| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Original Report |
1 All authors: Department of Radiology, Albert Einstein College of Medicine, Montefiore Medical Center, 111 E 210 St., Bronx, NY 10467.
Received October 3, 2003; accepted after revision December 18, 2003.
Address correspondence to L. B. Haramati
(lharamati{at}aecom.yu.edu).
OBJECTIVE. The aim of this study was to evaluate the ability of contrast-enhanced CT to detect acute myocardial infarction (MI), which has not been systematically assessed. On contrast-enhanced helical chest CT, we retrospectively identified 18 patients (10 women, eight men; mean age, 66 years) with an initial MI. Each patient underwent contrast-enhanced single-detector helical chest CT within 1 month after the MI between March 2001 and June 2002.
CONCLUSION. Acute MI is detectable on contrast-enhanced chest CT as an area of decreased left ventricular myocardial enhancement in a specific coronary arterial distribution.
Contrast-enhanced chest CT is not currently in general clinical use for the evaluation of myocardial infarction (MI). Historically, long scanning times caused CT to be of little use in evaluating the beating heart. However, CT has found a leading role in the diagnosis of entities that have clinical presentations overlapping those of MI, such as pulmonary embolism and aortic dissection [1]. Improvements in helical CT technology allow better evaluation of the heart, particularly by decreasing scanning time, permitting more accurate timing of the contrast bolus, and diminishing motion artifact [2].
In the setting of classical symptoms of acute MI, a prompt correct diagnosis is usually confirmed by typical electrocardiographic changes and elevation of cardiac enzymes. However, the presentation of acute MI is often atypical, especially in women [3]. Atypical presentations such as nausea, vomiting, syncope, or "tearing" chest pain generate a substantial differential diagnosis [4]. CT is commonly used in the emergency department to evaluate other diagnoses that present with symptoms similar to those of acute MI [2].
We have encountered several patients with acute MI who were evaluated with contrast-enhanced CT for other indications. The CT findings showed an area of diminished left ventricular myocardial enhancement in the coronary artery distribution of the infarct. The ability of helical CT to detect MI has not been systematically assessed. Therefore, the aim of this study was to evaluate the ability of contrast-enhanced CT to detect acute MI.
Materials and Methods
We retrospectively identified 69 consecutive patients from a single institution who had an acute MI and underwent contrast-enhanced chest CT within 1 month, between March 2001 and June 2002. The patients were identified by searching the hospital discharge database for the diagnosis of MI and then correlating that list with the CT database. Each medical chart was then reviewed to identify patients with a well-documented initial acute MI. Patients were excluded if the diagnosis of MI was not adequately documented, if they had a previous MI, if the CT images were unavailable, if they had revascularization between the MI and the CT, or if they had an inferior wall MI, because the inferior wall is poorly imaged in the axial plane. After we reviewed the CT images, we excluded three more cases from systematic analysis because of inadequate visualization of the myocardium resulting from poor contrast enhancement (n = 2) or myocardial thinning (n = 1). The remaining 18 patients composed our study population of 10 women and eight men with a mean age of 66 years (range, 36–94 years). The institutional review board approved the study and patient informed consent was not required.
In each patient the initial diagnosis of acute MI was confirmed when a note in the chart by a medical attending physician or cardiologist documented the diagnosis and either the cardiac enzyme levels were elevated (n = 14) or ECG changes consistent with MI were present (n = 11). The clinical location of the MI was determined by integrating the aggregate data from the results of cardiac catheterization (n = 12), echocardiography (n = 14), nuclear cardiology (n = 2), and ECG (n = 11). Cardiac catheterization results, when available, were the decisive choice for determining the location of the MI.
Each case was age- and sex-matched with a control who underwent contrast-enhanced helical CT during the same period, for any indication. The controls were randomly selected from the CT logbook. All controls whose charts indicated a history of MI were excluded, leaving 19 controls, 11 women and eight men, with a mean age of 66 (range, 35–93) years.
The CT scans for study cases and controls were obtained using single-detector helical CT scanners (HiSpeed, General Electric Medical Systems), except for one control who was scanned on a 4-MDCT scanner (LightSpeed plus, General Electric Medical Systems). All CT was performed in a craniocaudad direction with a collimation ranging from 3–5 mm, pitch ranging from 1–2, and with 150 mL of nonionic contrast material injected at a rate of 3 mL/sec with an empiric 15–30 sec delay, depending on the clinical indication for the CT.
