CLINICAL RESEARCH: CARDIAC IMAGING
Late gadolinium-enhanced magnetic resonance imaging in acute and chronic myocardial infarction
Improved prediction of regional myocardial contraction in the chronic state by measuring thickness of nonenhanced myocardium
Yasutaka Ichikawa, MD*,
Hajime Sakuma, MD ,*,
Naohisa Suzawa, MD*,
Kakuya Kitagawa, MD,
Katsutoshi Makino, MD ,
Tadanori Hirano, MD* and
Kan Takeda, MD
* Department of Radiology, Matsusaka Central Hospital, Mie, Japan
Department of Radiology, Mie University Hospital, Mie, Japan
Department of Internal Medicine, Matsusaka Central Hospital, Mie, Japan
Manuscript received April 18, 2004;
revised manuscript received November 19, 2004,
accepted November 29, 2004.
* Reprint requests and correspondence: Dr. Hajime Sakuma, Department of Radiology, Mie University Hospital, 2-174 Edobashi, Tsu, Mie 514-8507, Japan
(Email: sakuma{at}clin.medic.mie-u.ac.jp).
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Abstract
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OBJECTIVES: We sought to determine serial changes of enhanced and nonenhanced tissue on late gadolinium-enhanced cardiac magnetic resonance (CMR) imaging in patients with a myocardial infarction (MI) and to assess whether thickness of nonenhanced myocardium can improve the detection of preserved contractile function in the chronic state.
BACKGROUND: Previous studies demonstrated that enhancement on late gadolinium-enhanced CMR images indicates myocardial necrosis, and nonenhancement shows the presence of viable myocardium.
METHODS: The CMR studies were performed within one week (scan 1) and more than five months (scan 2) after the onset of MI in 18 patients. The area and mean thickness of enhanced tissue and nonenhanced myocardium were measured by using a 30-segment model. Systolic wall thickening on cine CMR at scan 2 was assessed for evaluating regional contractile function.
RESULTS: The amount of enhanced tissue significantly decreased from scan 1 to 2 (22.1 ± 14.0 ml vs. 15.0 ± 9.3 ml, p < 0.001). The averaged thickness of nonenhanced myocardium in the infarct segments significantly increased from scan 1 to 2 (5.2 ± 3.0 mm vs. 6.6 ± 3.2 mm, p < 0.001). Receiver operating characteristic analysis demonstrated that the measurement of thickness of nonenhanced myocardium, compared with measurement of percent transmural enhancement, had better diagnostic accuracy for predicting improved systolic wall thickening form scan 1 to 2 in dysfunctional segments (Az 0.650 vs. 0.594, p < 0.05).
CONCLUSIONS: The amounts of enhanced tissue and nonenhanced myocardium significantly altered from the acute to chronic state in MI patients. The diagnostic performance of CMR imaging for detection of preserved contractile function can be significantly improved by measuring thickness of nonenhanced myocardium in MI patients.
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Abbreviations and Acronyms
| | CMR = cardiac magnetic resonance | | ECG = electrocardiogram or electrocardiographic | | LV = left ventricle/ventricular | | MI = myocardial infarction | | ROC = receiver operating characteristics | | TIMI = Thrombolysis In Myocardial Infarction |
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In patients with an acute myocardial infarction (MI), myocardial salvage is the hallmark of successful coronary intervention and results in long-term reestablishment of myocardial contractile function and improved prognosis (1–4). Ventricular wall motion at rest cannot be used to quantify salvage early after infarction, as both necrotic and viable myocardium may demonstrate impaired regional myocardial contraction (5–7). Consequently, the distinction between reversible and irreversible dysfunction early after infarction is an important clinical issue. In patients with chronic ischemic heart disease who exhibit impaired myocardial contraction, the identification of viable and nonviable myocardium is important in predicting whether patients will have increased left ventricular (LV) ejection fractions and improved survival after revascularization (8–13).
Inversion-recovery cardiac magnetic resonance (CMR) imaging after administration of extracellular contrast agents has a high spatial resolution and can identify infarcted myocardium as an area of persistent enhancement (14). Previous studies demonstrated that the transmural extent of enhancement (percent transmural enhancement) revealed by late gadolinium-enhanced CMR imaging is correlated with a lack of improvement of regional contractile function in patients with acute MI (15–17). In the setting of chronic MI, percent transmural enhancement has been shown to be predictive of recovery of regional contraction after revascularization (18,19).
