Sodium Signal Intensity Research Articles

Temporal and Spatial Dynamics of Ischemic Stroke Lesions after Acute Therapy: A Comprehensive Edema Assessment Using Combined 1H- and 23Na-MRI.

Ischemic cerebral stroke initiates a complex cascade of pathophysiological events, involving various forms of molecular shifts and edema. Early intervention is pivotal in minimizing tissue loss and improving clinical outcomes. This study explores the temporal and spatial evolution of tissue sodium concentration (TSC) in acute ischemic lesions after acute therapy using 23Na-MRI in addition to conventional 1H-MRI. Prospectively, from examined 58 patients with acute ischemic stroke with a combined 1H/23Na-MRI within 72 h of symptom onset after receiving acute therapy, 31 patients were included in the evaluation of this study. After co-registration of the 23Na-MRI images to the morphological 1H-MRI images, manual segmentation of the ischemic lesions was performed, and the ADC and TSC measurements were quantified and correlated with the time of onset and lesion volume. The mean TSC in ischemic lesions correlated positively with lesion volume (r = 0.52, p = 0.002) and showed a significant association with the time of stroke onset (r = 0.8, p < 0.001). Patients who were treated only with intravenous rtPA showed homogenous sodium signal intensity in the ischemic lesions, whereas the patients who received mechanical recanalization exhibited distinctive sodium signal intensity patterns with focal significant TSC differences. The integration of 1H- and 23Na-MRI provides a nuanced understanding of temporal and spatial changes due to different types of edema in ischemic stroke lesions following acute treatment. Further exploration of these findings may enhance our understanding of stroke pathophysiology and guide personalized therapeutic interventions.

Sodium signal intensity of CSF using 1H-guided 23Na-MRI as a potential noninvasive biomarker in Alzheimer's disease.

Alzheimer's disease (AD) is characterized by cognitive decline and mnestic deficits. The pathophysiology of AD is not fully understood, which renders the development of accurate tools for early diagnosis and effective therapies exceedingly difficult. In this study, we investigated the use of 23Na-MRI to measure the relative sodium signal intensities (rSSIs) in CSF in patients with AD and healthy controls. We prospectively recruited 11 patients with biomarker-diagnosed early-stage AD, as well as 12 cognitively healthy age-matched controls. All participants underwent 23Na-MRI to measure rSSI. Statistical analyses were performed to compare CSF sodium signal intensities between groups and to evaluate the specificity and sensitivity of the rSSI in the diagnosis of AD. RSSIs in CSF were significantly higher in AD patients (mean=68.6%±7.7%) compared to healthy controls (mean=56.9%±5.5%) (p<.001). There was also a significant negative correlation between rSSI in CSF and hippocampus and amygdala volumes (r=-.54 and -.49, p<.05) as well as a positive correlation with total CSF volumes (r=.81, p<.05). Receiver operating characteristic analysis showed high diagnostic accuracy for rSSI in discriminating between AD patients and healthy controls (area under the curve=.94). Our study provides evidence that rSSI in CSF is increased in AD patients in comparison to healthy controls. rSSI may serve as a potential marker for early detection and monitoring of disease progression. Larger, longitudinal studies are needed to confirm our findings and to investigate the association between rSSI in CSF and the severity of cognitive impairment.

Redefining the concept of residual renal function with kidney sodium MRI: a pilot study.

