Serial magnetic resonance imaging in patients following acute myocardial infarction.

The detection of serial changes in magnetic resonance (MR) signal intensity of the heart following acute myocardial infarction may provide a useful method of characterizing tissue healing. Fourteen patients with acute Q-wave infarction underwent T2-weighted, spin-echo cardiac imaging during hospitalization, followed by one or more additional MR studies (total 31) over a 6- to 27-wk period (mean: 3 mo). Visual assessment of the images demonstrated a gradual reduction in signal intensity and localization of the bright signal to the subendocardium of the infarction region over the three-mo study period. A quantitative measurement of signal intensity (infarction/normal myocardium) fell from 1.81 +/- 0.42 on the initial study to 1.34 +/- 0.37 (p less than 0.05) at a mean of 14 wk. Two patients had an increase in signal intensity on the follow-up study and both patients had been readmitted with acute coronary syndromes. In summary, characterization of changes in signal intensity may provide a useful method of assessing myocardial healing following acute myocardial infarction. Further studies are indicated to determine the prognostic significance of these parameters.     

Imaging Perfusion Deficits in Ischemic Heart Disease with Susceptibility-Enhanced T2-Weighted MRI: Preliminary Human Studies

Aim: This feasibility study explores relative myocardial perfusion characterization with an investigational T₂/T₂1 contrast agent. Methods: Dysprosium-DTPA bis (methylamide) was administered peripherally in six patients with thallium defects. Rest and stress multi-section, gated, T₂-weighted images were acquired with a 1.5 T echo-planar imager. Change in transverse relaxation rate was calculated in four segments for each subject. Results: Magnetic resonance (MR) identified five of five instances of ischemia or infarction, at a dose of agent (0.25 mmol/kg) that was comparable to that currently used with clinically approved gadolinium agents. Injection at twice this dose resulted in saturation of the signal change, and the one ischemic segment corresponding to the higher dose was not identified by MR. MR was negative in two segments which, on final diagnosis, were determined to manifest thallium attenuation artifact. Conclusion: MR perfusion imaging with high susceptibility agents has the potential to characterize myocardial perfusion deficits.     

Visualization of myocardial infarction and subsequent coronary reperfusion with MRI using a dog model

Twelve anesthetized mongrel dogs underwent left thoracotomy with placement of a removable ligature around the left circumflex coronary artery. Following a 3 to 6 hour delay, ECG-gated spin-echo MRI was performed. The ligature was then removed reperfusing the heart, and after a 10-15 min period, MRI repeated. Finally, post-sacrifice images were obtained, and the hearts chemically stained for infarct evaluation. The MR images were subjectively and quantitatively evaluated for visibility of the endocardial border and of the injured myocardium, and for changes after reperfusion. The injured tissue was variably visible in vivo, the major limitation a result of motion blurring and artifact. The abnormal tissue was easily visible on MRI in 11 animals, and not clearly visible in one. The endocardial border was easily seen in 10 animals. The variation of calculated relaxation times was high for both normal and ischemic/infarcted myocardium in the beating hearts (normal: T1 = 566 +/- 288, T2 = 38 +/- 6; injured myocardium: T1 = 637 +/- 250, T2 = 41 +/- 12) in contrast, relatively stationary skeletal muscle measured in the same images had narrower ranges (T1 = 532 +/- 199, T2 = 28 +/- 2). Changes with reperfusion were seen, but not reliably. The infarcted or ischemic zones were easily visible on post-sacrifice images in all animals imaged. Post-sacrifice relaxation times were T1 = 564 +/- 69 msec, T2 = 39 +/- 3 msec for normal heart muscle, and 725 +/- 114, T2 = 47 +/- 5 for ischemic/infarcted tissue.(ABSTRACT TRUNCATED AT 250 WORDS)     

Measurement of kinetic perfusion parameters of gadoteridol in intact myocardium: Effects of ischemia/reperfusion and coronary vasodilation