Two experienced fellowship-trained cardiothoracic radiologists and a senior radiology resident jointly reviewed the chest CT scans and resolved differences by consensus. Previous experience with myocardial CT included initial training with several incidentally noted cases of confirmed MI detected on CT. To preserve objectivity, a medical student loaded the CT scans onto a digital workstation and displayed the cases and controls in random order. She recorded the interpretation of the reviewers but did not participate in the review or give any feedback. The reviewers were blinded to the clinical data and group assignment.
The enhancement of the left ventricular myocardium was visually assessed as normal or decreased. The location of decreased left ventricular myocardial enhancement was subjectively divided into three areas according to the major coronary artery territories [5]: the interventricular septum, the apicoanterior wall, and the lateroposterior wall. Left ventricular myocardial enhancement was measured in Hounsfield units by obtaining regions of interest (ROI) in the myocardium of the septum and the apicoanterior and the lateroposterior walls of the left ventricle. To avoid an erroneous measurement of Hounsfield units, we placed the ROI away from any artifact in the left ventricular myocardium, but as close as possible to the anatomic location being measured. The CT scans were reviewed at the workstation with a standard preset soft-tissue window. Adjustment of the window width and level was occasionally performed during review of the images to further assess visually noted differences in attenuation. The images were often magnified before placement of the ROI on the myocardium to minimize measurement of artifact and to avoid inclusion of enhanced blood in the ventricular cavity or epicardial fat, especially for the apex, which was often thin. If an artifact was present, an average of two to three separate ROIs was obtained. In the patients in whom no visual decrease in myocardial enhancement was detected, the ROI was placed on each of the three regions of myocardium that was most devoid of artifact. Each CT was evaluated for the degree of contrast enhancement by averaging the Hounsfield units for an ROI of blood in the left ventricular cavity and in the aorta.
Results
Eighty-three percent (15/18) of patients had a focal decrease in left ventricular myocardial enhancement of 20 H or more in the coronary artery distribution of the acute MI. In 50% (9/18), the area of decreased myocardial enhancement was also visually detected. The location of the MI in these patients was the lateroposterior wall (n = 6) (Figs. 1A, 1B and 2A, 2B), septum (n = 4), and apicoanterior wall (n = 3) (Fig. 3A, 3B). In these nine patients, the mean attenuation of the infarcted myocardium was 50 H (range, 8–87 H), compared with a mean attenuation of 118 H (range, 66–147 H) for the noninfarcted regions of the myocardium. Thirty-three percent (6/18) of patients had a decrease in left ventricular myocardial enhancement of 20 H or more at the site of the MI that was detected quantitatively but not visually. The location of the MI in this group was the lateroposterior wall (n = 3) or apicoanterior wall (n = 3) (Fig. 4A, 4B). In these six patients, the mean attenuation of the infarcted region was 74 H (range, 15–114 H), compared with a mean attenuation of 124 H (range, 100–144 H) in the noninfarcted regions.
|
|
|
|
|
|
|
|
In 17% (3/18) of patients, the MI was not detected on CT. One of these had poor enhancement of blood in the left ventricular cavity and in the aorta with a mean contrast enhancement of 90 H. Of the 19 controls, all except one was correctly identified as healthy (no MI). One control was incorrectly identified as having a septal MI.
The sensitivity of CT for detecting an initial acute MI in this series was 83% (15/18), the specificity was 95% (18/19), the positive predictive value was 94% (15/16), and the negative predictive value was 86% (18/21).
The mean contrast enhancement of the blood in the left ventricle and aorta for the 15 patients whose MI was detected on CT was 287 H (range, 170–380 H); for the nine visually detected cases, 275 H (range, 181–381 H); and for the six cases detected only quantitatively, 300 H (range, 177–350 H). Mean enhancement of the blood in the left ventricle and aorta for the three cases of MI that were not detected on CT was 226 H (range, 90–350 H). The corresponding mean contrast enhancement for the 19 controls was 243 H (range, 339–187 H). Mean interval from MI to CT for the nine of 18 patients whose MIs were visually detectable was 8 days (range, 1–26; median, 5 days); for the patients who had MIs detected only quantitatively, 11 days (range, 3–21; median, 12 days); and for the three of 18 whose MIs were not detected on CT, 6 days (range, 3–10; median, 4 days).