The concept of residual kidney function (RKF) is exclusively based upon urine volume and small solute clearance, making RKF challenging to assess in clinical practice. The aim of this study was to test the technical feasibility of obtaining useable 23Na-MRI kidney images in hemodialysis (HD) participants. We conducted an exploratory prospective study to quantify the cortico-medullary sodium gradient in healthy and HD participants. Participants fasted for eight hours prior to their study visit. Urine samples were collected to measure urinary osmolarity, before MRI. Proton and sodium pictures were merged; ROIs were delineated for the medulla and cortex when feasible. In cases where cortex could not be identified, we considered the cortico to medulla gradient (CMG) to be no longer present, resulting in a medulla-to-cortex ratio of 1. 17 healthy volunteers and 21 HD participants. Median (IQR) fasting medulla to cortex ratio was significantly higher 1.56 [1.5-1.61] in healthy volunteers compared to HD patients 1.22 [1.13-1.3], p<0.0001. Medulla to cortex ratio and median urinary osmolarity were correlated (r=0.87, p<0.0001) in the whole population. We found a significant association between HD vintage and medulla to cortex ratio whereas we did not find any association with urine volume. Sodium signal intensity distribution within healthy kidney describes two different peaks- relating to well defined cortex and medulla; whereas HD participants displays only a single peak indicative of the markedly lower sodium concentration. This study is only an exploratory study with a modest number of patients. the application of kidney sodium MRI to the study of RKF in patients receiving maintenance HD is practical and provides a previously unavailable ability to interrogate the function of remnant tubular function.

Abstract 13395: Dapagliflozin Reduces Myocardial Sodium Content and Correlates With Reverse Cardiac Remodeling in Nondiabetic Patients With Heart Failure and Preserved Ejection Fraction (Dapa-Sodium)

Introduction: Myocardial sodium overload is a major determinant of adverse cardiac remodeling in heart failure (HF). Sodium tissue content by 23Na magnetic resonance imaging (23Na-MRI) has been validated in human studies. SGLT-2 inhibition blocks sodium reabsorption in renal proximal tubular cells with remarkable cardiovascular outcomes in HF due to mechanisms not yet fully understood. Hypothesis: SGLT-2 inhibition will decrease myocardial sodium content and it will correlate with reverse remodeling in HFpEF. Aim: To determine whether Dapagliflozin leads to decreased myocardial sodium content and reverses pathological hypertrophy in HFpEF. Methods: Prospective, single-center, open-label study of sixty nondiabetic outpatients with HFpEF underwent baseline 23Na-MRI and initiated with dapagliflozin 10 mg once daily according to GDMT. Absolute changes in myocardium relative sodium signal intensity (rSSI) and left ventricular mass index (LVMi) were analyzed from baseline and at 3-month follow-up with 23Na-MRI. Results: All patients exhibited significantly high baseline myocardium rSSI [0.32 (0.28, 0.34)]; 66% above median [0.24 (0.20, 0.27), P = 0.004], decreasing -30% to [0.27 (0.22, 0.30), P&lt;0.001] at 3 months with Dapagliflozin therapy. These changes were correlated with a significant reduction in LVMi of -13 g/m 2 [from 84 g/m 2 (72, 120) to 71 g/m 2 (63, 95), P&lt;0.001]. Conclusions: Dapagliflozin reduces myocardial sodium content and reverses pathological hypertrophy in patients with HFpEF. These findings suggest that SGLT-2 inhibition acts directly on cardiomyocytes and explains the cardioprotective effects demonstrated though large randomized trials.

Primary hyperaldosteronism induces congruent alterations of sodium homeostasis in different skeletal muscles: a 23Na-MRI study.

BackgroundSodium homeostasis is disrupted in many cardiovascular diseases, which makes non-invasive sodium storage assessment desirable. In this regard, sodium MRI has shown its potential to reveal differences in sodium content between healthy and diseased tissues as well as treatment-related changes of sodium content. When different tissues are affected disparately, simultaneous assessment of these compartments is expected to provide better information about sodium distribution, reduce examination time, and improve clinical efficiency.ObjectivesThe objectives were (1) to investigate sodium storage levels in calf and pectoral muscle in healthy controls and patients and quantify changes following medical treatment and (2) to demonstrate homogeneous disruption in skeletal muscle sodium storage in patients with primary hyperaldosteronism (PHA).MethodsWe assessed sodium storage levels (relative sodium signal intensity, rSSI) in the calf and pectoral muscles of eight patients with PHA prior and after treatment and 12 age- and sex-matched healthy volunteers.ResultsCalf and pectoral muscle compartments exhibited similar sodium content both in healthy subjects (calf vs pectoral rSSI: 0.14 ± 0.01 vs 0.14 ± 0.03) and PHA patients (calf vs pectoral rSSI: 0.19 ± 0.03 vs 0.18 ± 0.03). Further, we observed similar treatment-related changes in pectoral and calf muscles in the patients (proportional rSSI change calf: 26%; pectoral: 28%).ConclusionWe found that sodium was distributed uniformly and behaved equally in different skeletal muscles in Conn’s syndrome. This allows to measure both heart and skeletal muscle sodium signals simultaneously by a single measurement without repositioning the patient. This increases 23Na-MRI’s clinical feasibility as an innovative technique to monitor sodium storage.