Quantitation of myocardial perfusion is feasible using contrast enhanced magnetic resonance imaging. A method to quantitate myocardial blood flow is provided by the Kety model modified to account for a diffusable tracer such as gadoteridol. In the present study, perfusion parameters of the modified Kety model (partition coefficient and extraction efficiency) were determined for gadoteridol in intact myocardium using a constant flow, isolated, perfused heart model. Perfusion conditions included hearts with normal perfusion, hearts made globally ischemic for 20 min then perfused normally, and hearts whose coronary flow was more than doubled with 9 μM adenosine. T1 relaxation times were rapidly measured at 0.5 T following step increases in perfusate gadoteridol concentration and at steady state. Both the partition coefficient and extraction efficiency were found to be significantly increased in ischemic/reperfused hearts compared to normal. While flow rates in adenosine hearts were too high for accurate extraction efficiency determination using this technique, the partition coefficient was no different between adenosine and normally perfused hearts. The method described in this article allowed the kinetic parameters of the modified Kety model to be determined in intact heart using NMR relaxation time measurements as the basis of the calculation.     

Differentiation between acutely ischemic myocardium and zones of completed infarction in dogs on the basis of frequency-dependent backscatter

The goal of this work was to determine whether the frequency dependence of apparent backscatter coefficient (not corrected for attenuation within the myocardium) could differentiate completed, remote infarction from acute myocardial injury in vivo. Myocardial infarcts were produced in six dogs by coronary artery occlusion. One to 12 months later, acute ischemic injury was induced in each dog by ligation of a coronary artery that supplied a region of myocardium adjacent to the established infarct. Infarct, ischemic, and normal regions were interrogated with a 5-MHz, circular, 0.5-in. diam, broadband, focused, piezoelectric transducer mounted in a water-filled stand-off device placed against the exposed, beating heart. Apparent backscatter coefficients were measured over the range of frequencies from 3-7 MHz. The frequency dependence was obtained from the slope of log apparent backscatter coefficient versus log frequency. No significant difference in frequency dependence was found between normal and acutely ischemic myocardium for periods of up to 2 h of ischemia. In contrast, frequency dependence in regions of remote infarct (1.8 +/- 0.1, mean +/- standard error) was significantly lower than that in acutely ischemic or nonischemic regions (2.3 +/- 0.1) (p less than 0.01). These results suggest that remote myocardial infarction can be differentiated from acutely injured but still potentially salvageable myocardium in vivo on the basis of the frequency dependence of backscatter.     

Intraventricular dispersion and temporal delay of early left ventricular filling after acute myocardial infarction. Assessment by magnetic resonance velocity mapping

This article aims to describe early left ventricular diastolic inflow using magnetic resonance velocity mapping in patients with recent acute myocardial infarction and in normal volunteers. Magnetic resonance velocity mapping was performed in a long axis plane through the hearts of 46 patients with recent, first time acute myocardial infarction and 43 age-matched normal volunteers. The peak velocities at six levels of the early diastolic inflow stream were recorded. A velocity index was calculated as the peak velocity in each position relative to the peak velocity at the mitral leaflet tips. Also, the temporal delay of velocity propagation was computed. Velocity index 4 cm downstream of mitral leaflet tips was lower in the acute myocardial infarction group (0.42 (0.17)) (mean (SD)) compared to controls (0.59 (0.25)) (p < 0.001). Temporal delay in the same position was longer in the acute myocardial infarction group (62 (67) ms) than in controls (32 (39) ms) (p < 0.02). Blood flow patterns in patients after acute myocardial infarction were characterized by increased dispersion of velocities and increased temporal delay of velocity propagation, probably reflecting impaired active left ventricular relaxation. Intraventricular flow measurements constitute a promising new technique for non-invasive assessment of left ventricular diastolic function.     

