An improved MR imaging technique for the visualization of myocardial infarction

PURPOSE: To design a segmented inversion-recovery turbo fast low-angle shot (turboFLASH) magnetic resonance (MR) imaging pulse sequence for the visualization of myocardial infarction, compare this technique with other MR imaging approaches in a canine model of ischemic injury, and evaluate its utility in patients with coronary artery disease. MATERIALS AND METHODS: Six dogs and 18 patients were examined. In dogs, infarction was produced and images were acquired by using 10 different pulse sequences. In patients, the segmented turboFLASH technique was used to acquire contrast material-enhanced images 19 days +/- 7 (SD) after myocardial infarction. RESULTS: Myocardial regions of increased signal intensity were observed in all animals and patients at imaging. With the postcontrast segmented turboFLASH sequence, the signal intensity of the infarcted myocardium was 1,080% +/- 214 higher than that of the normal myocardium in dogs-nearly twice that of the next best sequence tested and approximately 10-fold greater than that in previous reports. All 18 patients with myocardial infarction demonstrated high signal intensity at imaging. On average, the signal intensity of the high-signal-intensity regions in patients was 485% +/- 43 higher than that of the normal myocardium. CONCLUSION: The segmented inversion-recovery turboFLASH sequence produced the greatest differences in regional myocardial signal intensity in animals. Application of this technique in patients with infarction substantially improved differentiation between injured and normal regions.     

Enhanced viability imaging: improved contrast in myocardial delayed enhancement using dual inversion time subtraction.

In delayed contrast-enhanced MRI for the assessment of myocardial viability, the TI time in a gated inversion-recovery segmented gradient echo sequence is usually selected to null signal from normal myocardium. Although this TI time generates good contrast between the enhancing infarcted tissue and normal myocardium, there is usually less contrast between the infarct and the blood pool. A subtractive technique utilizing two acquisitions at a long and short TI time is proposed to improve the delineation between infarct-blood and infarct-myocardium. The concept was demonstrated in six mongrel dogs with reperfused myocardial infarction. Infarct-normal myocardium contrast (signal difference) using the proposed enhanced viability imaging (ENVI) technique was 142 +/- 50% (P < 0.001) that of standard magnitude inversion recovery (IR), while at the same TI time for the primary image, infarct-blood contrast, was 247 +/- 136% (P < 0.002) that of magnitude IR. Accounting for increased noise due to the subtraction, signal difference-to-noise ratios (SDNR) did not show a significant change for infarct-myocardium but infarct-blood SDNR for ENVI was 174 +/- 105% that of magnitude-IR (P < 0.03). Thus, marked improvement in the delineation of the infarcted zone was noted over a range of TI times.     

Assessment of myocardial infarction in humans with (23)Na MR imaging: comparison with cine MR imaging and delayed contrast enhancement

PURPOSE: To demonstrate the feasibility of sodium 23 ((23)Na) magnetic resonance (MR) imaging for assessment of subacute and chronic myocardial infarction and compare with cine, late enhancement, and T2-weighted imaging. MATERIALS AND METHODS: Thirty patients underwent MR imaging 8 days +/- 4 (subacute, n = 15) or more than 6 months (chronic, n = 15) after myocardial infarction by using a (23)Na surface coil with a double angulated electrocardiogram-triggered three-dimensional gradient-echo sequence at 1.5 T. In addition, cine, inversion-recovery gradient-echo, and, in the subacute group, T2-weighted images (n = 9) were obtained. Myocardial infarction mass was depicted as elevated signal intensity or wall motion abnormalities and expressed as a percentage of total left ventricular mass for all modalities. Correlations were tested with correlation coefficients. RESULTS: All patients after subacute infarction and 12 of 15 patients with chronic infarction had an area of elevated (23)Na signal intensity that significantly correlated with wall motion abnormalities (subacute; r = 0.96, P <.001, and chronic; r = 0.9, P <.001); three patients had no wall motion abnormalities or elevated (23)Na signal intensity. Only 10 patients in the subacute and nine in the chronic group revealed late enhancement; significant correlation with (23)Na MR imaging occurred only in subacute group (r = 0.68, P <.05). Myocardial edema in subacute infarction correlated (r = 0.71, P <.05) with areas of elevated (23)Na signal intensity but was extensively larger. CONCLUSION: (23)Na MR imaging demonstrates dysfunctional myocardium caused by subacute and chronic myocardial infarction.     

