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Cardiac Imaging |
1 From the Cardiovascular Division, Barnes-Jewish Hospital at Washington University Medical Center, St Louis, Mo (S.J.F., S.E.F., C.H.L.); and Philips Medical Systems, Best, the Netherlands (S.E.F.). Received April 26, 2000; revision requested June 12; revision received June 28; accepted July 6. Supported in part by the Wolff Charitable Trust and Philips Medical Systems. S.J.F. supported by a grant from the Deutsche Forschungsgemeinschaft. Address correspondence to C.H.L., Cardiovascular Magnetic Resonance Unit, Royal Brompton Hospital, Sydney St, London SW3 6NP, England (e-mail: chlorenz00@aol.com).
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMATERIALS AND METHODS RESULTS DISCUSSIONREFERENCES |
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) of gadopentetate dimeglumine in humans in vivo, evaluate the spatial and intersubject variation in the of normal myocardium, and compare these values on a regional basis with values of acute and chronic infarcted myocardium.
MATERIALS AND METHODS: Twelve healthy subjects and patients with acute (n = 5) or chronic (n = 5) myocardial infarction underwent magnetic resonance imaging at 1.5 T. Look-Locker images were acquired at four short-axis levels to measure myocardial and blood longitudinal relaxation time at baseline and after a 30–40-minute infusion of gadopentetate dimeglumine. was calculated as 
R1M/R1B, where M = myocardium, and B = blood.
RESULTS: The magnitude of the estimated in normal myocardium was uniform over the entire myocardium at 0.56 mL/g ± 0.10 (SD). The values in patients with acute (0.91 mL/g ± 0.11, P < .001) or chronic ( = 0.78 mL/g ± 0.09, P < .001) infarction were significantly elevated, as compared with those in healthy subjects. A 20% elevation in , as compared with the mean value of a corresponding normal circumferential segment, allowed identification of chronically (sensitivity, 88%; specificity, 96%) or acutely (sensitivity, 100%; specificity, 98%) infarcted segments.
CONCLUSION: Quantification of the in vivo allows differentiation between normal and acutely or chronically infarcted myocardium, with high sensitivity and specificity.
Index terms: Magnetic resonance (MR), contrast enhancement, 51.121412, 51.12143 • Myocardium, infarction, 511.771 • Myocardium, MR, 511.121412, 511.12143
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODS RESULTS DISCUSSIONREFERENCES |
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, is a key parameter in this type of evaluation but at the time this article was written had been measured only in animals or in humans in vivo indirectly from magnetic resonance (MR) imaging signal intensity changes (10–13). On the basis of the results of these studies, we presumed that an increased tissue-blood would indicate myocardial tissue death in acute infarction due to a loss of cell membrane integrity and a variable amount of interstitial edema; in healed infarctions, an increased tissue-blood would reflect the known increase of the extracellular space of collagenous scars (14,15). Therefore, the purposes of this study were to establish a method for measuring the of gadopentetate dimeglumine in humans in vivo, evaluate the spatial and intersubject variation in the of normal myocardium, and compare these values by using values in acutely and chronically infarcted myocardium. |
MATERIALS AND METHODS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODS RESULTS DISCUSSIONREFERENCES |
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Twelve randomly selected healthy subjects (age range, 21–64 years; mean age, 39 years) with no prior history of cardiovascular disease underwent MR imaging to determine the physiologic range of the of gadopentetate dimeglumine in the human myocardium.
For comparison, five consecutive patients (age range, 34–78 years; mean age, 61 years) with a prior history of myocardial infarction also underwent MR imaging. Patients were included in the study if the myocardial infarction had been diagnosed at least 1 year (mean, 8.4 years ± 3.6 [SD]) previously and event-related wall motion abnormalities at rest could be identified at echocardiography. Patients were excluded if dobutamine stress testing was contraindicated. These patients composed the chronic infarction group.
In addition, five consecutive patients (age range, 31–59 years; mean age, 47 years) who had recently had a myocardial infarction underwent imaging during the 1st days after admission (mean, 4.4 days ± 4.2). Patients were included in the study when acute myocardial infarction was confirmed with clinical criteria, electrocardiographic evidence, and a substantial troponin-I increase, and when rescue angioplasty had been performed. Patients who had had a prior cardiac event were excluded. Four of five patients underwent thrombolytic therapy. Angioplasty with stent placement was performed in four of five patients. In one patient, who had undergone prior coronary artery bypass graft surgery, no flow-obstructing lesion was identified within the graft and distal vessel distribution, but the bypassed vessel was occluded proximally. These patients composed the acute infarction group.
