWLEDGE
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- There is a close relationship between the presence and size of segmental myocardial hypoattenuation on initial scans and the likelihood of follow-up segment dysfunction after acute myocardial infarction (AMI) in both patent and occluded arteries.
- There is a close relationship between the presence and size of segmental myocardial hyperenhancement on late scans and the likelihood of follow-up segment dysfunction after AMI in both patent and occluded arteries.
- There is a strong association between the absence of segment myocardial hypoattenuation on initial scans and the likelihood of follow-up segment myocardial functional recovery (MFR) in patients with patent coronary arteries but not in occluded arteries.
- There is a strong association between the absence of segment myocardial hyperenhancement on delayed scans and the likelihood of follow-up segment MFR in patients with patent coronary arteries but not in occluded arteries.
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IMPLICATIONS FOR PATIENT CARE
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- In patients undergoing cardiac CT after acute myocardial infarction, enhancement patterns may be used to predict the extent of segment myocardial dysfunction at late follow-up.
- Likewise in patients with a reperfused infarct-related artery, CT may be useful to predict myocardial functional recovery.
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FOOTNOTES
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Abbreviations: AMI = acute myocardial infarction • ED = early perfusion defect • LE = late enhancement • LV = left ventricular • MFR = myocardial functional recovery
Author contributions: Guarantors of integrity of entire study, J.L., S.R., E.G.; study concepts/study design or data acquisition or data analysis/interpretation, all authors; manuscript drafting or manuscript revision for important intellectual content, all authors; approval of final version of submitted manuscript, all authors; literature research, J.L., R.D., D.L., E.G.; clinical studies, J.L., R.D., D.M., S.R., D.L., A.E., Y.A., M.K., H.H., E.G.; statistical analysis, J.L.; and manuscript editing, J.L., R.D., S.R., R.B., D.L., Y.A., E.G.
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ABSTRACT
INTRODUCTION