Phase-sensitive inversion-recovery MR imaging in the detection of myocardial infarction

PURPOSE: To prospectively determine if phase-sensitive inversion-recovery (IR) magnetic resonance (MR) imaging eliminates the need to find the precise inversion time (TI) to null the signal of normal myocardium to achieve high contrast between infarcted and normal myocardium. MATERIALS AND METHODS: Informed consent was obtained from each patient for this prospective MR imaging research study, which was approved by the institutional review board. Twenty patients (16 men; four women; mean age, 56 years +/- 12.3) who experienced Q-wave myocardial infarction 2 weeks earlier were examined with a 1.5-T MR system 10 minutes after administration of 0.1 mmol per kilogram of body weight gadobenate dimeglumine. To determine the optimal TI, a TI scout sequence was used. A segmented two-dimensional IR turbo fast low-angle shot (FLASH) sequence and a segmented two-dimensional IR true fast imaging with steady-state precession (FISP) sequence that produces both phase-sensitive and magnitude-reconstructed images were used at TI values of 200-600 msec (TI values were varied in 100-msec steps) and at optimal TI (mean value, 330 msec). Contrast-to-noise ratios (CNRs) of normal and infarcted myocardium and the area of infarcted myocardium were determined. Magnitude-reconstructed IR turbo FLASH images were compared with magnitude-reconstructed and phase-sensitive IR true FISP images. Two-tailed unpaired sample Student t test was used to compare CNRs, and two-tailed paired-sample Student t test was used to compare area of infarction. RESULTS: Mean CNR of images acquired with IR turbo FLASH and IR true FISP (phase-sensitive and magnitude-reconstructed images) at optimal TI (mean value, 330 msec) were 6.6, 6.2, and 6.1, respectively. For a TI of 200 msec, CNR values were -4.3, -4.0, and 7.2, respectively; for TI of 600 msec, CNR values were 3.1, 3.3, and 4.3, respectively. Area of infarcted myocardium was underestimated on magnitude-reconstruction images (P = .002-.03) for short TI values (ie, 200 msec) for both sequences and for a TI of 300 msec for IR true FISP but not on phase-sensitive reconstructed IR true FISP images when compared with IR turbo FLASH images obtained at optimal TI. CONCLUSION: Phase-sensitive image reconstruction results in reduced need for precise choice of TI and more consistent image quality.     

Normal and infarcted myocardium: differentiation with cellular uptake of manganese at MR imaging in a rat model

PURPOSE: To assess whether normal myocardium can be distinguished from infarction at magnetic resonance (MR) imaging with low doses of manganese dipyridoxyl diphosphate (Mn-DPDP). MATERIALS AND METHODS: After 1-hour coronary arterial occlusion and 2-hour reperfusion, three groups of eight rats each were injected with 25, 50, or 100 micromol of Mn-DPDP per kilogram of body weight. The longitudinal relaxation rate (R1) in normal myocardium, reperfused infarction, and blood was repeatedly measured at inversion-recovery echo-planar imaging before and for 1 hour after the administration of contrast material. Afterward, several animals from each group were examined at high-spatial-resolution inversion-recovery spin-echo (SE) MR imaging. RESULTS: Manganese accumulated in normal myocardium but was cleared from reperfused infarction and blood. One hour after the administration of Mn-DPDP, R1 in normal myocardium (1.53 sec(-1) +/- 0.03, 1.73 sec(-1) +/- 0.03, and 1.94 sec(-1) +/- 0.02, respectively, for 25, 50, and 100 micromol/kg) was significantly (P <.05) faster than that of reperfused infarction (0.99 sec(-1) +/- 0.03, 1.11 sec(-1) +/- 0.03, and 1.48 sec(-1) +/- 0.06). Normal myocardium appeared hyperintense on T1-weighted inversion-recovery SE MR images and was clearly distinguishable from reperfused infarction. CONCLUSION: Mn-DPDP-enhanced inversion-recovery echo-planar and SE MR images demonstrated retention of manganese in normal myocardium and clearance of manganese from infarction. Mn-DPDP has characteristics similar to those of widely used thallium and may be useful in the assessment of myocardial viability at MR imaging.     

