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Analysis of First-Pass and Delayed Contrast-Enhancement Patterns of Dysfunctional Myocardium on MR Imaging

Use in the Prediction of Myocardial Viability

¹ Department of Radiology, Universität Würzburg, Josef-Schneider-Str. 2, D-97080 Würzburg, Germany.
² Department of Internal Medicine, Universität Würzburg, D-97080 Würzburg, Germany.

Received May 3, 1999; accepted after revision September 9, 1999.

 
Supported by a grant from the Interdisziplinäres Zentrum für Klinische Forschung, Universität Würzburg, part F2.

Address correspondence to J. J. W. Sandstede

Abstract

Top Abstract Introduction Subjects and Methods Results Discussion References

 
OBJECTIVE. The purpose of the study was to analyze first-pass and delayed contrast-enhancement patterns of dysfunctional myocardial regions on MR imaging after injection of gadopentetate dimeglumine to predict myocardial viability in patients with coronary artery disease.

SUBJECTS AND METHODS. Twelve patients with wall motion abnormalities and related coronary artery disease revealed by conventional coronary angiography underwent MR imaging at 1.5-T before and 3 months after revascularization therapy. Short-axis images were acquired using a cine gradient-echo sequence. Each slice was divided into eight segments. Overall, 73 segments with impaired contractility were imaged during the first-pass and 14 ± 2 min after injection of 0.05-mmol/kg gadopentetate dimeglumine at a flow of 3 ml/sec using a T1-weighted turbo fast low-angle shot sequence. Improved systolic wall thickening 3 months after revascularization served as the criterion of viability.

RESULTS. At study entry, 26 dysfunctional segments showed delayed hyperenhancement compared with the adjacent functional segments within the same slice, and 47 did not reveal hyperenhancement. After revascularization, 25 (96%) of the 26 hyperenhanced segments did not recover function, whereas 39 (83%) of the 47 segments without hyperenhancement showed mechanical improvement. Segment-related sensitivity and specificity for the correlation of lack of delayed hyperenhancement with myocardial viability were 39 (98%) of 40 and 25 (76%) of 33, respectively. Hypoenhancement during first-pass did not serve as a reliable criterion of viability.

CONCLUSION. Evidence of delayed hyperenhancement of dysfunctional myocardium may be used to predict lack of mechanical improvement or nonviability, whereas the lack of hyperenhancement can be correlated with improvement of regional contractility or viability after revascularization.

Introduction

Top Abstract Introduction Subjects and Methods Results Discussion References

 
The success of a revascularization therapy concerning mechanical improvement of regionally dysfunctional myocardium depends on the presence of viable myocardial cells in these ischemically injured regions. Cardiac MR imaging follows two potential strategies for the prediction of regional wall motion improvement after revascularization therapy. Cine MR imaging provides measurement of diastolic wall thickness and of dobutamine-induced systolic wall thickening. Both parameters were evaluated against positron emission tomography and contractile recovery after revascularization and found useful for the detection of myocardial viability [1, 2]. The other strategy involves the use of MR imaging contrast agents. Using gadopentetate dimeglumine, contrast-enhanced MR imaging may be used to reveal myocardial infarction and estimate the infarct size [3,4,5]. More recent experimental and clinical studies have investigated how different delayed contrast-enhancement patterns relate to the extent and severity of myocardial injury and to myocardial viability [6,7,8,9,10,11]. Fedele et al. [8], Lima et al. [9], and Ramani et al. [10] found a correlation between late enhancement and nonviability. Contrary to the cited studies and our study, Rogers et al. [11] reported predictability of late functional recovery after reperfused myocardial infarction with a normal first-pass followed by hyperenhanced signal on delayed images.

The aim of our study was to correlate the presence or absence of first-pass hypoenhancement and delayed hyperenhancement of dysfunctional myocardial regions with myocardial viability after injection of gadopentetate dimeglumine. The functional recovery of these regions 3 months after revascularization therapy served as the criterion of viability.

Subjects and Methods

Top Abstract Introduction Subjects and Methods Results Discussion References

 
Twelve patients (10 men, two women; age range, 49-79 years; mean, 61 ± 9 years) with hypokinetic or akinetic myocardial regions and associated coronary artery disease revealed by left ventriculography and coronary angiography were included regarding usual MR contraindications. Ten patients had a history of previous myocardial infarction (27 ± 9 days before the examination) and two patients had dysfunctional myocardia without a history of infarction. All patients underwent revascularization therapy, 10 underwent percutaneous transluminal coronary angioplasty with (n = 6) or without (n = 4) coronary stent implantation and two underwent coronary artery bypass grafting. The revascularization was based on clinical issues; the results of the MR imaging examination at study entry had no impact on the patient's treatment. MR imaging was performed at study entry and repeated 3 months after revascularization. Written informed consent was obtained from all patients, and the study was approved by the ethics committee at our institution.