SAT-386 Assessment Of Tissue Sodium Content By23Na-MRI In Patients With Adrenal Insufficiency

Patients with chronic primary adrenal insufficiency (PAI) depend on lifelong replacement therapy with gluco- (GC) and mineralocorticoids (MC). Monitoring is based on clinical parameters assessing hemodynamic stability, electrolyte status and plasma renin concentration (PRC). Reduced subjective well-being is however often described by these patients in absence of objectifiable abnormalities, thus suggesting a gap between the concept of adequate hormone substitution and physiological requirements. This study investigated the potential role of 23Na-MRI for noninvasive assessment of sodium status in PAI. Tissue sodium was initially analyzed both in the calf muscle and in the skin of 16 patients with chronic PAI and 16 sex-, age- and BMI-matched controls. Patients were classified into 3 groups (optimal/subtherapeutic/supraphysiological) according to the quality of GC and MC substitution assessed separately by clinical scores based on subjective wellbeing and clinical/laboratory parameters. We additionally performed a longitudinal analysis in 8 patients with newly diagnosed PAI. Muscle and skin sodium content (Muscle-SC, Skin-SC) were determined using a 23NA-MRI protocol on a 3T scanner implementing a 3D sequence. A vial with 100mmol/L of sodium was scanned with every participant. Tissue sodium is presented as the ratio of tissue sodium signal intensity to sodium signal intensity of the reference vial. Muscle-SC was significantly higher in patients with chronic PAI compared to controls (19.1 vs. 16.0, p<0.05), whereas Skin-SC was similar between the two groups (16.1 vs. 17.1). These results were replicated in the subgroups classified as receiving optimal GC and MC replacement, respectively. Skin-SC was significantly correlated with 24h-urine sodium level in the whole cohort. When comparing Muscle-SC and Skin-SC with obtained clinical scores a trend from lower SC for low scores to higher SC for higher scores was observed. The longitudinal analysis of 8 patients with newly diagnosed PAI revealed that Skin-SC was significantly lower at primary diagnosis compared to sex-, age- and BMI-matched controls (12.1 vs. 15.8, p=0.05), whereas the difference in Muscle-SC was less pronounced (14 vs. 16.1, p=0.18). A significant increase in both Muscle- and Skin-SC at follow-up compared to first diagnosis was detected (19.4 vs. 14, p<0.05 and 19.3 vs. 12.1, p<0.05), consistent with a significant decrease in PRC (200 vs. 31.2 ng/l, p<0.05). Interestingly, patients with chronic PAI under replacement therapy exhibited significantly higher Muscle-SC compared to controls. The agreement between tissue SC and clinical scores as well as the significant increase in tissue SC under replacement therapy in newly diagnosed patients indicate that 23Na-MRI might be a quantitative method to assess steroid replacement. Further studies on a larger cohort are, however, needed to prove these initial findings.

Increased myocardial sodium signal intensity in Conn's syndrome detected by 23Na magnetic resonance imaging.