MR Imaging
All MR imaging was performed with a 1.5-T imager (Gyroscan NT; Philips Medical Systems, Best, the Netherlands). In all subjects, scout images were acquired to determine the four-chamber view and a Look-Locker sequence (16–18) (3,000/3.53 [repetition time msec/echo time msec]; flip angle, 10°; field of view, 320 mm; matrix, 128 x 128; 2.5 x 2.5 x 8-mm resolution, one signal acquired) was performed at four short-axis levels by using a phased-array cardiac coil to measure myocardial and blood longitudinal relaxation times. After a 180° radio-frequency prepulse triggered by the R peak of the electrocardiographic examination, 50 gradient-recalled echo images were acquired at different intervals throughout the cardiac cycle, with a phase interval of 50 msec between images before and a phase interval of 30 msec after contrast material administration. During the acquisition time of 1 minute per section, the patient was breathing continuously. Each subject underwent imaging prior to contrast agent administration and again 30–40 minutes afterward. The radio-frequency excitation pulse of the Look-Locker sequence was small (10°) for minimization of signal intensity variations that were induced by time-of-flight effects.
The contrast material administration protocol consisted of a 5 mL/sec intravenous bolus injection with a power injector (Spectris; Medrad, Maastricht, the Netherlands) of gadopentetate dimeglumine (Magnevist; Berlex, Wayne, NJ) at a dose of 0.1 millimole per kilogram of body weight followed by a constant 30–40-minute infusion (0.002 mmol/kg per minute) to establish equilibrium distribution of gadopentetate dimeglumine between the blood and myocardium. Tong et al (19) have shown that a gadopentetate dimeglumine bolus immediately followed by constant infusion ensures a 90% equilibrium between the myocardium and blood in less than 1 hour if the bolus–constant infusion ratio is 50:1 and normal renal clearance is assumed.
Rest and dobutamine (Dobutrex; Eli Lilly, Indianapolis, Ind) (20 µg/kg per minute) cine MR imaging were performed at the same four short-axis levels and one vertical long-axis level to assess the responsiveness to dobutamine of dysfunctional segments in the five patients with chronic infarction. Breath-hold segmented gradient-recalled echo planar imaging was performed (1 RR/5.8; flip angle, 30°; in-plane spatial resolution, 2.5 x 3.2 mm; temporal resolution, 32 msec; one signal acquired; breath-hold duration, 12 heartbeats; echo-planar imaging factor, seven). The same sequence was performed in all other participants to assess wall motion at rest.
Image Analysis and Calculation of
MR images obtained for the assessment of wall motion were displayed in a cine loop and analyzed at a consensus reading by two experienced observers (C.H.L., S.J.F.) who were aware of clinical and imaging data but not of the calculated values and late enhancement imaging findings. Wall motion at rest was graded qualitatively for eight circumferential segments of each of the four short-axis levels as normokinetic, hypokinetic, akinetic, or dyskinetic. In the group of patients with chronic infarction, segments with wall motion abnormalities at rest and systolic wall thickening of less than 2 mm under dobutamine stress were graded as nonviable (20). In the group of patients with acute infarction, myocardial segments with wall motion abnormalities at rest within the distribution of the occluded vessel, with a corresponding wall motion abnormality on the angiogram and abnormal echocardiographic changes, were judged as reflecting acute infarction.
Look-Locker images were analyzed by using MASS software (Medis, Leiden, the Netherlands) and defining the epicardial and endocardial borders of each frame. Signal intensity time curves were generated for eight circumferential sectors of myocardium and the left ventricular cavity blood pool. The inferior right ventricle–left ventricle junction was used to define the first-sector starting point in all subjects. The curves were fit to the predicted longitudinal magnetization curves for these images, as previously described, to determine the T1 for each circumferential myocardial sector and blood (16–18,21). From these data, the of gadopentetate dimeglumine was calculated for each circumferential sector of the four imaging sections, as described subsequently.