The indications for performing chest CT in the patients with MI were suspected pulmonary embolism (n = 7), suspected aortic aneurysm or dissection (n = 6), malignancy (n = 3), and other (n = 2).
Discussion
This series showed that an initial acute MI is detectable on contrast-enhanced chest CT as a focal area of decreased left ventricular myocardial enhancement in a specific coronary arterial distribution. This finding is clinically relevant because contrast-enhanced chest CT is performed for indications such as suspected pulmonary embolism and aortic dissection, which have clinical features that overlap those of acute MI [4]. Atypical presenting symptoms occur in 20–60% of patients with acute MI [4]; this trend is especially true for women [3, 6]. If acute MI is evident on CT, the diagnosis can be suggested, leading to appropriate triage of the patient.
After seeing several incidental cases, we became aware that acute MI could be detected on contrasted-enhanced CT as diminished left ventricular myocardial enhancement in the coronary artery distribution of the clinical infarct. As CT scanning times have diminished, the quality and timing of contrast enhancement have improved [2]. In the late 1970s and early 1980s, animal studies used CT to detect experimentally induced MI [7–9]. Although these studies were the first indication that CT may be useful in the diagnosis of acute MI, the findings from these experimental animal studies did not translate into clinical practice. With the advent of helical CT, the assessment of myocardial perfusion may develop a clinical role. Recently, Paul et al. [10] and Hilfiker et al. [11] have shown a single case of MI detected on MDCT. In this retrospective series, we set out to systematically evaluate the ability of CT to detect acute MI in a larger group of patients.
We designed this study as a retrospective case control series to examine a larger number of patients, because patients with acute MI rarely undergo contrast-enhanced chest CT. The relatively high sensitivity and specificity of this series may differ in the clinical setting, in which CT is rarely performed on patients with acute MI. Although we were unable to exclude patients who had a previous "silent" MI, our aim in studying a group of patients with an initial acute MI was to create a relatively homogeneous population. This study was a pilot, and we did not know with confidence how acute MI would appear on CT. Therefore, we did not include the more complex group of patients with reinfarction. Hence, our data set had few variables and was easy to analyze. The study group was randomly interspersed with an approximately equal number of controls to provide the highest yield and help avoid significant selection bias.
CT is not traditionally used to evaluate the myocardium, so all the CT scans included in this study were obtained for other indications. Often the studies were performed many days after the acute MI. We set an arbitrary interval of 1 month between the acute MI and the CT to recruit our study group. We realize that this arbitrary interval may not be ideal because the myocardium may reperfuse spontaneously. We also understand that we may have witnessed delayed myocardial hyperenhancement as a late manifestation of the infarction [12]. Delayed hyperenhancement is an MRI feature of nonviable myocardium in acute MI [12]. A similar phenomenon was observed in the animal studies performed by Newell et al. [7]. Our series was not designed to detect this phenomenon.
Quantitative measurement of differences in myocardial attenuation was important in detecting the MI on CT in one third (6/18) of the patients in this series. We empirically chose a quantitative decrease of 20 H as an indication of significant reduction in myocardial enhancement for this pilot study, but further evaluation is needed to determine the optimal decrease in enhancement to be used to diagnose MI.
Our study design has several limitations. Because this review was retrospective, the clinical information was culled from documented charts, which are often incomplete. In clinical medicine, the diagnosis of an acute MI is often subjective when it is based on classic symptoms [4]. Because of the retrospective study design, we had to rely exclusively on objective results as evidence for acute MI. Another limitation is the small sample size of our population, which precludes us from drawing broad conclusions.
Varied CT protocols and the exclusive use of single-detector helical CT in our study are both technical limitations. Although only single-detector helical CT equipment was available in our institution during most of the study period of 2001–2002, the technology is changing rapidly. Because of motion artifact and poor contrast enhancement, we excluded three cases from review and erroneously failed to exclude one case with poor enhancement that resulted in a false-negative finding. We anticipate that using multidetector scanners will improve the diagnostic yield. Furthermore, with the routine use of MDCT, multiplanar reformations can be performed with minimal artifact, which may enable us to evaluate the inferior wall of the heart.