AimsSodium intake has been linked to left ventricular hypertrophy independently of blood pressure, but the underlying mechanisms remain unclear. Primary hyperaldosteronism (PHA), a condition characterized by tissue sodium overload due to aldosterone excess, causes accelerated left ventricular hypertrophy compared to blood pressure matched patients with essential hypertension. We therefore hypothesized that the myocardium constitutes a novel site capable of sodium storage explaining the missing link between sodium and left ventricular hypertrophy.Methods and resultsUsing 23Na magnetic resonance imaging, we investigated relative sodium signal intensities (rSSI) in the heart, calf muscle, and skin in 8 PHA patients (6 male, median age 55 years) and 12 normotensive healthy controls (HC) (8 male, median age 61 years). PHA patients had a higher mean systolic 24 h ambulatory blood pressure [152 (140; 163) vs. 125 (122; 130) mmHg, P < 0.001] and higher left ventricular mass index [71.0 (63.5; 106.8) vs. 55.0 (50.3; 66.8) g/m2, P = 0.037] than HC. Compared to HC, PHA patients exhibited significantly higher rSSI in the myocardium [0.31 (0.26; 0.34) vs. 0.24 (0.20; 0.27); P = 0.007], calf muscle [0.19 (0.16; 0.22) vs. 0.14 (0.13; 0.15); P = 0.001] and skin [0.28 (0.25; 0.33) vs. 0.19 (0.17; 0.26); P = 0.014], reflecting a difference of +27%, +38%, and +39%, respectively. Treatment of PHA resulted in significant reductions of the rSSI in the myocardium, calf muscle and skin by −13%, −27%, and −29%, respectively.ConclusionMyocardial tissue rSSI is increased in PHA patients and treatment of aldosterone excess effectively reduces rSSI, thus establishing the myocardium as a novel site of sodium storage in addition to skeletal muscle and skin.

Changes in Cartilage and Tendon Composition of Patients With Type I Diabetes Mellitus: Identification by Quantitative Sodium Magnetic Resonance Imaging at 7 T.

The aim of this study was to investigate possible biochemical alterations in tendons and cartilage caused by type 1 diabetes mellitus (DM1), using quantitative in vivo 7 T sodium magnetic resonance (MR) imaging. The institutional review board approved this prospective study, and written informed consent was obtained. Eight DM1 patients with no history of knee trauma and 9 healthy age- and weight-matched volunteers were examined at 7 T using dedicated knee coils.All participants underwent morphological and sodium MR imaging. Region-of-interest analysis was performed manually for the non-weight-bearing area of the femoral condyle cartilage and for the patella tendon. Two readers read the image data sets independently, twice, for intrareader and interreader agreement. Normalized mean sodium signal intensity (NMSI) values were compared between patients and volunteers for each reader using analysis of variance. On morphological images, cartilage in the non-weight-bearing area and the patellar tendon was intact in all patients. On sodium MR imaging, bivariate analysis of variance showed significantly lower mean NMSI values in the cartilage (P = 0.008) and significantly higher values in the tendons (P = 0.025) of patients compared with those of volunteers. Our study showed significantly different NMSI values between DM1 patients and matched volunteers. Differences observed in the cartilage and tendon might be associated with a DM1-related alteration of biochemical composition that occurs before it can be visualized on morphological MR sequences.

In Vivo Sodium MRI for Mouse Model of Ischemic Stroke at 7 T: Preliminary Results

Previous studies have used sodium magnetic resonance imaging (MRI) to investigate the increase in tissue sodium concentration that occurs during a stroke by using various animal models of brain ischemia. However, most of these studies have involved rats, cats, or nonhuman primates. Although studies involving mice are relatively scant, mice have become the principal animal model for studying many human diseases, particularly in the field of genetics. Accordingly, this study employed sodium MRI to monitor changes in the intensity of sodium signals in a mouse model of ischemic stroke. The experiments were conducted using a 7-T MRI system, and a commercial double-tuned sodium/proton transmit-receive surface coil was used to capture the sodium and proton signal images. Sodium MRI was performed using a fast low-angle shot pulse sequence. The mice underwent middle cerebral artery occlusion to induce focal brain ischemia 48 h before the MRI scans were performed. The signal intensity of the sodium image was determined for a region of interest (ROI) in the ischemic area, and an ROI contralateral to this area. The average signal intensity in the sodium images of the mouse brains exhibited a 2.51-fold increase and a standard deviation was 0.93. The results of this study demonstrate the feasibility of using a 7-T MRI system to perform sodium MRI of a mouse model of ischemic stroke. The sodium signal intensity of the mouse brain revealed a substantial increase in sodium levels in the ischemic area compared with that in the contralateral brain hemisphere.