Acute myocardial infarction: MR evaluation in 29 patients

This study evaluated the ability of MR to identify and characterize the region of myocardial infarction in humans. Twenty-nine patients, all with ECG and enzyme rises consistent with an acute myocardial infarction, were studied by MR 3-17 days from the onset of acute chest pain. Four patients were excluded because of inability to acquire adequate MR studies. For comparison, 20 normal subjects were studied who also had gated MR examinations. The site of infarction was visualized in 23 patients as an area of high signal intensity in relation to the normal myocardium, a contrast that increased on the second-echo image. The regions of abnormal signal intensity corresponded to the anatomic site of infarction as defined by the ECG changes. The mean T2 relaxation time of the infarcted myocardium (79 +/- 22 msec) was significantly prolonged in comparison with the mean T2 (43.9 +/- 9 msec) of normal myocardium (p less than .01). The mean percentage of contrast (intensity difference) between normal and infarcted myocardium was much greater on the second-echo images (65.6 +/- 34.0%) than the first-echo images (27.5 +/- 18.7%). In the normal subjects there was no difference in T2 between the anterolateral (40.3 +/- 5.7 msec) and septal (39.5 +/- 7.4 msec) regions, and percentages of contrast between these two regions of myocardium on the first-echo (9.1 +/- 7.4%) and second-echo (15.0 +/- 13.3%) images were similar. Thus, MR can be used to directly visualize acute infarcts. However, it has several pitfalls, including the necessity to differentiate signal from slowly flowing blood in the ventricle, from increased signal from a region of infarction and artifactual variation of signal intensity in the myocardium due to respiratory motion or residual cardiac motion.     

Infarcted myocardium in pigs: MR imaging enhanced with slow-interstitial-diffusion gadolinium compound P760.

PURPOSE: To assess the value of P760, a gadolinium chelate with slow interstitial diffusion and high relaxivity, for magnetic resonance (MR) imaging of acute myocardial infarction in pigs. MATERIALS AND METHODS: First-pass gradient-echo MR imaging and spin-echo MR imaging were performed with P760 and then with gadoterate meglumine in eight pigs with occlusive acute myocardial infarction. P760 signal intensity enhancement and clearance were compared with those of gadoterate meglumine. RESULTS: The first-pass enhancement ratio of P760 in normal myocardium was higher than that in infarcted myocardium (1.37 +/- 0.06 [SEM] vs 1.05 +/- 0.03, P = .03). The myocardial first pass showed a blood pool-like curve for P760. The blood pool enhancement ratio 40 seconds after injection was higher for P760 than for gadoterate meglumine (left ventricular cavity, 1.75 +/- 0.06 vs 1.45 +/- 0.06, P = .009). Spin-echo MR imaging showed improved contrast between normal and infarcted myocardium after P760 administration: The ratio before contrast material administration was 0.21 +/- 0.03, that at 15 minutes was 0.48 +/- 0.05 (P = .002), and that at 25 minutes was 0.47 +/- 0.07 (P = .003). CONCLUSION: P760 is an MR imaging contrast agent characterized by low diffusion, a blood pool effect soon after low-dose administration, and fast elimination. This agent is useful for improved myocardial perfusion MR imaging of acute myocardial infarction.     

Blood pool contrast agent CMD-A2-Gd-DOTA-enhanced MR imaging of infarcted myocardium in pigs.

The purpose of this study was to assess the ability of the new blood pool contrast agent meglumine-carboxymethyldextran-ethylenediamino-gadoterate (CMD-A2-Gd-DOTA) to depict acute occlusive myocardial infarction (AMI). First-pass gradient-echo and delayed spin-echo magnetic resonance imaging (MRI) was performed 5 days after induction of AMI in a pig model. MRI was correlated with pathology. First-pass imaging with CMD-A2-Gd-DOTA allowed detection of infarcted myocardium in all pigs (n = 7). The infarction was recognized as a black spot on MRI as well as on a parametric image. The signal intensity (SI) amplitudes of normal versus infarcted myocardium were 80.55 +/- 18.61 versus 8.48 +/- 15.50 on MRI and 81.62 +/- 18.50 versus 1.61 +/- 3.73 on the parametric image (both P values < 0.001. The contrast ratio between normal and infarcted myocardium was not significantly improved on spin-echo MRI, suggesting largely intact vascular integrity outside the occluded area. CMD-A2-Gd-DOTA is useful for depicting occlusive myocardial infarction by first-pass MRI. Spin-echo imaging is promising in assessing vascular integrity. J. Magn. Reson. Imaging 1999;10:170-177.     