In summary, this series shows that acute MI is detectable on contrast-enhanced chest CT as decreased left ventricular enhancement in a specific coronary artery distribution, related to the clinical infarct. Chest CT is performed for indications such as suspected pulmonary embolism and aortic dissection, which have clinical features similar to those of acute MI. If findings indicative of acute MI are evident on CT, that diagnosis can be suggested, leading to appropriate triage of the patient. Although our results are promising, further study is needed to define the clinical role and optimal technique for CT in evaluating patients with MI.
References
CiteULike 
Complore 
Connotea 
Del.icio.us 
Digg 
Reddit 
Technorati What's this?
This article has been cited by other articles:
|
|
 |
|
  K. Thygesen, J. S. Alpert, H. D. White, and on behalf of the Joint ESC/ACCF/AHA/WHF Task Force Universal Definition of Myocardial Infarction J. Am. Coll. Cardiol., November 27, 2007; 50(22): 2173 - 2195. [Full Text] [PDF]
|
|
|
|
 |
|
 K. Thygesen, J. S. Alpert, H. D. White, on behalf of the Joint ESC/ACCF/AHA/WHF Task Force, TASK FORCE MEMBERS: Chairpersons: Kristian Thygese, Biomarker Group: Allan S. Jaffe, Coordinator (USA), ECG Group: Bernard Chaitman, Co-ordinator (USA), P, Imaging Group: Richard Underwood, Coordinator (UK), Intervention Group: Jean-Pierre Bassand, Co-ordina, Clinical Investigation Group: Paul W. Armstrong, C, et al. Universal Definition of Myocardial Infarction Circulation, November 27, 2007; 116(22): 2634 - 2653. [Full Text] [PDF]
|
|
|
|
 |
|
 Task Force Members, K. Thygesen, J. S. Alpert, H. D. White, Biomarker Group, A. S. Jaffe, F. S. Apple, M. Galvani, H. A. Katus, L. K. Newby, et al. Universal definition of myocardial infarction: Kristian Thygesen, Joseph S. Alpert and Harvey D. White on behalf of the Joint ESC/ACCF/AHA/WHF Task Force for the Redefinition of Myocardial Infarction Eur. Heart J., October 2, 2007; 28(20): 2525 - 2538. [Full Text] [PDF]
|
|
|
|
 |
|
 J H Arnett, K Mohajer, and S A Okon Evidence of acute myocardial infarction on CT Br. J. Radiol., September 1, 2007; 80(957): e219 - e221. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. Baks, F. Cademartiri, A. D. Moelker, W. J. van der Giessen, G. P. Krestin, D. J. Duncker, and P. J. de Feyter Assessment of Acute Reperfused Myocardial Infarction with Delayed Enhancement 64-MDCT Am. J. Roentgenol., February 1, 2007; 188(2): W135 - W137. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. Baks, F. Cademartiri, A. D. Moelker, A. C. Weustink, R.-J. van Geuns, N. R. Mollet, G. P. Krestin, D. J. Duncker, and P. J. de Feyter Multislice Computed Tomography and Magnetic Resonance Imaging for the Assessment of Reperfused Acute Myocardial Infarction J. Am. Coll. Cardiol., July 4, 2006; 48(1): 144 - 152. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. F. Bruzzi, M. Remy-Jardin, D. Delhaye, A. Teisseire, C. Khalil, and J. Remy When, Why, and How to Examine the Heart During Thoracic CT: Part 1, Basic Principles Am. J. Roentgenol., February 1, 2006; 186(2): 324 - 332. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. F. Bruzzi, M. Remy-Jardin, D. Delhaye, A. Teisseire, C. Khalil, and J. Remy When, Why, and How to Examine the Heart During Thoracic CT: Part 2, Clinical Applications Am. J. Roentgenol., February 1, 2006; 186(2): 333 - 341. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. J. Gibbons and P. A. Araoz The year in cardiac imaging J. Am. Coll. Cardiol., November 16, 2004; 44(10): 1937 - 1944. [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