All MR imaging examinations were performed with a 1.5-T scanner (Magnetom VISION; Siemens, Erlangen, Germany) with 25 mT/m maximum gradient strength and a phased array body coil. Patients were examined in the supine position. Short-axis cine MR images were acquired during a breath-hold using an ECG-triggered two-dimensional cine fast low-angle shot sequence with a slice thickness of 8 mm without gap (TR/TE, 80/4.8; flip-angle, 30°; rectangular field of view, 320 x 320; matrix 256 x 256). The number of cardiac phases imaged depended on the heart rate. After determination of up to five slices with wall motion abnormalities, these slices were imaged during first-pass and 15 min after injection of 0.05 mmol/kg of gadopentetate dimeglumine into an antecubital vein. A multislice T1-weighted turbo fast low-angle shot sequence was used (TR/TE, 2.4/1.2; TI, 10 msec; flip-angle, 8°; matrix 60 x 128; field of view, 350 x 350; acquisitions, 40). For the first-pass examination, at least five images were acquired before the contrast agent reached the heart to assess steady-state of the magnetization.

For data analysis, each slice was divided into eight segments. By consensus interpreting by two experienced observers, regional wall motion was judged as normal, hypokinetic, or akinetic. Any improvement of systolic wall thickening after revascularization of the affected segments served as the criterion of viability. An infarcted region was defined as homogeneous if all the segments in this region were either viable or nonviable at follow-up and heterogenous if the infarcted regions consisted of a mixture of viable and nonviable segments. To compensate for changes in localization within the heart between study entry and follow-up, identification of the short heart axis was always performed using double-angulated scout images positioned perpendicular to the septum, and the examination was always started at the same level at the base of the heart. Additionally, image planes were matched using internal landmarks such as papillary muscles, right ventricular shape, and the absolute distance from the base.

For each of these dysfunctional segments, the presence or absence of hypoenhancement during the first-pass of the contrast agent or delayed hyperenhancement was stated both qualitively and by signal-intensity measurements. These measurements were performed with manually drawn regions of interest and the signal intensity was expressed as the percentage of increase over the baseline intensity. The signal intensities of the dysfunctional segments were compared with the signal intensities of the adjacent nondysfunctional segments within the same slice. During first-pass, the image with the clearest depiction of hypoenhancement was chosen for evaluation, whereas, in the of absence of hypoenhancement, the image with the highest myocardial signal intensity was evaluated. All data are presented as mean ± standard deviation, and Wilcoxon's rank sum test was used to identify differences between dysfunctional and adjacent normal segments with p < 0.05 considered statistically significant.

Results

Top Abstract Introduction Subjects and Methods Results Discussion References

 
The dysfunctional myocardial regions shown by MR imaging were consistent with the regions revealed by left ventriculography. All patients had only a single area of dysfunctional myocardium. The wall motion abnormalities were located in the anterior (n = 3), anteroseptal (n = 4), septal (n = 1), posterior (n = 2), posterolateral (n = 1), and lateral (n = 1) wall, respectively. Overall, 73 segments with wall motion abnormalities distributed among an average of 3.6 ± 1.1 slices and 5.9 ± 2.8 segments per patient were evaluated by contrast-enhancement patterns. At study entry, 34 segments showed hypoenhancement during first-pass (16% ± 14% increase over baseline of the dysfunctional segments versus 61% ± 21% increase over baseline of the adjacent segments, p < 0.001), and 39 segments had normal enhancement (91% ± 42% increase over baseline of the dysfunctional segments versus 95% ± 28% increase over baseline of the adjacent segments, p = 0.39). Of the hypoenhanced segments, 25 showed delayed enhancement (group I) (Figs. 1A,1B,1C,1D), and nine remained unchanged (group II). Concerning the normal segments during first-pass, one segment revealed delayed enhancement (group III), and 38 segments did not (group IV). Regarding only delayed-contrast-enhancement patterns, 26 segments showed delayed hyperenhancement (57% ± 37% increase over the baseline versus 21% ± 13% increase over the baseline of the adjacent segments, p < 0.001), and 47 segments did not (37% ± 27% versus 29% ± 16%, p = 0.11).