Recent myocardial infarction: assessment with unenhanced T1-weighted MR imaging

The purpose of the study was to prospectively evaluate a T1-weighted technique for detection of myocardial edema resulting from recent myocardial infarction (MI) or intervention. This study was HIPAA compliant and institutional review board approved. Fifteen men and one woman (mean age, 57.8 years+/-11.5 [standard deviation]) were examined with T1-weighted magnetic resonance (MR) imaging and inversion-recovery cine pulse sequence in two groups, recent MI and chronic MI, and gave informed consent. T1 relaxation times of MI and adjacent myocardium were compared (Student t test and correlation analysis). In patients with recent MI, areas of myocardial edema were well depicted with T1-weighted MR imaging. T1 relaxation times of recent infarcts were longer than those of older MIs (925 msec+/-169 vs 551 msec+/-107, P<.001). From local edema, T1 relaxation time of infarcted myocardium is increased, may remain elevated for 2 months, and enables imaging with T1-weighted techniques.     

Effects of preinfarction angina on myocardial injury in patients with acute myocardial infarction: a study with resting 123I-BMIPP and 201T1 myocardial SPECT.

METHODS: Recent studies have suggested that patients with preinfarction angina have smaller infarcts and a better in-hospital outcome than those without angina. The mechanisms responsible for limitation of infarct size in the presence of preinfarction angina are unclear. We examined the effects of preinfarction angina on myocardial injury in patients with the first acute myocardial infarction with resting 123I-15-(p-iodophenyl)-3-(R,S)-methylpentadecanoic acid (BMIPP) 201TI myocardial scanning performed within 1 mo of infarction. RESULTS: Of 136 patients tested, 48 (35%) had preinfarction angina within 72 h before infarction, whereas 88 (65%) did not. BMIPP and 201TI defects were scored in 9 segments of the left ventricle (0 = normal, 1 = mild defect, 2 = moderate defect, 3 = severe defect, and 4 = no uptake). The total defect score was defined as the sum of the defect scores. There was no significant difference in percentage diameters of stenoses of infarct-related arteries, collateral circulation, total defect scores for BMIPP, or 201TI between the groups with and without preinfarction angina. However, the ratio of total defect score for 201TI to that for BMIPP was significantly smaller for patients with than for those without preinfarction angina (0.64 +/- 0.21 versus 0.74 +/- 0.25, respectively; P = 0.007). CONCLUSION: Preinfarction angina did not affect the areas at risk in acute myocardial infarction, as shown by BMIPP defect, but decreased necrotic myocardium in the areas at risk, as shown by 201TI defect, and increased metabolically damaged but viable myocardium, as shown by BMIPP and 201TI mismatch through unidentified mechanisms other than collateral circulation (e.g., ischemic preconditioning).     

Myocardial viability: assessment with three-dimensional MR imaging in pigs and patients