A previous study using animal models (20) demonstrated that the amount of enhanced necrotic tissue at three days after the onset of MI was substantially higher than that at eight weeks after the onset of MI. Consequently, the optimal threshold of percent transmural enhancement for predicting preserved regional contractile function may be different between acute and chronic MI. On late gadolinium-enhanced CMR images, noninfarcted myocardium with preserved intracellular space is shown as nonenhanced myocardium (20). Thus, regional myocardial viability might be assessed by measuring the amount of nonenhanced noninfarcted tissue rather than the transmural extent of enhanced necrotic tissue. However, there have been no reports eliciting the relationship between the amount of nonenhanced myocardium on late gadolinium-enhanced CMR images in the ischemically injured region and preserved regional myocardial contraction in the chronic state.
In the current study, we evaluated the amounts of enhanced necrotic tissue and nonenhanced noninfarct tissue in the acute and chronic states in patients with MI. In addition, we compared the diagnostic value of measuring the thickness of nonenhanced myocardium and that of measuring percent transmural enhancement in predicting preserved regional myocardial contraction in the chronic state.
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Methods
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Patients.
This study protocol was approved by the institutional review board, and all patients gave written, informed consent. Twenty-five patients (17 men and 8 women; mean age 63.2 ± 11.1 years) admitted to the coronary care units at our hospital with the diagnosis of acute MI, as defined by typical chest pain, characteristic abnormal findings on the electrocardiogram (ECG), and an increased cardiac creatine kinase-MB fraction enzyme level (>9 µg/l) were prospectively enrolled. Patients were included if they had no history of MI, showed single-vessel disease, underwent successful percutaneous transluminal coronary angioplasty with <50% residual stenosis, were clinically stable, had no contraindications to CMR imaging, and could be scanned within one week.
The study population consisted of the 18 patients who had a second MR scan more than five months later (scan 2). Of the seven patients without a second CMR study, three moved to other hospitals and four refused to undergo a second CMR scan. No patient was excluded for technical or image quality reasons. No patient had clinical evidence of a new MI or restenosis of the coronary artery between the first and second scans.
Protocol for MR imaging.
The patient was placed supine in a clinical 1.5-T imager (Magnetom Vision; Siemens, Erlangen, Germany) with body-array coils around the chest. The CMR images were gated to the ECG and obtained during repeated breath-holds. The first CMR imaging was performed at a mean of 4.2 ± 1.4 days after the onset of MI (scan 1). The second CMR image (scan 2) was obtained at a mean of 294.3 ± 122 days after the onset of MI and a mean of 290 ± 121 days after the first CMR imaging.
Late gadolinium-enhanced CMR images were obtained with a segmented inversion-recovery, fast, low-angle shot sequence on contiguous short-axis imaging planes 15 min after intravenous administration of 0.15 mmol/kg gadopentetate dimeglumine (Magnevist, Schering AG, Berlin, Germany) (21). The CMR imaging parameters included a repetition time of 6.0 ms, an echo time of 3.4 ms, an inversion time of 200 to 250 ms, a trigger delay time for inversion recovery pulse of 200 ms, a section thickness of 10 mm, a field of view of 240 x 320 mm, and image matrix of 192 x 256.
Cine CMR images encompassing the entire LV were acquired on contiguous short-axis imaging planes with a segmented, fast, low-angle shot cine sequence. The following imaging parameters were used: a repetition time of 50 ms for each cine frame, an echo time of 4.8 ms, a section thickness of 10 mm, a field of view of 240 x 320 mm, and an image matrix of 192 x 256. The scan parameters were same for scan 1 and scan 2.
Image analysis.
Cine and late gadolinium-enhanced CMR images were assessed on separate days. For the assessments of global LV volume, ejection fraction, and mass and the total volume of enhanced and nonenhanced tissue, all short-axis planes encompassing the entire LV on cine and late gadolinium-enhanced CMR imaging were analyzed. For the segment-to-segment comparison between cine and late gadolinium-enhanced CMR images, we used a 30-segment model in which the LV was divided into six circumferential segments on five basal and mid-ventricular short-axis views. Apical segments were omitted from the segment-to-segment analysis because precise evaluation of systolic wall thickening, percent transmural enhancement, and thickness of nonenhanced tissue was difficult to determine due to partial-volume averaging.