A double-tuned (1) H/(23) Na resonator allows (1) H-guided (23) Na-MRI in ischemic stroke patients in one session.

Established imaging methods are still not confident in the determination of stroke onset. Sodium imaging in animal models and lately in humans implicates that the sodium signal intensity within the ischemic lesion increases in a time-dependent fashion. Sodium imaging usually requires a time-consuming change of resonators or magnetic resonance imaging systems. To avoid this, we used a double-tuned (1) H/(23) Na birdcage head coil in combination with a protocol minimizing T1 - and T2 *-weighting effects for measurement of sodium intensity in acute stroke patients. Multinuclear (1) H/(23) Na data sets were obtained from 16 stroke patients [75 ± 9·9 (standard deviation) years old] 4-130 h after symptom onset. The protocol was acquired on a clinical 3T magnetic resonance imaging site using a double-tuned (1) H/(23) Na birdcage head coil. Sodium signal intensity within the lesion and homologous contralateral side was measured and compared. With an acquisition time of the complete magnetic resonance imaging protocol of 22 min, a nonlinear sodium signal intensity increase within the lesion over time after stroke onset was acknowledged. Onset time within six-hours showed an increase of only 8% or less, whereas onset time beyond 8·5 h demonstrated increases of 36% or more reaching a maximum of 170% > 120 h. In addition, some patients showed a difference in sodium signal intensity compared with diffusion weighted imaging lesion. The use of a double-tuned (1) H/(23) Na birdcage head coil in a clinical setting 'allowed sodium intensity measurements' in a justifiable time also for acute stroke patients, and heterogenous sodium signal intensity in the diffusion weighted imaging lesion might represent differences in tissue damage or repair.

Bilateral kidney sodium‐MRI: Enabling accurate quantification of renal sodium concentration through a two‐element phased array system

To develop a sodium-MRI ((23) Na-MRI) method for bilateral renal sodium concentration (RSC) measurements in rat kidneys at 9.4 Tesla (T). To simultaneously achieve high B1 -field homogeneity and high receive sensitivity a dual resonator system composed of a double-tuned linearly polarized (1) H/(23) Na volume resonator and a newly developed two-element (23) Na receive array was used. In conjunction with three-dimensional (3D) ultra-short Time-to-Echo sequence a quantification accuracy of ± 10% was achieved for a nominal spatial resolution of (1 × 1 × 4) mm(3) in 10 min acquisition time. The technique was applied to study the RSC in six kidneys before and after furosemide-induced diuresis. The loop diuretic agent induced an increase of cortical RSC by 22% from 86 ± 16 mM to 105 ± 18 mM (P = 0.02), whereas the RSC in the inner medulla decreased by 38% from 213 ± 24 mM to 132 ± 25 mM (P = 0.8×10(-4) ). The RSC changes measured in this study agreed well with the qualitative sodium signal intensity variations reported elsewhere. Furosemide-induced diuresis has been investigated accurately with herein presented quantitative (23) Na-MRI technique. In the future, RSC quantification could allow for defining pathological and nonpathological RSC ranges to assess sodium concentration changes, e.g., induced by drugs.

Sodium MR Imaging of the Lumbar Intervertebral Disk at 7 T: Correlation with T2 Mapping and Modified Pfirrmann Score at 3 T—Preliminary Results