PURPOSE: To prospectively evaluate the correlation between a three-dimensional (3D) delayed enhancement magnetic resonance (MR) imaging sequence and a two-dimensional (2D) delayed enhancement MR imaging sequence for noninvasive assessment of myocardial viability in pigs and patients. MATERIALS AND METHODS: The pig and patient studies were approved by the responsible authorities, and patients gave written informed consent. MR imaging was performed by using a rapid 3D inversion-recovery balanced steady-state free precession sequence and a 2D segmented inversion-recovery fast low-angle shot sequence as the reference standard. Fourteen pigs with reperfused (n=7) or nonreperfused (n=7) myocardial infarction and 17 patients (13 men, four women; mean age, 64.9 years+/-8.6 [standard deviation]) suspected of having myocardial infarction were included. Linear regression analysis and Bland-Altman analysis were used to compare the infarction volumes. RESULTS: In 10 of the 14 pigs the induction of myocardial infarction was successful. In these pigs, altogether 81 segments with myocardial infarction were demonstrated by both MR sequences, and agreement between the two sequences for classification of transmural extent of myocardial infarction was 99.7%. The infarction volume determined by using 3D MR imaging (4.64 cm3+/-2.48) in the pigs highly correlated with that of 2D MR imaging (4.65 cm3+/-2.39, r=0.989, P<.001) and that of staining by using triphenyltetrazolium chloride (4.67 cm3+/-2.44, r=0.996, P<.001). Thirteen of the 17 patients examined showed myocardial infarction in 34 myocardial segments with both sequences, and agreement between the two sequences for classification of transmural extent of myocardial infarction was 98.6%. In the patients, the infarction volume determined with both sequences highly correlated (9.71 cm3+/-7.47 for the 3D sequence vs 10.01 cm3+/-8.04 for the 2D sequence, r=0.982, P<.001). The breath-hold time necessary for the 3D MR imaging (21.0+/-2.3 seconds) was significantly shorter than that for 2D MR imaging (188.3+/-20.2 seconds, P<.001). CONCLUSION: Myocardial infarction volumes obtained with the 3D MR imaging sequence are highly correlated and in good agreement with volumes obtained with the 2D MR imaging standard approach and reduced the acquisition time by a factor of nine.     

MRI of reperfused myocardial infarct in dogs

The current study evaluated the capability of magnetic resonance imaging (MRI) to detect acutely injured myocardium in the first 5 hr after a 1-hr period of occlusion followed by reperfusion of the coronary artery and to determine if magnetic relaxation times could be used to differentiate injured from normal myocardium. Fourteen dogs underwent left anterior descending coronary arterial occlusion for 1 hr, followed by reperfusion. Electrocardiographic gated MRI was performed before and during coronary artery occlusion and immediately after reperfusion, and serially up to 5 hr postreperfusion. In all dogs with postmortem evidence of myocardial infarction (n = 7), regional increase of signal intensity was observed in the anterior wall of the left ventricle as early as 30 min after reestablishing blood flow to the jeopardized myocardium. The area of increased signal intensity in the myocardium conformed to the site of myocardial infarction found at autopsy. The signal intensities of the jeopardized myocardium were significantly (p less than 0.01) greater than those of normal myocardium at 30 to 300 min postreperfusion. The T2 (spin-spin) relaxation time was significantly (p less than 0.05-p less than 0.01) prolonged in the region of the reperfused myocardial infarct at 30 min (59.6 +/- 13.1 msec) and remained prolonged up to 300 min (62.6 +/- 12 msec) postreperfusion compared with the T2 of normal myocardium (40.6 +/- 5.2 msec). Of the remaining seven dogs, four developed fatal arrhythmias during the reperfusion procedure and three dogs had no evidence of myocardial infarction at pathologic examination. Signal intensities and T2 relaxation times in these three dogs did not change during the experiment. Thus, acutely infarcted and reperfused myocardium can be detected by in vivo gated MRI, using the spin-echo technique, as early as 30 min after reperfusion. The jeopardized myocardium is characterized by a prolonged T2 relaxation time and, therefore, best visualized on T2-weighted images.     

Inversion-recovery-prepared SSFP for cardiac-phase-resolved delayed-enhancement MRI.

Delayed-enhancement magnetic resonance imaging (DE-MRI) can be used to visualize myocardial infarction (MI). DE-MRI is conventionally acquired with an inversion-recovery gradient-echo (IR-GRE) pulse sequence that yields a single bright-blood image. IR-GRE imaging requires an accurate estimate of the inversion time (TI) to null the signal from the myocardium, and a separate cine acquisition is required to visualize myocardial wall motion. Simulations were performed to examine the effects of a steady-state free precession (SSFP) readout after an inversion pulse in the setting of DE-MRI. Using these simulations, a segmented IR-SSFP sequence was optimized for infarct visualization. This sequence yields both viability and wall motion images over the cardiac cycle in a single breath-hold. Viability images at multiple effective TIs are produced, providing a range of image contrasts. In a study of 11 patients, IR-SSFP yielded infarct sizes and left ventricular ejection fractions (LVEFs) similar to those obtained by IR-GRE and standard SSFP, respectively. IR-SSFP images yielded improved visualization of the infarct-blood border because of the simultaneous nulling of healthy myocardium and blood. T(1) (*) recovery curves were extracted from IR-SSFP images and showed excellent qualitative agreement with theoretical simulations.     