Late gadolinium-enhanced images from scans 1 and 2 were randomized and evaluated by two observers who were blinded to patient identity. Two observers manually traced the borders of the epicardium, endocardium, and enhanced tissue on short-axis, contrast-enhanced CMR images, by consensus with the use of commercial software (MASSPlus, MEDIS Medical Imaging Systems, Leiden, the Netherlands). Papillary muscles were excluded from the myocardium. After determining the total volume of enhanced tissue, the percentage of enhanced tissue for total LV myocardium was calculated as follows: (volume of enhanced tissue x 100/total volume of LV myocardium) (%). The total volume of nonenhanced myocardium was calculated as follows: (total volume of LV wall – volume of enhanced tissue) (ml). For segmental analysis, the thickness of enhanced tissue and that of nonenhanced tissue were measured along 100 chords that were equally distributed along the circumference of the LV. The mean thickness of nonenhanced myocardium and the mean percent transmural enhancement in each segment were determined by averaging the measurements in each segment.
Cine images from scan 2 were randomized and analyzed by two observers who were blinded to patient identity and results on late enhancement. Two observers manually traced the borders of the epicardium and endocardium on short-axis cine CMR images by consensus with the use of MASSPlus. Papillary muscles were excluded from the myocardium. Left ventricular end-diastolic volume, end-systolic volume, ejection fraction, and mass were measured. Ejection fraction was calculated as follows: ([end-diastolic volume – end-systolic volume] x 100/end-diastolic volume) (%). For segmental analysis, the systolic wall thickening on scan 2 was determined as followed: ([end-systolic wall thickness – end-diastolic wall thickness] x 100/end-diastolic wall thickness) (%).
The threshold of regional percent wall thickening for separating the segments with preserved and impaired contractile function was determined as follows. First, we selected 132 normal segments without any enhancement and 21 segments with transmural enhancement by assessing late gadolinium-enhanced CMR images. Then, receiver operating characteristic (ROC) analysis was performed to obtain an optimal threshold of regional percent wall thickening for distinguishing the segments with preserved and impaired contraction function. The optimal cut-off value of 22% was determined by the intersection of the ROC curve with the second bisectrix at which the sensitivity and specificity were identical (22). The sensitivity and specificity were 90.7% at this threshold value.
Statistical analysis.
All values were expressed as the mean value ± SD. The statistical significance of differences between the areas under ROC curves was evaluated with a univariate z score test. A value of p < 0.05 was considered to be statistically significant.
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Results
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Table 1 summarizes the clinical data of the patient population. The mean time between the onset of MI and reperfusion was 3.0 ± 1.0 h, and the mean Thrombolysis In Myocardial Infarction (TIMI) flow grade after reperfusion was 2.9 ± 0.3 in the patients who underwent both CMR scans 1 and 2. At coronary angiography, the infarct-related artery was the left anterior descending coronary artery territory in nine patients, the right coronary arterial territory in seven patients, and the left circumflex coronary arterial territory in two patients. Late gadolinium-enhanced CMR images demonstrated enhancement in all subjects. Myocardial enhancement was observed in 216 (40%) of the 540 segments (18 patients x 30 segments = 540). The LV end-diastolic volume, LV end-systolic volume, LV ejection fraction, and total LV mass measured by cine CMR imaging at scans 1 and 2 are summarized on Table 2. No significant difference was observed between scan 1 and 2 for the LV volume, LV ejection fraction, and total LV mass.
Total volumes of late-enhanced tissue and nonenhanced myocardium in the acute and chronic states.
Table 2 summarizes total volumes of enhanced tissue and nonenhanced myocardium at scans 1 and 2. The total volume of enhanced tissue significantly decreased from scan 1 to 2 (22.1 ± 14.0 ml vs. 15.0 ± 9.3 ml, p < 0.001) (Figs. 1 and 2). The percentage of enhanced tissue compared with total LV mass significantly decreased from scan 1 to 2 as well (19.4 ± 9.1% vs. 13.6 ± 6.6%, p < 0.001). No significant difference was observed between scan 1 and 2 for the total volume of nonenhanced myocardium and LV mass.