Quantitation of renal perfusion using arterial spin labeling with FAIR-UFLARE

Quantitative perfusion imaging of human kidneys was performed using arterial spin labeling MRI with a fast spin echo readout-sequence. Perfusion maps of centrally located single slices were obtained in axial and coronal orientations. In ten healthy volunteers, the mean value of perfusion was 213+/-55 mL/(100g min) with a range from 140 to 319 mL/(100g min). These results are in accordance with literature data, considering the fact that FAIR only measures the perfusion component normal to the imaging plane. Intra-individual reproducibility errors of +/-11% were smaller than the natural interindividual variability of renal perfusion (SD = +/- 25%). Perfusion in the cortex was approximately 3-4 times higher compared to the medulla. Considering the relatively high resolution of 2x2x10 mm3, the ability to quantify perfusion, and the lack of ionizing radiation and contrast media, this technique should prove useful in diagnosing renal pathologies that are associated with reductions in tissue perfusion.     

T2-based area-at-risk and edema are influenced by ischemic duration in acute myocardial infarction

The purpose of our study was to assess whether T2 MRI identifies the infarcted myocardium or the true area-at-risk (AAR) and whether edema is present in the salvageable region following acute myocardial infarction (MI). The study involved a porcine model of MI with a coronary occlusion model of either 60 min or 90 min. Imaging was performed on a 3T MRI pre-occlusion and at day 3 post-MI. Prior-MI, myocardial perfusion territory (MPT) maps were obtained under MRI via direct intracoronary injection of contrast agent. Post-MI, edema extent was quantified by T2 mapping while infarction and microvascular obstruction (MVO) were assessed by late gadolinium enhancement (LGE). Anatomically registered short-axis slices were analyzed for MPT, T2-AAR and infarct areas and T2 relaxation values. Animals were divided into groups with (MVO+) and without MVO (MVO-). T2-AAR area was significantly greater than infarct area in both groups. In the MVO+ group, T2-AAR and MPT were comparable and highly correlated, whereas, in the MVO- group, T2-AAR significantly underestimated MPT without any trend. T2 values in the salvageable myocardium were found to be significantly higher than those in remote myocardium. Our methodology offers the advantage that all images are acquired within the same MRI reference as opposed to complex co-registration with gross pathology. Our study suggests that edema may expand beyond the infarct zone over the entire ischemic bed. T2-AAR may be more clinically relevant than true AAR by perfusion territory since it identifies the “salvageable” myocardium.     

Measurement of regional brain temperature using proton spectroscopic imaging: validation and application to acute ischemic stroke

A magnetic resonance proton spectroscopic imaging (SI) technique was developed to measure regional brain temperatures in human subjects. The technique was validated in a homogeneous phantom and in four healthy volunteers. Simulations and calculations determined the theoretical measurement precision as approximately +/-0.3 degrees C for individual 1-ml voxels. In healthy volunteers, repeated measurements on individual voxels had an S.D. = 1.2 degrees C. In a clinical study, 40 patients with acute ischemic stroke were imaged within 26 h (mean, 10 h) of onset. Temperatures were highest in the region that appeared abnormal (i.e., ischemic) on diffusion-weighted imaging (DWI) compared with a normal-appearing brain. The mean temperature difference between the DWI "lesion" area and the "normal brain" was 0.17 degrees C [P < 10(-3); range, 2.45 degrees C (hotter)-2.17 degrees C (cooler)]. Noninvasive temperature measurement by SI has sufficient precision to be used in studies of pathophysiology in stroke and in other brain disorders and to monitor therapies.     