To compare sodium imaging of lumbar intervertebral disks in asymptomatic volunteers at 7-T magnetic resonance (MR) imaging with quantitative T2 mapping and morphologic scoring at 3 T. Following ethical board approval and informed consent, the L2-3 to L5-S1 disks were examined in 10 asymptomatic volunteers (nine men, one woman; mean age, 30 years; range, 23-43 years). At 7 T, normalized sodium signal-to-noise ratios were calculated, by using region-of-interest analysis. At 3 T, T2 mapping was performed with a multiecho spin-echo sequence (repetition time msec/echo times msec, 1500/24, 36, 48, 60, 72, 84, 96, 108, 120, 132, 144, 156). T2 values were calculated over the nucleus, with a pixelwise, monoexponential nonnegative least-squares-fit analysis. Morphologic grading according to a modified Pfirrmann score was assessed independently by three experienced musculoskeletal radiologists, and Pearson correlation analysis of the covariates was performed. The mean normalized sodium signal intensity was 275.5±115.4 (standard deviation). The T2 mapping showed a mean value of 89.8 msec±19.34. The median modified Pfirrmann score was 2b (90% had score≤3c). The Pearson correlation coefficient showed a cubic function between sodium imaging and the modified Pfirrmann score, a moderate inverse correlation between T2 mapping and the modified Pfirrmann score (r=-0.62), and no correlation between sodium imaging and T2 mapping (r=0.06). The results suggest that MR imaging of the intervertebral disk, using sodium imaging and T2 mapping, can help characterize different component changes and that both of these methods are to some degree related to the Pfirrmann score.

Relationship between sodium intensity and perfusion deficits in acute ischemic stroke

To assess the relationship between sodium signal intensity changes and oligemia, measured with perfusion-weighted imaging (PWI), in ischemic stroke patients. Nine ischemic stroke patients (55 ± 13 years), four with follow-up scans, underwent sodium and proton imaging 4-32 hours after symptom onset. Relative sodium intensity was calculated as the ratio of signal intensities in core (identified as hypertintense lesions on diffusion-weighted imaging [DWI]) or putative penumbra (PWI-DWI mismatch) to contralateral homologous regions. Sodium intensity increases in the core were not correlated with the severity of hypoperfusion, measured with either cerebral blood flow (rho = 0.157; P = 0.61) or cerebral blood volume (rho = -0.234; P = 0.44). In contrast, relative sodium intensity was not elevated (4-7 hours 0.96 ± 0.07; 17-32 hours 1.00 ± 0.07) in PWI-DWI mismatch regions. Sodium signal intensity cannot be predicted by the degree of hypoperfusion acutely. Sodium intensity also remains unchanged in PWI-DWI mismatch tissue, indicating preservation of ionic homeostasis. Sodium magnetic resonance imaging (MRI), in conjunction with PWI and DWI, may permit identification of patients with viable tissue, despite an unknown symptom onset time.

3D 23Na MRI of human skeletal muscle at 7 Tesla: initial experience

To evaluate healthy skeletal muscle pre- and post-exercise via 7 T (23)Na MRI and muscle proton T(2) mapping, and to evaluate diabetic muscle pre- and post-exercise via 7 T (23)Na MRI. The calves of seven healthy subjects underwent imaging pre- and post-exercise via 7 T (23)Na MRI (3D fast low angle shot, TR/TE = 80 ms/0.160 ms, 4 mm x 4 mm x 4 mm) and 1 week later by (1)H MRI (multiple spin-echo sequence, TR/TE = 3,000 ms/15-90 ms). Four type 2 diabetics also participated in the (23)Na MRI protocol. Pre- and post-exercise sodium signal intensity (SI) and proton T(2) relaxation values were measured/calculated for soleus (S), gastrocnemius (G), and a control, tibialis anterior (TA). Two-tailed t tests were performed. In S/G in healthy subjects post-exercise, sodium SI increased 8-13% (p < 0.03), then decreased (t(1/2) = 22 min), and (1)H T(2) values increased 12-17% (p < 0.03), then decreased (t(1/2 )= 12-15 min). In TA, no significant changes in sodium SI or (1)H T(2) values were seen (-2.4 to 1%, p > 0.17). In S/G in diabetics, sodium SI increased 10-11% (p < 0.04), then decreased (t(1/2) = 27-37 min) without significant change in the TA SI (-3.6%, p = 0.066). It is feasible to evaluate skeletal muscle via 3D (23)Na MRI at 7 T. Post-exercise muscle (1)H T(2) values return to baseline more rapidly than sodium SI. Diabetics may demonstrate delayed muscle sodium SI recovery compared with healthy subjects.