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Figure 1 Contrast-enhanced magnetic resonance images in the acute state (A) and chronic state (B), and cine images in the chronic state (C, diastole; D, systole) in Patient #11 after an inferior myocardial infarction. The inferior wall demonstrated normal wall thickening on the cine images acquired in the chronic state.
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Late-enhanced tissue and nonenhanced myocardium in the infarct segments in the acute and chronic states.
The mean thickness of enhanced tissue at scan 2 (5.4 ± 3.3 mm) was significantly less than that at scan 1 (7.7 ± 3.3 mm, p < 0.001). The percent transmural enhancement at scan 2 (44.8 ± 22.2%) was also significantly less than that at scan 1 (59.7 ± 21.2%, p < 0.001). In contrast, the mean thickness of nonenhanced myocardium at scan 2 (6.6 ± 3.2 mm) significantly increased compared with that at scan 1 (5.2 ± 3.0 mm, p < 0.001).
Relationship between the measurements on late-enhanced CMR images and systolic wall thickening in the chronic state.
Figure 3 shows the relationship between the thickness of nonenhanced myocardium at scans 1 and 2 and systolic wall thickening in the chronic state, as well as the relationship between the percent transmural enhancement at scans 1 and 2 and systolic wall thickening in the chronic state in the 216 segments showing late enhancement. A significant positive correlation was observed between the thickness of nonenhanced myocardium measured in the acute and chronic states and systolic wall thickening in the chronic state (scan 1: r = 0.51, p < 0.001; scan 2: r = 0.56, p < 0.001). The percent transmural enhancement measured in the acute and chronic states demonstrated a significant negative correlation with systolic wall thickening in the chronic state (scan 1: r = –0.51, p < 0.001; scan 2: r = –0.48, p < 0.001).
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Figure 3 The relationship between the thickness of nonenhanced myocardium on scan 1 (A) and scan 2 (B) and systolic wall thickening in the chronic state, as well as the relationship between the percent transmural enhancement on scan 1 (C) and scan 2 (D) and systolic wall thickening in the chronic state in the 216 segments showing late enhancement.
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The ROC curves of late gadolinium-enhanced CMR imaging for detecting preserved contractile function on scan 2 are shown in Figure 4. The area under the ROC curve with the measurements of thickness of nonenhanced myocardium was 0.872 for scan 1 and 0.928 for scan 2, being significantly higher than those obtained by the measurements of percent transmural enhancement (scan 1: 0.846, p < 0.05; scan 2: 0.819, p < 0.001).
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Figure 4 The receiver operating characteristic curves of contrast-enhanced cardiac magnetic resonance imaging with the measurements of percent transmural enhancement (dotted line) and with measurements of thickness of nonenhanced myocardium (solid line) for detecting preserved contractile function in the chronic state. The area under the receiver operating characteristic curve with the measurements of thickness of nonenhanced myocardium was significantly higher than that with the measurements of percent transmural enhancement for both scans 1 and 2.
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The optimal threshold of the thickness of nonenhanced myocardium for predicting preserved systolic wall thickening (>22%) in the chronic state, as determined by ROC analysis, was 3.9 mm for scan 1 and 5.1 mm for scan 2. The optimal thresholds of percent transmural enhancement for detecting preserved systolic wall thickening in the chronic state was 69.7% for scan 1 and 52.4% for scan 2 for the chronic phase. The sensitivity, specificity, and diagnostic accuracy of late contrast-enhanced CMR imaging for predicting preserved systolic wall thickening with the measurements of thickness of nonenhanced myocardium were 79.6%, 79.7%, and 79.6% in the acute phase and 88.7%, 87.8%, and 88.4% in the chronic phase, respectively (Table 3). The sensitivity, specificity, and diagnostic accuracy of late-enhanced CMR imaging for predicting preserved systolic wall thickening with the measurements of percent transmural enhancement were 78.2%, 78.4%, and 78.2% in the acute phase and 76.1%, 75.7%, and 75.9% in the chronic phase, respectively.
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Table 3. Test Performance of Contrast-Enhanced Magnetic Resonance Imaging in the Diagnosis of Preserved Wall Thickening in the Chronic Phase
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Prediction of the improvement of regional wall thickening from the acute to chronic phase in dysfunctional segments by measuring thickness of nonenhanced myocardium.