Differences between arterial occlusive and cortical photothrombosis stroke models with magnetic resonance imaging and microtubule-associated protein-2 immunoreactivity

The differences between two models of cerebral ischemia [middle cerebral arterial transection (MCAT) and cortical photothrombosis (PT)] were explored with multiparametric MRI of apparent diffusion coefficient trace (ADCtr), cerebral blood flow (CBF) and T1. Microtubule-associated protein-2 (MAP2) immunoreactivity sections aligned with the MR images in the same coronal plane were used to map the infarct and to guide region-of-interest selection. In ischemic cortex, the larger T1 increase in PT versus MCAT (42+/-7% vs. 16+/-5%) is related to the different character of edema between these models; yet, neither CBF nor ADCtr discriminated between them at 3.5 h, suggesting that different mechanisms of ischemic damage to the brain cells resulted in the same ADCtr value. CBF and ADCtr were depressed in immediately adjacent ischemic border by 27+/-7% and 47+/-10%, respectively, in MCAT but not in PT, suggesting marginal perfusion in MCAT. CBF in homotopic normal cortex in the opposite hemisphere was higher for PT compared with MCAT (199+/-20 and 134+/-10 ml/100 g/min, respectively). Different pathological processes in the two models affect CBF, ADCtr and T1 in a unique, regionally specific manner. The PT model differs substantially from the MCAT and is not a model of cortical ischemia with an appreciable border zone.     

Elevations of diffusion anisotropy are associated with hyper-acute stroke: a serial imaging study

Diffusion tensor imaging (DTI) studies of human ischemic stroke within 24 h of symptom onset have reported variable findings of changes in diffusion anisotropy. Serial DTI within 24 h may clarify these heterogeneous results. We characterized longitudinal changes of diffusion anisotropy by analyzing discrete ischemic white matter (WM) and gray matter (GM) regions during the hyperacute (2.5-7 h) and acute (21.5-29 h) scanning phases of ischemic stroke onset in 13 patients. Mean diffusivity (MD), fractional anisotropy (FA) and T2-weighted signal intensity were measured for deep and subcortical WM and deep and cortical GM areas in lesions outlined by a > or =30% decrease in MD. Average reductions of approximately 40% in relative (r) MD were observed in all four brain regions during both the hyperacute and acute phases post stroke. Overall, 9 of 13 patients within 7 h post symptom onset showed elevated FA in at least one of the four tissues, and within the same cohort, 11 of 13 patients showed reduced FA in at least one of the ischemic WM and GM regions at 21.5-29 h after stroke. The fractional anisotropy in the lesion relative to the contralateral side (rFA, mean+/-S.D.) was significantly elevated in some patients in the deep WM (1.10+/-0.11, n=4), subcortical WM (1.13+/-0.14, n=4), deep GM (1.07+/-0.06, n=1) and cortical GM (1.22+/-0.13, n=5) hyperacutely (< or =7 h); however, reductions of rFA at approximately 24 h post stroke were more consistent (rFA= 0.85+/-0.12).     

Assessment of myocardial perfusion using multisection first-pass MRI and color-coded parameter maps: a comparison to 99mTc Sesta MIBI SPECT and systolic myocardial wall thickening analysis

The most recently reported magnetic resonance first-pass myocardial perfusion studies were restricted to single slice imaging or a data analysis based on interactively placed regions of interest. This study was designed to investigate a new saturation recovery TurboFLASH sequence for multisection myocardial perfusion imaging and to develop a pixel-based software tool to calculate qualitative perfusion parameters. The findings of perfusion imaging were compared to percent systolic myocardial wall thickening analysis and 99mTc Sesta MIBI SPECT. Six healthy volunteers and twelve patients with proven coronary artery disease (CAD) or chronic myocardial infarction were examined. Diagnostic images were acquired for all volunteers and patients with the multisection saturation recovery TurboFLASH sequence. Perfusion defects could be visualized on parameter maps for signal intensity increase over baseline and signal intensity upslope. Sensitivity and specificity were 76.9% and 97.1% for first-pass perfusion MRI, and respectively 84.6% and 94.3% for CINE imaging. All perfusion defects determined with 99mTc Sesta MIBI SPECT were identified by the combined analysis of myocardial perfusion and wall thickening. The presented software demonstrated a pixel-based analysis of first-pass perfusion studies and simplified image interpretation in a clinical setting. The combination of perfusion and wall motion imaging provided complementary information for the treatment of patients suffering from CAD.     