View larger version (150K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 1A. —49-year-old man with recovery from acute myocardial infarction (arrows, A-F). Two-dimensional cine fast low-angle shot MR images at midventricular short-axis view obtained 24 days after myocardial infarction show wall motion defect of anteroseptal wall from diastole (A) to systole (B).

View larger version (148K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 1B. —49-year-old man with recovery from acute myocardial infarction (arrows, A-F). Two-dimensional cine fast low-angle shot MR images at midventricular short-axis view obtained 24 days after myocardial infarction show wall motion defect of anteroseptal wall from diastole (A) to systole (B).

View larger version (145K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 1C. —49-year-old man with recovery from acute myocardial infarction (arrows, A-F). T1-weighted turbo fast low-angle shot MR image reveals hypoenhancement of this region during first-pass of gadopentetate dimeglumine.

View larger version (131K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 1D. —49-year-old man with recovery from acute myocardial infarction (arrows, A-F). T1-weighted turbo fast low-angle shot MR image obtained 15 min after injection shows delayed hyperenhancement compared with adjacent lateral and inferior wall. This hyperenhancement is less distinct than average hyperenhancement of nonviable segments at study entry.

After revascularization, four segments with former normal enhancement during first-pass showed hypoenhancement, whereas eight segments with former hypoenhancement changed to normal signal intensity. Delayed contrast-enhancement patterns of all segments did not differ from results at study entry (delayed enhancement, 66% ± 24% increase over the baseline of the dysfunctional segments versus 22% ± 21% increase over baseline of the adjacent segments, p < 0.001; normal enhancement, 37% ± 17% versus 33% ± 15%, p = 0.11). Concerning global viability of the infarcted regions at follow-up, seven patients had homogeneous viability or nonviability, but five patients had heterogeneous infarcted regions of up to 50% viable and nonviable segments. Overall, 40 segments with former wall motion abnormalities showed improved systolic contractility and were diagnosed as viable, and 33 segments did not improve and were judged nonviable (Figs. 1E,1F). No discrepancies occurred between the two observers concerning the judgment of regional wall motion abnormalities before and after revascularization. Results of groups I-IV are shown in Table 1.

View larger version (152K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 1E. —49-year-old man with recovery from acute myocardial infarction (arrows, A-F). Two-dimensional cine fast low-angle shot MR image obtained 3 months after percutaneous transluminal coronary angioplasty of infarct-related left anterior descending coronary artery with stent implantation proves unchanged wall motion defect at systole as sign of scarred tissue.

View larger version (131K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 1F. —49-year-old man with recovery from acute myocardial infarction (arrows, A-F). T1-weighted turbo fast low-angle shot MR image obtained 15 min after injection of gadopentetate dimeglumine still reveals delayed hyperenhancement. This hyperenhancement is more distinct than average hyperenhancement of nonviable segments at follow-up.

Analysis of only the delayed contrast-enhancement patterns revealed that 25 of the 26 hyperenhanced segments remained dysfunctional, whereas 39 of the 47 segments without hyperenhancement showed mechanical improvement. Concerning the prediction of viability, 39 of the 40 viable segments were not enhanced, and 25 of the 33 nonviable segments showed delayed hyperenhancement. Despite the small number of patients, sensitivity and specificity for the correlation of the absence of delayed hyperenhancement with myocardial viability were 98% and 76%, and positive and negative predictive values were 83% and 96%, respectively.

Discussion

Top Abstract Introduction Subjects and Methods Results Discussion References

 
Tissue contrast-enhancement patterns generally depend on perfusion, blood pool, diffusion of the contrast agent from the intravascular space into the extracellular space, and size of the extracellular space. Myocardial injury leads to muscle necrosis, consecutive interstitial edema, and leucocyte infiltration within the first 4 days, followed by subsequent penetration of blood capillaries and connective tissue from the periphery. Muscle fibers are removed until the third week and then replaced by collagen formation in the following weeks [12]. This reparation leads to an enlarged extracellular space. Thus, one possible mechanism of delayed hyperenhancement may be increased uptake of gadopentetate dimeglumine because of a larger extracellular volume. Inoue et al. [6] compared reperfused infarcted tissue with occluded infarcted or normal tissue and found the highest gadopentetate dimeglumine concentration in the reperfused tissue, with a correspondingly high water content. Additionally, a positive correlation was found between tissue water content and gadopentetate dimeglumine in both the occluded and reperfused infarcted tissue. On the other hand, Kim et al. [7] reported delayed washin and washout of gadopentetate dimeglumine of the infarcted myocardium after acute reperfused infarction in rabbits. Therefore, delayed hyperenhancement patterns of reversibly and irreversibly injured myocardium may be caused by differences in both size of extracellular space and in washin and washout time constants. However, hypoenhancement during first-pass is caused by reduced blood flow [13]. This reduction can be caused by either a severely stenosed hypoperfused coronary artery already at rest or an impaired microvascular blood flow in infarcted regions [14].