Figure 5 shows ROC curves of late gadolinium-enhanced CMR imaging for predicting improved systolic wall thickening from scan 1 to 2 in the 110 segments showing impaired contractile function on scan 1 (<22% wall thickening). The area under the ROC curve by measuring thickness of nonenhanced myocardium was 0.650, being significantly higher than that by measuring percent transmural enhancement (0.594, p < 0.05).
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Figure 5 The receiver operating characteristic curves of late gadolinium-enhanced cardiac magnetic resonance imaging with the measurements of percent transmural enhancement (dotted line) and with measurements of thickness of nonenhanced myocardium (solid line) for detecting improved contractile function from scan 1 to 2 in the 110 segments showing impaired contractile function on scan 1 (<22% systolic wall thickening). The area under the receiver operating characteristic curve with the measurements of thickness of nonenhanced myocardium was significantly higher than that with measurements of percent transmural enhancement.
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Discussion
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Late gadolinium-enhanced CMR imaging of the myocardium has become increasingly important as a noninvasive method for demonstrating MI. In the current study, we found that the total volume and transmural extent of enhanced necrotic tissue significantly decreased, and the mean thickness of nonenhanced myocardium in infarct segments significantly increased from the acute to chronic state. The ROC analysis (Fig. 4) indicated that regional systolic wall thickening in the infarcted segments in the chronic state has a more close association with thickness of nonenhanced myocardium than with percent transmural enhancement. These results indicate the value of measuring thickness of nonenhanced myocardium in the infarct segments in predicting regional myocardial contractile function.
In this study, we evaluated the changes in enhanced tissue and nonenhanced myocardium from the acute and chronic state in patients with MI and observed a significant reduction in the total volume of enhanced tissue by  32% (22.1 ± 14.0 ml vs. 15.0 ± 9.3 ml). The mean thickness of enhanced tissue in the infarct segments decreased similarly by 30% (7.7 ± 3.3 mm vs. 5.4 ± 3.3 mm), and the mean thickness of nonenhanced myocardium in the infarct segments increased by 27% (5.2 ± 3.0 mm vs. 6.6 ± 3.2 mm, p < 0.001). These findings in clinical patients agree with the results of previous studies using animal models (20,23). Kim et al. (20) measured the total volume of late-enhanced tissue in the dogs at both three days and eight weeks after the onset of MI in a single coronary artery territory. They reported that the total volume of the enhanced necrotic tissue decreased by a factor of 3.4 ± 1.4, and the total volume of nonenhanced noninfarcted myocardium increased by 1.2 ± 0.2-fold at eight weeks in comparison with three days after the onset of MI. A time-related reduction of infarcted tissue was observed in humans as well after the onset of acute MI (24). The reduction of late-enhanced area from the acute to chronic state can be explained that the spatial extent of collageneous scar in the chronic sate is smaller than the spatial extent of myocyte necrosis in the acute state. Although the exact mechanism for the increase in nonenhanced myocardium has not been determined, it can be explained by compensatory hypertrophy. Compensatory hypertrophy may occur not only in noninfarcted myocardium in the infarct-related segments but also in the adjacent segments without infarction.
The assessment of percent transmural enhancement has been proven to be useful in evaluating patients with a recent MI, as well as those with chronic MI. In this study, we found that the optimal threshold for predicting the segments with preserved contractile function is different between acute and chronic MI. This observation has an important implication when assessing infarct segments with an intermediate extent of enhancement. Choi et al. (15) reported that in patients within one week after the onset of MI, 67% of myocardial segments with a 1% to 25% transmural extent of enhancement exhibited improved contractile function in the chronic state, but only 5% of segments with 76% to 100% transmural extent of enhancement showed improvement. Similarly, in patients with chronic MI, Kim et al. (18) found that 60% of the myocardial segments with a 1% to 25% transmural extent of enhancement improved after revascularization, and the likelihood of functional recovery was very limited in the segments with a 76% to 100% transmural extent of enhancement. In the segments showing a 50% to 75% transmural extent of enhancement, no functional recovery was observed in 90% of the segments. In contrast, Choi et al. (15) observed a higher likelihood of the functional recovery (35%) in the segments showing a 50% to 75% transmural extent of enhancement in patients with acute MI. In our current study, the optimal threshold of percent transmural enhancement in predicting the segments with preserved contractile function was 69.7% for acute MI and 52.4% for chronic MI, which corresponds clearly with previous studies.