Magnetic resonance imaging with superparamagnetic iron oxide particles for the detection of myocardial reperfusion

The effect of superparamagnetic iron oxide particles on magnetic resonance myocardial signal intensity was examined in order to define the ability of this agent to identify normal, ischemic, and reperfused myocardium. Data were obtained from 6 normal rats (group 1) and from 6 heterotopic isogenic rat heart transplants (group 2) at 4.7 T with a multislice spin-echo sequence. Images were acquired in (a) normal rats before and after the infusion of 36 μmol Fe/kg of AMI-25 (group 1) and (b) rat heart transplants during control, global myocardial ischemia (before and after the injection of 72 μmol Fe/kg of AMI-25), and following reperfusion (group 2). Myocardial signal intensity decreased by 36 ± 4%, p < 0.001, following contrast infusion in normal hearts (group 1). The intensity remained constant in the rat heart transplants (group 2) during coronary occlusion, both before and after the infusion of AMI-25 and decreased by 61 ± 7%, p < 0.001, upon reperfusion. The larger effect of AMI-25 in reperfused as compared to normal myocardium suggests the presence of ischemia-induced hyperemia. There was no significant difference (analysis of variance) among intensities from different myocardial regions in either group at any stage of the experiment. We conclude that the use of AMI-25 permits identification of normal, ischemic, and reperfused myocardium and may therefore be helpful for the early detection of reperfusion following thrombolytic therapy for acute myocardial infarction.     

Identification of human myocardial infarction in vitro based on the frequency dependence of ultrasonic backscatter.

It has been reported previously that acute and mature myocardial infarction in dogs can be differentiated in vitro and in vivo by ultrasonic tissue characterization based on measurement of the frequency dependence of ultrasonic backscatter. To characterize human infarction with an index of the frequency dependence of backscatter that could be obtained in patients, cylindrical biopsy specimens from 7 normal regions and 12 regions of infarction of 6 fixed, explanted human hearts in 2-deg steps around their entire circumference with a 5-MHz broadband transducer were insonified. One to six consecutive transmural levels were studied for each specimen. The dependence of apparent (uncompensated for attenuation or beam width) backscatter, /B(f)/2, on frequency (f) was computed from spectral analyses of radio-frequency data as /B(f)/2 = afn, where from theoretical considerations the magnitude of n decreases as scatterer size increases. Apparent integrated backscatter was computed as the average of /B(f)/2 from 3 to 7 MHz. The average value for n for normal tissue (0.9 +/- 0.1) exceeded that for tissue from regions of infarction (0.6 +/- 0.1; p less than 0.05). Infarct manifested a significant decrease of n from epicardial to endocardial levels (epi----mid----endo: 0.9----0.7----0.2; p less than 0.05) whereas normal tissue manifested similar values for n at each transmural level (0.8----1.1----0.9; p = NS). Average integrated backscatter across all transmural levels for infarct was significantly greater than for normal tissue (-48.3 +/- 0.5 vs -53.4 +/- 0.4 dB, infarct versus normal; p less than 0.05). The presence of fibrosis was associated with smaller values of n and greater integrated backscatter.(ABSTRACT TRUNCATED AT 250 WORDS)     

Magnetic resonance tissue analysis of acute renal vascular occlusion in the rabbit: enhancement with gadolinium-DTPA complex