Accurate quantification of the reperfused infarction size by contrast enhancement is possible with experimental studies after injection of gadolinium tetraazacyclododecane tetraacetic acid or gadodiamide [15, 16]. With clinical studies, de Roos et al. [3, 4] also showed significantly increased enhancement of infarcted areas. They included patients with suspected acute myocardial infarction after coronary angiography and thrombolytic treatment. A delayed hyperenhancement was found 15-20 min and 25-30 min after injection with no significant difference between both imaging times. In this acute situation, a distinction between reperfused and nonreperfused infarction based on delayed enhancement was not possible. Nevertheless, patients with reperfused myocardial infarction showed significantly smaller infarct sizes than patients without reperfusion [5].

For the detection of myocardial viability, Fedele et al. [8] examined 19 patients more than 3 months after previous myocardial infarction with dysfunctional areas related to the left anterior descending coronary artery. Spin-echo sequences were used to measure signal intensity 4, 8, 12, and 30 min after injection of gadopentetate dimeglumine. The sequences showed high signal intensity in necrotic tissue compared with normal or hibernating myocardium judged by ¹²³I phenylpentadecanoic acid scintigraphy. This hyperenhancement was seen only 12 and 30 min after injection. Comparing thallium scintigraphy and late enhancement, Lima et al. [9] found a close correlation between hyperenhancing segments and fixed scintigraphic defects 10 min after contrast injection. In a recent study, 24 patients with stable coronary artery disease and regional wall motion abnormalities were examined at least 6 months after myocardial infarction [10]. Delayed hyperenhancement 3-15 min after contrast administration was correlated with a diagnosis of viability by a ²⁰¹Tl scan and dobutamine echocardiography. A significantly greater enhancement was seen each time after contrast injection with the nonviable regions, even in patients without a history of myocardial infarction.

Unlike the results of other reports and our study, Rogers et al. [11] found that 5 ± 2 days after reperfused first acute myocardial infarction only regions with a normal first-pass signal followed by hyperenhanced signal on delayed images (HYPER) showed systolic-wall-motion improvement 7 weeks later. Regions with hypoenhancement at first-pass (HYPO) did not improve, and regions with additional delayed hyperenhancement (COMB) only tended to improve. Referring to this nomenclature, we found only one of 73 segments in the HYPER group revealed nonviability compared with 13 of 28 regions described by Rogers et al. representing viable myocardium. In our study, 24 of the 25 segments in the COMB group were nonviable, whereas 10 regions in the study by Rogers et al. showed a borderline improvement and were considered to contain a mixture of viable and necrotic myocardium. In the HYPO group, five of the nine segments were viable in our study and none of the five regions were viable in the study by Rogers et al. However, with our data, nearly all functionally improved segments were predicted by the absence of delayed hyperenhancement. Concerning hypoenhancement at first-pass, we also found that 28 of the 38 segments did not improve. Nevertheless, 24 of these 28 segments also showed delayed hyperenhancement, and nine out of 10 segments that did improve had no hyperenhancement. This might be explained by the different mechanisms for first-pass hypoenhancement concerning either microvascular or macrovascular damage, which we have previously mentioned. Our data indicate that delayed contrast-enhancement patterns are a more reliable criterion of viability.

Whether these contradictory results concerning the prediction of myocardial viability are explained by varying examination times after myocardial infarction or by other differences concerning patient selection needs to be further investigated. With our patients, a delayed enhancement of the nonviable segments was seen on the first examination and on follow-up 3 months later. Therefore, we postulate, in agreement with the results by Fedele et al. [8] and Ramani et al. [10], that delayed hyperenhancement is not only a sign of nonviability related to recent myocardial infarction, but also indicates chronic coronary artery disease.