Measurement of the distribution volume of gadopentetate dimeglumine at echo-planar MR imaging to quantify myocardial infarction: comparison with 99mTc-DTPA autoradiography in rats.

PURPOSE: To measure the fractional distribution volume of gadopentetate dimeglumine in normal and reperfused infarcted myocardium at magnetic resonance (MR) imaging by using the fractional distribution volume of technetium 99m-diethylenetriaminepentaacetic acid (DTPA) as an independent reference. MATERIALS AND METHODS: Rats were subjected to 1 hour of coronary artery occlusion and 1 hour of reperfusion before inversion-recovery echo-planar imaging or autoradiography. Regional change in relaxation rate (delta R1) ratios for myocardium over blood were compared with radioactivity ratios for myocardium over blood after the injection of 99mTc-DTPA. RESULTS: Both delta R1 and radioactivity ratios demonstrated equilibrium distribution and hence represent partition coefficients (lambda). The fractional distribution volumes were greater in infarcted myocardium (0.90 +/- 0.05 for gadopentetate dimeglumine and 0.89 +/- 0.04 for 99mTc-DTPA) than in normal myocardium (0.23 +/- 0.02 for gadopentetate dimeglumine and 0.16 +/- 0.01 for 99mTc-DTPA). Area at risk at autoradiography was not significantly different from that at histomorphometry. The infarction size defined by using triphenyltetrazolium chloride was 13% +/- 4 smaller than that defined by using autoradiography. CONCLUSION: The fractional distribution volumes of gadopentetate dimeglumine and 99mTc-DTPA are similar and indicate extracellular distribution in normal myocardium and intracellular as well as extracellular distribution in reperfused infarction. Because the failure of cells to exclude these agents is indicative of necrosis, contrast medium-enhanced MR imaging may be useful to quantify myocardial infarction.     

Fast inversion-recovery MR: the effect of hybrid RARE readout on the null points of fat and cerebrospinal fluid.

PURPOSETo evaluate the effect of the hybrid RARE (rapid acquisition with relaxation enhancement) readout, commonly coupled to inversion-recovery pulse sequences, on the null inversiton time (TI) of fluid and fat using both phantoms and human volunteers.METHODSTwo phantoms, simulating fat (phantom A) and cerebrospinal fluid (phantom B), respectively, were imaged using a fast inversion-recovery sequence that coupled an inversion-recovery preparation pulse to a hybrid RARE readout. At repetition times (TRs) ranging from 700 to 20,000, the TI necessary to null the signal from each phantom (null TI) was determined for an echo train length of 4, 6, 8, 10, 12, 14, 16, 18, and 20, respectively. Plots of null TI versus echo train length at different TRs were generated for both phantoms. Fast inversion-recovery MR imaging of the cervical spine and brain was performed in healthy volunteers. At a fixed TR and TI, the adequacy of signal suppression from bone marrow and cerebrospinal fluid was assessed as a function of echo train length.RESULTSThere was a gradual decrease of null TI for both phantoms with echo train length. This decrease persisted at longer TRs for phantom B (T1 = 3175 +/- 70 milliseconds) than for phantom A (T1 = 218 +/- 5 milliseconds). In the human volunteers, there was a gradual loss of suppression of signal from bone marrow and cerebrospinal fluid, with changes in the hybrid RARE readout.CONCLUSIONTo optimize specific tissue suppression, radiologists implementing fast inversion-recovery MR imaging should be aware of the effects of the hybrid RARE readout on null TI.     