There has been no previous report investigating the value of measuring the thickness of nonenhanced myocardium in the infarcted segment on late gadolinium-enhanced CMR images in patients with MI. Accordingly, we determined the diagnostic accuracy of measuring thickness of nonenhanced myocardium by using ROC analysis (Fig. 4) and found that thickness of nonenhanced myocardium is a better predictor of preserved regional myocardial contraction in the chronic state. In the chronic state, the thickness of nonenhanced myocardium had a more close relation to systolic wall thickening, and thickness of nonenhanced myocardium of  5.1 mm can predict preserved systolic wall thickening with excellent sensitivity (88.7%) and specificity (87.8%). For late gadolinium-enhanced CMR images acquired in the acute phase, thickness of nonenhanced myocardium exhibited significantly improved diagnostic performance in comparison with percent transmural extent for the prediction of preserved contractile function in the chronic phase. Thickness of nonenhanced myocardium of 3.9 mm in the acute phase can predict preserved systolic wall thickening (>22%) in the chronic state with a sensitivity of 79.6% and specificity of 79.7%. However, the difference in the area under the ROC curves was relatively small for gadolinium-enhanced CMR images obtained in the acute phase. In order to clarify the value of measuring the thickness of nonenhanced myocardium in patients with acute MI, we analyzed the relationship between nonenhanced wall thickness in the acute state and improvement of systolic wall thickening between scans 1 and 2 in the segments showing impaired wall thickening on scan 1. The ROC curve analysis (Fig. 5) demonstrated that the thickness of nonenhanced myocardium on scan 1 is a significantly better predictor of functional improvement during the following five months, compared with percent transmural enhancement.
Several potential limitations should be acknowledged. In the current study, the relationship between the thickness of nonenhanced myocardium and systolic wall thickening was investigated by using a segment-to-segment comparison. In managing patients with MI, it is important to determine the relationship between the amount and distribution of nonenhanced myocardium on late-enhanced CMR imaging and improved global LV function over time. Further study will be required to determine whether assessment of nonenhanced myocardium on late-enhanced CMR imaging can predict improved LV function in the chronic phase. The diagnostic performance of late gadolinium-enhanced CMR was significantly improved by measuring the thickness of nonenhanced myocardium instead of percent transmural extent of enhancement. However, it should be acknowledged that the difference of diagnostic performance was relatively limited, and sufficient diagnostic accuracy was obtained by assessing percent transmural extent of enhancement. Regional systolic wall thickening was used as a reference method in determining regional myocardial contractility. Despite the use of standard imaging procedures and anatomic landmarks, misregistration may be caused by infarction due to scar formation and remodeling. In addition, the effect of through-plane motion, especially in basal segments, cannot be eliminated when cine CMR imaging is employed. A recent study (25) reported that in patients with thinned myocardial segments and LV dilation, these regions with thinned myocardium (<5.5 mm thickness) may demonstrate significantly improvement after revascularization. The difference of the observations of the Shah et al. (25) study from those of our current study seems to be primarily related to the fact that the Shah et al. (25) study focused on patients demonstrating severely dilated LVs. In our current study, all patients had successful reperfusion, and the average TIMI flow grade after coronary intervention was 2.9 ± 0.3. Consequently, global LV function was relatively preserved in most patients. The diagnostic value of measuring the thickness of nonenhanced myocardium and percent transmural enhancement in MI patients should be further evaluated by studying a larger number of MI patients exhibiting various LV dimensions.
Conclusions.
The amounts of enhanced tissue and nonenhanced myocardium significantly altered from the acute to chronic state in patients with MI. The diagnostic performance of late gadolinium-enhanced CMR imaging for detection of preserved contractile function can be significantly improved by measuring the thickness of nonenhanced myocardium in MI patients without severe LV dilation.
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Figure 2 Contrast-enhanced magnetic resonance images in the acute state (A) and chronic state (B), and cine images in the chronic state (C, diastole; D, systole) in Patient #12 after an anteroseptal myocardial infarction. The contractility of the anteroseptal wall was not improved in the chronic state in this patient.
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Abstract
Methods