In order to assess the sensitivity of nuclear magnetic resonance (NMR) in detecting acute renal vascular insufficiency, in vitro NMR spectroscopy (at 0.25 T) was performed on rabbit renal cortices following 45 min of unilateral renal artery (RAO) or renal vein occlusion (RVO). Data were obtained both with and without paramagnetic enhancement with gadolinium-DTPA (Gd-DTPA). In the absence of contrast material, RVO was distinguished by markedly elevated spin-lattice (T1) and spin-spin (T2) relaxation times when compared to the contralateral control kidney [mean increase of 29% in T1 (p less than 0.001) and 19% in T2 (p less than .001)]. RAO produced no change in T1 (p = N.S.) and a small change in T2 (mean increase of 11%, p less than .01). Five min following injection of 0.05 mM/kg of Gd-DTPA, relaxation times of control kidneys were markedly shortened [mean decrease 75% in T1 (p less than .001) and 12% in T2 (p less than 0.01)]. With Gd-DTPA, kidneys with RVO continued to have elevated T1 and T2 relaxation time, and kidneys with RAO maintained their essentially normal pre-contrast relaxation time values. We conclude that non-contrast NMR tissue analysis clearly differentiated normal from congested (RVO) kidneys, but not from acutely ischemic (RAO) kidneys. Paramagnetic enhancement with Gd-DTPA allows the differentiation of normally perfused from acutely ischemic or congested kidneys.     

Phosphorus-31 MR spectroscopic imaging (MRSI) of normal and pathological human brains.

The goals of this study were to evaluate 31P MR spectroscopic imaging (MRSI) for clinical studies and to survey potentially significant spatial variations of 31P metabolite signals in normal and pathological human brains. In normal brains, chemical shifts and metabolite ratios corrected for saturation were similar to previous studies using single-volume localization techniques (n = 10; pH = 7.01 +/- 0.02; PCr/Pi = 2.0 +/- 0.4; PCr/ATP = 1.4 +/- 0.2; ATP/Pi = 1.6 +/- 0.2; PCr/PDE = 0.52 +/- 0.06; PCr/PME = 1.3 +/- 0.2; [Mg2+]free = 0.26 +/- 0.02 mM.) In 17 pathological case studies, ratios of 31P metabolite signals between the pathological regions and normal-appearing (usually homologous contralateral) regions were obtained. First, in subacute and chronic infarctions (n = 9) decreased Pi (65 +/- 12%), PCr (38 +/- 6%), ATP (55 +/- 6%), PDE (47 +/- 9%), and total 31P metabolite signals (50 +/- 8%) were observed. Second, regions of decreased total 31P metabolite signals were observed in normal pressure hydrocephalus (NPH, n = 2), glioblastoma (n = 2), temporal lobe epilepsy (n = 2), and transient ischemic attacks (TIAs, n = 2). Third, alkalosis was detected in the NPH periventricular tissue, glioblastoma, epilepsy ipsilateral ictal foci, and chronic infarction regions; acidosis was detected in subacute infarction regions. Fourth, in TIAs with no MRI-detected infarction, regions consistent with transient neurological deficits were detected with decreased Pi, ATP, and total 31P metabolite signals. These results demonstrate an advantage of 31P MRSI over single-volume 31P MRS techniques in that metabolite information is derived simultaneously from multiple regions of brain, including those outside the primary pathological region of interest. These preliminary findings also suggest that abnormal metabolite distributions may be detected in regions that appear normal on MR images.     

Whole-body T2* mapping at 1.5 T

This study investigated the feasibility of an MRI protocol providing whole-body T2* maps at 1.5 T. Seven healthy volunteers (mean age=30.1+/-3.7, three women and four men) and two patients (both male, 53 and 46 years old) affected by transfusion-dependent anemias participated in the study. Coronally oriented images of five subsequent body levels were acquired using a fat-suppressed multiecho 2D gradient-echo sequence (12 echo times ranging from 4.8 to 76.3 ms were selected) and afterwards composed. Parametrical T2* maps of the whole body were reconstructed on a pixel-by-pixel basis. For both, healthy volunteers and patients, representative T2* values were computed from extended regions of interest (ROIs). Good-quality whole-body T2* maps were computed in all volunteers and patients. In healthy volunteers, T2* values were assessed in the cerebral white (58.5+/-4.2 ms) and gray (81.4+/-5.5 ms) matter, liver (34.3+/-7.0 ms), spleen (63.5+/-3.3 ms), kidneys (65.4+/-10.3 ms) and skeletal muscles (~30 ms). The liver presented faster relaxation rates in males as compared to females. One patient (serum ferritin concentration=927 microg/dl) showed shortened T2* values in liver (3.6+/-5.5 ms), spleen (3.1+/-4.8 ms), kidneys (11.1+/-7.1 ms) and muscles (25.1+/-3.4 ms). The second patient (serum ferritin concentration=346 microg/dl) presented reduced T2* values in liver (3.9+/-7.3 ms), spleen (20.1+/-9.8 ms) and kidneys (24.6+/-7.7 ms). The presented technique may find clinical application in the assessment of the iron burden in the entire body, and in monitoring of chelation therapies in patients treated with frequent blood transfusions.     