The (mL/g) of gadopentetate dimeglumine was defined as the ratio of the tissue tracer concentration to the blood tracer concentration at equilibrium (11,12): = [GDM (
)]/[GDA ()], where GD = gadopentetate dimeglumine, M = myocardial, and A = arterial. By assuming that the concentration of gadopentetate dimeglumine is related to the R1, the of each circumferential sector was calculated by using the pre- and postcontrast blood and myocardial T1 values, in accordance with equation 1:
R1 is 1/T1Post - 1/T1Pre for either blood or myocardium, Post = postcontrast, Pre = precontrast, M = myocardium, and B = blood. Inherent in this derivation of are two assumptions: (a) The relaxation rate of gadopentetate dimeglumine is equal in myocardial tissue and blood; this has been shown previously by Donahue and colleagues (22). (b) For the biologically compartmentalized gadopentetate dimeglumine, fast exchange of water between intracellular and extracellular spaces in blood and myocardial tissue exists, such that a single R1 value characterizes the entire voxel. This assumption holds true for blood, in which the exchange rate of water between serum and blood cells is considered to be fast at the concentrations of gadopentetate dimeglumine used in the current study. In tissue, the exchange rate between cellular and interstitial spaces is considered to be intermediate to fast (23). The water exchange rate between the intravascular and extravascular spaces is variable. However, at equilibrium concentration during the constant infusion of gadopentetate dimeglumine and distribution in the intravascular and extravascular spaces, the exchange rate between these two compartments can also be expected to be fast (22–26).
The was related to the distribution volume of gadopentetate dimeglumine by the following relation: distribution volume = (1 - hematocrit level) · . However, because we did not measure the peripheral hematocrit level, we could not calculate the distribution volume but only report itself.
The calculated values for were averaged per sector and per section for all healthy subjects to determine spatial variation in the estimation. In addition, a pooled mean of the was determined for all healthy subjects, sections, and sectors.
The values in patients with acute or chronic infarctions were compared with the mean values in patients with corresponding normal sectors. The ratio of the patient value to the value of the corresponding normal sector was determined for each circumferential sector. A cutoff value of 20% (approximately 1 SD of the normal values) above baseline measurements, which corresponded to a ratio of 1.2, was chosen to determine sensitivity and specificity of this ratio for the delineation of increased values of in nonviable or acutely infarcted segments. For visualization, this ratio was also displayed in a "bull’s-eye" view for all four sections imaged.
Statistical Methods
Measurements were expressed as means plus or minus the SD. Magnitude differences in the of the sectors of each of the four sections were compared by performing a one-way analysis of variance and a Scheffé post hoc test. Differences between the values of the of acutely and chronically infarcted myocardium and the corresponding values for each normal sector were assessed by performing a paired two-tailed Student t test. A nonpaired two-tailed Student t test was performed to compare the pooled means of normal and acutely and chronically infarcted segments. For all statistical analyses, a P value of 
.05 was considered to indicate a significant difference.
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RESULTS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODS RESULTS DISCUSSIONREFERENCES |
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in Healthy Volunteers in the healthy volunteers was 0.56 mL/g ± 0.10. The magnitude of the estimated was uniform, with a small SD over the entire myocardium. Regional variations of the magnitude are shown in Figure 2. Increased values of were observed within the septal segments of each section and reached significance for segments at the inferior intersection of the left and right ventricles (Table 2).
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of these segments was 0.78 mL/g ± 0.09. This mean differed significantly from the calculated mean in normal segments (P < .001). The difference between the mean of a nonviable segment and that of the corresponding normal segment was 0.19 mL/g ± 0.08, which corresponded to a mean increase of 33% ± 16%. The paired differences between normal and chronically infarcted segments were highly significant (P < .001). In only four of the 34 segments was the increase of in the nonviable segment less than 20% of the normal value for the corresponding segment (Fig 3). These four were thin segments of the apical inferior septum or septal wall, in which the normal mean values were also elevated, as compared with the rest of the ventricle.
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value. These segments could not be differentiated from chronically infarcted segments on the basis of the calculated ratio (specificity, 96%). Four of these five segments were adjacent to nonviable segments.
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ratio of chronically infarcted segments to normal segments was calculated with the mean normal value of 0.56 mL/g and the same cutoff value for this ratio of 1.2 was chosen, 32 of the 34 nonviable segments were correctly identified (sensitivity, 94%), with seven false-positive results in the 126 normally contracting segments (specificity, 94%).
Partition Coefficients in Acutely Infarcted Tissue
By using the criteria outlined earlier, 15 of a possible 160 segments were identified as being acutely infarcted. The mean of these segments was 0.91 mL/g ± 0.11, which was significantly higher than that of the normal segments (P < .001) and nonviable myocardium (P < .001). The difference between the mean of the acutely infarcted segments and that of the corresponding normal segments was 0.38 mL/g ± 0.12, which corresponded to a mean increase of 73% ± 26%. The paired difference between normal and acutely infarcted segments was highly significant (P < .001). The minimum increase of , as compared with the value of the corresponding normal segment, was 38% (Fig 3).