Sodium imaging intensity increases with time after human ischemic stroke

Establishing time of onset is important in acute stroke management. Current imaging modalities do not allow determination of stroke onset time. Although correlations between sodium magnetic resonance imaging signal intensity within ischemic lesions and time of onset have been shown in animal models, the relation to onset time has not been established in human stroke. Utilizing high-quality sodium images, we tested the hypothesis that sodium signal intensity increases with time from symptom onset in human ischemic stroke. Twenty-one stroke patients (63 +/- 15 years old) were scanned 4 to 104 hours after symptom onset. Follow-up images were obtained in 10 patients at 23 to 161 hours after onset, yielding a total of 32 time points. A standard stroke imaging protocol was acquired at 1.5 Tesla, followed by sodium magnetic resonance imaging at 4.7 Tesla. Relative sodium signal intensity within each lesion was measured with respect to the contralateral side. The sodium image quality was sufficient to visualize each acute lesion (lesion volume range, 1.7-217cm(3)). Relative sodium signal intensity increased nonlinearly over time after stroke onset. Sodium images acquired within 7 hours (n = 5) demonstrated a relative increase in lesion intensity of 10% or less, whereas the majority beyond 9 hours demonstrated increases of 23% or more, with an eventual leveling at 69 +/- 18%. Increases of sodium signal intensity within the ischemic lesion are related to time after stroke onset. Thus, noninvasive imaging of sodium may be a novel metabolic biomarker related to stroke progression. Ann Neurol 2009;66:55-62.

Low-Grade Glioma: Correlation of Short Echo Time1H-MR Spectroscopy with23Na MR Imaging

There is considerable variability in the clinical behavior and treatment response of low-grade (WHO grade II) gliomas. The purpose of this work was to characterize the metabolic profile of low-grade gliomas by using short echo time (1)H-MR spectroscopy and to correlate metabolite levels with MR imaging-measured sodium ((23)Na) signal intensity. Based on previous studies, we hypothesized decreased N-acetylaspartate (NAA) and increased myo-inositol (mIns), choline (Cho), glutamate (Glu), and (23)Na signal intensity in glioma tissue. Institutional ethics committee approval and informed consent were obtained for all of the subjects. Proton ((1)H-MR) spectroscopy (TR/TE = 2200/46 ms) and sodium ((23)Na) MR imaging were performed at 4T in 13 subjects (6 women and 7 men; mean age, 44 years) with suspected low-grade glioma. Absolute metabolite levels were quantified, and relative (23)Na levels were measured in low-grade glioma and compared with the contralateral side in the same patients. Two-sided Student t tests were used to test for statistical significance. Significant decreases were observed for NAA (P < .001) and Glu (P = .004), and increases were observed for mIns (P = .003), Cho (P = .025), and sodium signal intensity (P < .001) in low-grade glioma tissue. Significant correlations (r(2) > 0.25) were observed between NAA and Glu (P < .05) and between NAA and mIns (P < .01). Significant correlations were also observed between (23)Na signal intensity and NAA (P < .01) and between (23)Na signal intensity and Glu (P < .01). Ratios of NAA/mIns, NAA/(23)Na, and NAA/Cho were altered in glioma tissue (P < .001); however based on the t statistic, NAA/(23)Na (t = 9.6) was the most significant, followed by NAA/mIns (t = 6.1), and NAA/Cho (t = 5.0). Although Glu concentration is reduced and mIns concentration is elevated in low-grade glioma tissue, the NAA/(23)Na ratio was the most sensitive indicator of pathologic tissue.