荧光标记法分析心绞痛血瘀证的差异蛋白

应用荧光标记法寻找心绞痛血瘀证血浆差异蛋白,探索心绞痛血瘀证的蛋白质组学特点。方法 采用三种荧光染料(Cy2, Cy3, Cy5)分别标记心绞痛血瘀证患者和正常人血浆样品,双向电泳检测后进行荧光扫描,分析图谱,寻找心绞痛血瘀证血浆差异蛋白,并对差异蛋白点进行质谱鉴定。结果发现Fibrinogen β chain,Fibrinogen γ chain,α1-Antitrypsin,Haptoglobin β chain,Haptoglobin α2 chain在心绞痛血瘀证患者中高表达,ApoA-Ⅳ,ApoA-Ⅰ,Transthyretin在心绞痛血瘀证患者中低表达。表达上调的差异蛋白主要是急性时相反应蛋白,表达下调的差异蛋白根据功能可分为：(1)急性时相反应负相蛋白;(2)载脂蛋白。研究表明, 心绞痛血瘀证可能属于一种炎症反应,并且与脂代谢紊乱有关,新发现的差异蛋白可能为研究或发现抗心绞痛药物作用的新靶标提供线索。荧光标记法适合于差异蛋白组学研究。     

Comparison of NMR Water Proton T1 Measurements in Healthy and Pathological Blood

water proton T1 in blood from healthy volunteers and patients with acute leukaemia, lymphoma; iron deficiency anaemia, post hepatitic cirrhosis and tuberculosis, was measured by a FT-NMR spectrometer. Relaxation measurements were performed at 60MHz frequency and a temperature of (20 ± 0.5)C. The T1 measured for each disease correlates strongly with hemoglobin content. The spin-lattice relaxation time in each abnormal group was signaficantly (p < 0.001) elevated over normal group. There is little overlap between the healthy and abnormal groups. On the contrast, T1 ranges obtained for malignant groups and non-malignant diseases do overlap.     

Prolonged bone marrow T1-relaxation in acute leukaemia. In vivo tissue characterization by magnetic resonance imaging

In vivo tissue characterization by measurement of T1- and T2-relaxation processes is one of the greatest potentials of magnetic resonance imaging (MRI). This may be especially useful in the evaluation of bone marrow disorders as the MRI-signal from bone marrow is not influenced by the overlying osseous tissue. Nine patients with acute leukaemia, one patient with myelodysplastic syndrome, and ten normal volunteers were included in the study. The T1- and T2-relaxation processes were measured in the lumbar spine bone marrow using a wholebody superconductive MR-scanner operating at 1.5 Tesla. In the patients MRI was done at the time of diagnosis and during follow-up of chemotherapy and related to bone marrow biopsies taken within three days of the MRI. At the time of diagnosis T1-relaxation time was increased two to three times in the patients (range 0.7-3.0 sec.) compared to the controls (range 0.38-0.60 sec.). No significant difference was seen in the T2-relaxation process. In relation to chemotherapy T1 decreased towards the normal range in the patients who obtained complete remission, whereas T1 remained prolonged in the patients who did not respond successfully to the treatment. The results indicate that MRI may be a non-invasive clinically useful tool in the evaluation of acute leukaemia especially as a follow-up control of chemotherapy.