Fifteen of 15 acutely infarcted myocardial segments were identified on the basis of the calculated ratio of patient to normal values (sensitivity, 100%) (Fig 5). In one patient, three segments with normal wall motion that were adjacent to a large anterior wall infarction had an increased ratio of (>1.2) and an appearance similar to that of the acute infarction on the bull’s-eye display. The other 142 of the 145 noninfarcted segments could be clearly differentiated from the acutely infarcted segments (specificity, 98%).
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by using the same cutoff value for the calculated ratio, all 15 acutely infarcted segments were identified (sensitivity, 100%). Eleven of the 145 normal segments had an increased ratio (specificity, 92%). |
DISCUSSION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODS RESULTS DISCUSSIONREFERENCES |
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value of gadopentetate dimeglumine in humans in vivo, as determined by performing the Look-Locker sequence, is 0.56 mL/g ± 0.10 and (b) the gadopentetate dimeglumine measurements in chronically and acutely infarcted myocardium are significantly higher than those in normal myocardium.
T1 Values
The measurement of relaxation times by using a Look-Locker technique has been validated in vitro and in vivo (16,27–29). Precontrast measurements of myocardial and blood relaxation times are in keeping with data in the literature (16,27,30). A remaining problem with such T1 measurements in vivo is the fact that MR imaging can be used to measure the effect of gadopentetate dimeglumine on water in a voxel rather than the concentration of gadopentetate dimeglumine itself. Not knowing the differences in water exchange rates between acutely or chronically infarcted and normal myocardium may lead to uncertainty in measurement (31). However, Arheden et al (10) have shown that indirect MR imaging measurement of myocardial gadopentetate dimeglumine content on the basis of T1 correlates well with the more direct radioisotope measurement of technetium 99m–diethylenetriaminepentaacetic acid.
Additional variability in the T1 measurement with the fast Look-Locker sequence is related to the nature of the data acquisition. Because data are acquired during multiple phases throughout the entire cardiac cycle, heart rate variability and spatial smearing during ventricular contraction can introduce uncertainties. However, SDs of the presented data that we obtained by using the Look-Locker sequence were not greater than those obtained by using other researchers’ T1 measurement techniques (30,32,33).
Magnitude and Spatial Distribution of in Normal Myocardium
The magnitude of in normal human myocardium was higher than that previously reported in animals (11,12,19) and varied throughout the heart. Such spatial variations have been described for measurements of in dogs and may be explained by true organ heterogeneity (11,12). In the current study, however, a systematic variation of with the location in the myocardium was noted, with increased values in the septum of each section. This elevation likely was due to partial volume effects of mixed blood-myocardium voxels that resulted from the limited spatial resolution with the Look-Locker technique we used. Such partial volume effects are more pronounced at the right-left ventricular junction with the blood pool on both sides of the myocardium, especially if the septum is thin.
Similar partial volume effects may also account for the insignificant trend of increase of at the apex; mixed blood-myocardium voxels are more likely to be included within the more prominent trabeculation near the apex of the heart. In addition, the greater curvature of the heart at the apex increases the partial volume contribution within a section of 8-mm thickness. These partial volume effects potentially yield increased T1 measurements of myocardium before contrast material administration, because blood T1 is longer than myocardial T1; these effects also yield decreased T1 measurements of myocardium after administration of gadopentetate dimeglumine, because the postcontrast T1 values of blood are lower than those of myocardium. As a result, the calculated we measured in healthy myocardium in vivo may be slightly higher than that measured with other methods (10–12,33). However, in cases of chronic and acute infarction, these measurement uncertainties can be expected to be smaller, because the differences in postcontrast T1 values between infarcted myocardium and blood are smaller.
in Acute and Chronic Infarctions
In animals, an increase in the distribution volume has been described for extracellular markers of a molecular weight similar to that of gadopentetate dimeglumine after myocyte death due to a loss of sarcomere integrity, which allows the extracellular tracers to be passively distributed into the intracellular spaces of irreversibly injured myocardial cells (34,35). A loss of sarcomere membrane integrity has been observed in regions of high signal intensity in cases of acute infarction (1), and the fractional distribution volume of gadopentetate dimeglumine in reperfused infarctions in another study (10) was close to that of the combined intra- and extracellular spaces (10). Our study data show that, similar to those in animals, the value of gadopentetate dimeglumine and thus the distribution volume are increased in acute infarctions in humans. This finding is consistent with observed late enhancement patterns after acute myocardial infarction (36). Our data also show that was increased in healed infarctions, which is consistent with the known increase of extracellular space of collagenous scars (14,15). The more subtle increase of in healed infarctions may explain in part the controversial description of late enhancement patterns in chronic infarction (5–9). In our analysis, we failed to identify three nonviable segments in chronic myocardial infarction in the ventricular septum on the basis of the measurement. In such areas, the effect of an increased distribution volume for gadopentetate dimeglumine may be mimicked by the effect of partial volume contribution of mixed blood-myocardial voxels and thus reduce sensitivity.