Irreversible myocardial injury: assessment with cardiovascular delayed-enhancement MR imaging and comparison of 1.5 and 3.0 T--initial experience

PURPOSE: To prospectively compare visualization and quantification of irreversible myocardial injury in patients with chronic myocardial infarction at 1.5- and 3.0-T magnetic resonance (MR) imaging. MATERIALS AND METHODS: The institutional research ethics committee approved the study. Participants gave written informed consent. Sixteen male patients (mean age, 66 years +/- 13 [standard deviation]) with myocardial infarction were imaged with the same sequence by the same operator at 1.5 and 3.0 T. After cine imaging, a bolus of gadodiamide was administered. Short-axis images of entire left ventricle (LV) were acquired with a breath-hold T1-weighted segmented inversion-recovery turbo fast low-angle shot (FLASH) sequence. Agreement for myocardial hyperenhancement (HE) mass between field strengths was assessed with Bland-Altman method; agreement for detection and transmural extent of HE was assessed with kappa statistics. Intra- and interobserver reproducibility of mass and transmural extent of HE were assessed at 1.5 and 3.0 T. RESULTS: Bland-Altman analysis revealed no systematic bias (mean difference, 0.2 g; 95% confidence interval: -0.7 g, 1.2 g) and acceptable limits of agreement (-3.3 to 3.8 g) between field strengths for HE mass. HE mass measurements were strongly correlated (R(2) = 0.99); there was no significant difference in measurements at 1.5 and 3.0 T (28.1 g +/- 15.7 [22.6% +/- 10.9 of LV mass] vs 27.8 g +/- 15.7 [22.3% +/- 10.7 of LV mass], respectively; P = .599). For all segments, there was a high degree of agreement for HE detection (kappa = 0.90) and transmural grade (kappa = 0.79) between field strengths. Intra- and interobserver variability were low between both field strengths. Initial inversion time selected to null the signal of normal myocardium at 3.0 T was 57 msec +/- 20 longer than at 1.5 T (P < .01). CONCLUSION: By using the same turbo FLASH MR pulse sequence, there was strong agreement in mass and transmural extent of myocardial HE between 1.5 and 3.0 T.     

Quantitation of reperfused myocardial infarction by Gd-DOTA-enhanced magnetic resonance imaging. An experimental study.

Because there is evidence that myocardial infarct size is modified by coronary artery reperfusion, an ex vivo experimental model of myocardial infarction was developed to determine the influence of the timing of gadolinium-tetraazacyclododecane tetraacetic acid (Gd-DOTA)-enhanced magnetic resonance imaging (MRI) on the accuracy of infarct size quantitation. Eighteen dogs underwent a 2-hour coronary occlusion followed by 1 (n = 6), 6 (n = 6), or 48 (n = 6) hours of reperfusion. Gd-DOTA was injected 10 minutes before the dogs were killed. T1 (SE 250/26) and T2 (SE 1500/78) weighted images were performed on excised hearts. Gd-DOTA concentration was measured in myocardium by atomic emission spectrometry, and correlated with myocardial blood flow evaluated by radioactive microspheres. All dogs presented with myocardial infarction (mean size 20.4% +/- 3.1% of the left ventricle), and a corresponding area of increased signal intensity on T1-weighted MR images. In none of the three groups did the area of high signal intensity correlate with the ischemic area. By contrast, after 6 and 48 hours of reperfusion, the high signal intensity area (17.9% +/- 2.4%) closely matched the area of nonreversible jeopardized tissue (16.4% +/- 2.5%), as determined on tetrazolium-stained heart slices. Although a noreflow phenomenon was observed in the jeopardized tissue, Gd-DOTA concentration was higher in the subendocardial central ischemic zone than in normally perfused myocardium. Gd-DOTA imaging enhancement seems to be the consequence of a delayed clearance of the agent from the injured tissue. Gd-DOTA-enhanced MRI accurately quantitates the size of reperfused myocardial infarction on the ex vivo heart for more than 6 hours after the beginning of reperfusion. It remains to be determined whether the in vitro results obtained here can be applied to assess the myocardial infarct size in vivo.     

In vivo myocardial tissue kinetics of Gd(ABE-DTTA), a tissue-persistent contrast agent.