In summary, our preliminary data suggest that evidence of delayed hyperenhancement of dysfunctional myocardium may predict lack of mechanical improvement or nonviability, whereas the absence of hyperenhancement is correlated with improvement of regional contractility or viability after revascularization. This interpretation of delayed hyperenhancement in reperfused myocardium differs from previously published results and, thus, needs to be further studied.

References

Top Abstract Introduction Subjects and Methods Results Discussion References

 

1. Baer FM, Voth E, Schneider CA, Theissen P, Schicha H, Sechtem U. Comparison of low-dose dobutamine-gradient-echo magnetic resonance imaging and positron emission tomography with 18F-Fluorodeoxyglucose in patients with chronic coronary artery disease: a functional and morphological approach to the detection of residual myocardial viability. Circulation 1995;91:1006 -1015[Abstract/Free Full Text]
2. Baer FM, Theissen P, Schneider CA, et al. Dobutamine magnetic resonance imaging predicts contractile recovery of chronically dysfunctional myocardium after successful revascularization. J Am Coll Cardiol 1998;31:1040 -1048[Abstract/Free Full Text]
3. de Roos A, Doornbos J, van der Wall EE, van Voorthuisen AE. MR imaging of acute myocardial infarction: value of Gd-DTPA. AJR 1988;150 : 531-534[Abstract/Free Full Text]
4. de Roos A, van Rossum AC, van der Wall E, et al. Reperfused and nonreperfused myocardial infarction: diagnostic potential of Gd-DTPA-enhanced MR imaging. Radiology 1989;172:717 -720[Abstract/Free Full Text]
5. de Roos A, Matheijssen NA, Doornbos J, van Dijkman PR, van Voorthuisen AE, van der Wall EE. Myocardial infarct size after reperfusion therapy: assessment with Gd-DTPA-enhanced MR imaging. Radiology 1990;176:517 -521[Abstract/Free Full Text]
6. Inoue S, Murakami Y, Ochiai K, et al. The contributory role of interstitial water in Gd-DTPA-enhanced MRI in myocardial infarction. J Magn Reson Imaging 1999;9:215 -219[Medline]
7. Kim RJ, Chen EL, Lima JA, Judd RM. Myocardial Gd-DTPA kinetics determine MRI contrast enhancement and reflect the extent and severity of myocardial injury after acute reperfused infarction. Circulation 1996;94:3318 -3326[Abstract/Free Full Text]
8. Fedele F, Montesano T, Ferro-Luzzi M, et al. Identification of viable myocardium in patients with chronic coronary artery disease and left ventricular dysfunction: role of magnetic resonance imaging. Am Heart J 1994;128:484 -489[Medline]
9. Lima JA, Judd RM, Bazille A, Schulman SP, Atalar E, Zerhouni EA. Regional heterogeneity of human myocardial infarcts demonstrated by contrast-enhanced MRI: potential mechanisms. Circulation 1995;92:1117 -1125[Abstract/Free Full Text]
10. Ramani K, Judd RM, Holly RA, et al. Contrast magnetic resonance imaging in the assessment of myocardial viability in patients with stable coronary artery disease and left ventricular dysfunction. Circulation 1998;98:2687 -2694[Abstract/Free Full Text]
11. Rogers WJ Jr, Kramer CM, Geskin G, et al. Early contrast-enhanced MRI predicts late functional recovery after reperfused myocardial infarction. Circulation 1999;99:744 -750[Abstract/Free Full Text]
12. Mallory GK, White PD, Salcedo-Salgar J. The speed of healing of myocardial infarction: a study of the pathologic anatomy in seventy-two cases. Am Heart J 1939;18:647 -671
13. Wilke N, Jerosch-Herold M, Wang Y, et al. Myocardial perfusion reserve: assessment with multi-section, quantitative, first-pass MR imaging. Radiology 1997;204:373 -384[Abstract/Free Full Text]
14. Kloner RA, Ganote CE, Jennings RB. The "no-reflow" phenomenon after temporary coronary occlusion in the dog. J Clin Invest 1974;54:1496 -1508
15. Ovize M, Revel D, de Lorgeril M, et al. Quantitation of reperfused myocardial infarction by Gd-DOTA-enhanced magnetic resonance imaging: an experimental study. Invest Radiol 1991;26:1065 -1070[Medline]
16. Saeed M, Wendland MF, Masui T, Higgins CB. Reperfused myocardial infarctions on T1- and susceptibility-enhanced MRI: evidence for loss of compartmentalization of contrast media. Magn Reson Med 1994;31:31 -39[Medline]

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