Clinical Utility of in the Assessment of Viability
The overall sensitivity and specificity for the detection of nonviable myocardial segments on the basis of the calculated ratio was greater than 90%, regardless of the comparison between corresponding segments or between patient segments and the measured mean value in healthy volunteers. Therefore, the method used in the current study may be used as an independent measurement of myocardial viability.
The determination of at equilibrium distribution overcomes difficulties that are related to direct imaging of signal intensity changes after administration of gadopentetate dimeglumine; these difficulties include (a) the sensitivity of the imaging sequence to changes in T1 contrast between tissues and (b) the influence of tissue perfusion and gadopentetate dimeglumine pharmacokinetics on signal intensity in infarcted tissue (28,29). Recently introduced imaging techniques such as inversion recovery have been shown to be highly sensitive and accurate for the delineation of acutely infarcted myocardium (2). The direct measurement of , as described in the current study, provides information in addition to detecting infarcted myocardium. The precontrast T1 values did not differ between normal and infarcted myocardium. Postcontrast T1 values in infarcted myocardium were significantly different from those in normal myocardium, but postcontrast T1 values alone were not sensitive enough to differentiate between acute and chronic infarctions (Table 1). However, differences in values between chronic and acute infarction, as measured in the current study, were highly significant. These results suggest that direct measurements of may allow a noninvasive regional evaluation of ventricular remodeling after ischemic injury.
Clinical Applicability
The time requirement for data acquisition and analysis with the presented technique is 1–2 minutes for acquiring and 10 minutes for postprocessing each section, for a total of approximately 45 minutes. With more automated image analysis procedures, time requirements may be substantially reduced; this would allow determination of unambiguous values of on a routine clinical basis.
Limitations
The major potential limitation of this study was the partial volume effect. The spatial resolution of the Look-Locker imaging sequence contributes to uncertainties in the measurement of T1 values. In addition, was assessed artificially by averaging values for the total area included in a circumferential sector. Although such an approach is practical and allows a formal comparison with wall motion analysis, it has several shortcomings: Averaging values over a sector may lead to an underestimation of the values of infarcted tissue if noninfarcted tissue also is included. Furthermore, anatomic reference points were used to define the eight sectors, and their position may vary from patient to patient and does not usually account for the variation in individual vessel distribution. The sector-based comparison of wall motion and values may also lead to a discrepancy in the case of a "patchy" infarction pattern, in which remaining viable myocytes maintain a normal wall motion, but is increased because of scattered cell death. Such patterns in the rim of larger infarctions may have led to the four false-positive results in the current study.
Another limitation of this study was that we did not attempt to predict functional recovery after revascularization or test for it at follow-up examinations. We presumed cell death on the basis of other criteria. However, in the setting of chronic infarction, the results of using as a discrimination factor, as compared with low-dose dobutamine, show that can be used with high accuracy as an independent variable to assess myocardial viability. Further research will be necessary to determine whether hibernating myocardium can be identified as abnormal resting wall motion that is accompanied by a normal .
In conclusion, quantification of allows differentiation between normal and nonviable myocardium in acute and chronic myocardial infarction in humans. The high sensitivity and specificity of this type of measurement may allow use of of gadopentetate dimeglumine as an independent measurement of myocardial viability.
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ACKNOWLEDGMENTS |
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FOOTNOTES |
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R1 = change in R1,
= partition coefficient Author contributions: Guarantor of integrity of entire study, C.H.L.; study concepts, S.J.F., C.H.L.; study design, S.J.F., S.E.F., C.H.L.; definition of intellectual content, C.H.L., S.J.F.; literature research, S.J.F.; clinical studies, S.J.F., C.H.L.; data acquisition, S.J.F., C.H.L.; data analysis, S.J.F., S.E.F., C.H.L.; statistical analysis, S.J.F.; manuscript preparation and editing, S.J.F.; manuscript review, S.J.F., C.H.L.
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REFERENCES |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODS RESULTS DISCUSSIONREFERENCES |
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S. Flacke, J. S. Allen, J. M. Chia, J. H. Wible, M. P. Periasamy, M. D. Adams, I. K. Adzamli, and C. H. |
= section 1, 
= section 2, 
= section 3, 
= section 4.