The phenomenological tissue kinetics of Gd(ABE-DTTA) was investigated in myocardial infarction (MI). Reperfused infarction was generated by balloon catheter in closed-chest canines (N=11). Forty-eight hours thereafter, inversion-recovery (IR)-prepared fast gradient-echo control images were acquired with varying inversion times (TIs). Precontrast R(1) maps were calculated from the TI dependence of signal intensity (SI) using nonlinear curve fitting. Then 0.05 mmol/kg Gd(ABE-DTTA) was administered I.V. In 11 dogs postcontrast R(1) maps were generated at 24 hr and 48 hr postcontrast. In five dogs measurements were also repeated at 108 hr and 12 days. In one dog early measurement was carried out at 4 hr. Delta R(1) values for blood and viable and infarcted myocardium were calculated at each time point by subtracting the precontrast R(1) from the postcontrast R(1). Gd(ABE-DTTA) showed significant, progressive accumulation into infarcts during the first 2 days (k(in)=0.39 hr(-1)) and a delayed clearance (k(out) = 0.005 hr(-1)). Among the time points sampled, the maximum infarct Delta R(1) was detected at 48 hr (1.72 s(-1)). Contrast agent (CA) in infarcted tissue was detectable for 12 days. Clearance from blood and viable myocardium occurred in parallel and was completed by 108 hr. Gd(ABE-DTTA) displays slow, tissue-persistent kinetics and partly intravascular, partly extravascular characteristics. It demonstrates high affinity for infarcted myocardium and induces highlighting of infarcts between 4 hr and 12 days following administration.     

Planar myocardial perfusion imaging with technetium-99m-teboroxime: comparison by vascular territory with thallium-201 and coronary angiography.

Myocardial perfusion agents labeled with 99mTc offer improved physical imaging properties compared to 201TI. Teboroxime is a new 99mTc-labeled compound for myocardial perfusion imaging that shows a high myocardial extraction and rapid clearance. Sixty-seven patients underwent planar teboroxime imaging with a rapid acquisition protocol. Agreement of teboroxime and 201TI for the presence or absence of disease occurred in 56/65 patients (86%). There was agreement (normal or abnormal) between the two agents in 156/195 vessels (80%) and 457/585 segments (78%). When abnormal segments (ischemia or infarction) were compared, teboroxime showed significantly more ischemic segments (89/135, 66%) than did 201TI (73/135, 54%, p < 0.05). Teboroxime offers accuracy comparable to 201TI for the diagnosis of coronary artery disease and may improve the detection of ischemic or viable myocardium. In addition, its rapid myocardial clearance permits stress/rest imaging in 60-90 min.     

Left ventricular postmyocardial infarction remodeling studied by combining MR-tagging with delayed MR contrast enhancement

OBJECTIVES: We sought to monitor the evolution of noninfarcted and infarcted myocardium function in the process of left ventricular (LV) remodeling after a reperfused myocardial infarction. MATERIAL AND METHODS: Pigs (n = 8) were subjected to reperfused infarction. Magnetic resonance imaging (MRI) was performed at 3 days and 8 weeks after infarction. Regional circumferential shortening (Ecc) and principal strain L1 in the infarcted, peri-infarcted, and remote myocardium were evaluated by tagged cine MRI combined with matched late enhancement data (Gadolinium-DOTA-enhanced IR-GRE) Global LV function was evaluated by cine MRI. Animals were euthanized after the second imaging session and tissue samples from the different myocardial regions were obtained for histopathologic study. RESULTS: There was a significant deterioration in Ecc between the 3-day and 8-week studies in the peri-infarcted myocardium at apex (-9.9% +/- 4.5% to -6.5 +/- 3.9; P = 0.046) whereas it remained stable for all other regions at all levels. A trend toward improvement in Ecc existed in the infarcted myocardium when infarction transmurality was less than 50% of the LV wall (-7.5% +/- 0.8% to -12.2% +/- 2.9% P = 0.06). Ecc in infarcted myocardium was significantly inferior (P < 0.002) to that in remote and peri-infarcted myocardium at the apical level (2.7% +/- 2.6% vs. -14.4% +/- 3.3% and -9.9% +/- 4.5%, respectively). Global LV function substantially deteriorated after infarction and was associated with a significant LV dilation. CONCLUSION: These results confirm the hypothesis that scarred myocardium imposes additional functional burden to the peri-infarcted myocardium.