(23)sodium MRI for infarct imaging of the human heart

Sodium is elevated in acute/subacute myocardial infarction due to three distinct mechanisms: Breakdown of ion homeostasis with accumulation of intracellular sodium, extracellular edema formation and, during scar formation, increase of extracellular vs. intracellular space as cardiomyocytes are replaced by connective tissue. 23Na MRI has previously been shown to have the potential to demonstrate myocardial infarction in an animal model. Aim of this study was, therefore, to demonstrate myocardial infarction with the use of 23Na-MRI in patients. 10 patients were examined 14 +/- 7 days after first myocardial infarction using a 23Na surface coil at 1.5 T. Double angulated short axis images of the entire heart were imaged using an ECG-triggered 3d-FLASH-sequence (FOV, 450 mm; matrix, 64 x 128; spatial resolution, 3.5 x 7 mm2; slice thickness, 16 mm; 32 acquisitions). Areas of elevated sodium signal intensity were correlated with infarct-related wall motion abnormalities imaged by Cine MRI in breathhold-technique. All patients showed an area of elevated sodium signal intensity that correlated well with the clinically determined localization of myocardial infarction as well as with regional wall motion abnormalities detected by Cine MRI. Elevated 23Na MR image signal intensity demonstrates subacute myocardial infarction in patients.

Early changes in cerebral sodium distribution following ischaemia monitored by 23Na magnetic resonance imaging

23Na magnetic resonance imaging has been used in this preliminary study to investigate early changes in brain sodium signal intensity during and after cerebral ischaemia in a gerbil model. The total sodium signal in selected brain regions decreased between 15 and 30% within 4 min of the onset of ischaemia, and then remained constant throughout the ischaemic period. The same pattern was observed in the eyes. On reperfusion, there was no significant change in the sodium signal over the first 4 min, but by 8 min the signal intensity had returned to or passed through control levels in all regions measured, with the exception of the eyes. These observations are consistent with the loss and resynthesis of ATP as seen in this model, and may be reflecting the redistribution of tissue sodium resulting from energy failure and recovery.

Sodium, ATP, and intracellular pH transients during reversible complete ischemia of dog cerebrum.

We tested the hypotheses that with the onset of cerebral ischemia, massive cellular sodium influx does not occur until adenosine triphosphate is fully depleted and that on reperfusion, neuronal sodium efflux does not occur until adenosine triphosphate is fully restored. We examined the temporal relationships among transcellular sodium, energy metabolism, and intracellular pH with sodium and phosphorus magnetic resonance spectroscopy in a new, hemodynamically stable, brain stem-sparing model of reversible, complete cerebral ischemia in eight anesthetized dogs. Inflation of a neck tourniquet after placement of glue at the tip of the basilar artery resulted in decreased blood flow to the cerebrum from 29 +/- 5 to 0.3 +/- 0.5 ml/min/100 g. Medullary blood flow was not significantly affected, and arterial blood pressure was unchanged. Sodium signal intensity decreased and did not lag behind the fall in adenosine triphosphate. After 12 minutes of ischemia, reperfusion resulted in a more rapid recovery of sodium intensity (12.4 +/- 4.8 minutes) than either adenosine triphosphate (16.5 +/- 3.7 minutes) or intracellular pH (38.9 +/- 1.8 minutes). Because intracellular sodium has a weaker signal than extracellular sodium, the decreased sodium intensity is interpreted as sodium influx and indicates that sodium influx does not require full depletion of adenosine triphosphate. Rapid recovery of sodium intensity during early reperfusion may represent sodium efflux, although increased plasma volume and sodium uptake from plasma may also contribute. If our interpretation of the sodium signal is correct, delayed recovery of adenosine triphosphate may be due to the utilization of adenosine triphosphate for the restoration of transcellular sodium gradient.

Sodium NMR imaging of lung water in rats.

Coronal proton and sodium images of control rats and rats with either increased permeability edema produced by intravenous alloxan (300 mg/kg) or increased pressure edema produced by saline infusion (2 ml/min) were obtained. Axial chest CT images were used to monitor the development of pulmonary edema. Immediately after the imaging session compartmental lung water was measured gravimetrically. The sodium and proton imagings were done sequentially in a 31-cm-bore 1.9-T magnet without moving the animal. The anatomical boundaries of the lung on the proton images were transferred to the sodium images for calculation of the average sodium signal intensity which was determined by extrapolating the mean values from five echoes to time zero. The sodium signal intensity was correlated (r = 0.7) with the total water fraction. There was poor correlation (r = 0.56) with the extravascular water due to confounding by the sodium vascular signal.