Accurate assessment of carotid artery stenosis in atherosclerotic mice using accelerated high-resolution 3D magnetic resonance angiography.

OBJECT: High-resolution magnetic resonance angiography (MRA) enables non-invasive detection and longitudinal monitoring of atherosclerosis in mouse models of human disease. However, MRA is hampered by long acquisition times putting high demands on the physiological stability of the animal. Therefore, we evaluated the feasibility of accelerated MRA using the parallel imaging technique SENSE with regard to both lesion detection and quantification. MATERIALS AND METHODS: MRA acquisitions of supra-aortic vessels were performed in ApoE (-/-) mice that have been shown to develop atherosclerotic plaques. Findings obtained from accelerated data sets were compared to fully sampled reference data sets and histology. RESULTS: Our results revealed only minor differences in detecting vascular lesions for data collections accelerated by factors of up to 3.3 using a four-element coil array. For vessels with a mean lumen diameter of 500 µm, morphometry of stenotic lesions revealed no substantial deviations from reference (fully sampled) data for all investigated acceleration factors. For the highest acceleration factor of 3.3, an average deviation of the degree of stenosis of 4.9 ± 3.6% was found. Common carotid stenoses assessed by in vivo MRA displayed a good correlation with histological analyses (slope of linear regression = 0.97, R (2) = 0.98). CONCLUSION: According to the results of this work, we have demonstrated the feasibility and accuracy of accelerated high-resolution 3D ToF MRA in mice suitable for detailed depiction of mouse supra-aortic vessels and amenable to non-invasive quantification of small atherosclerotic lesions.

Assessment of brain responses to innocuous and noxious electrical forepaw stimulation in mice using BOLD fMRI.

Functional magnetic resonance imaging (fMRI) using the blood oxygen level-dependent (BOLD) contrast was used to study sensory processing in the brain of isoflurane-anesthetized mice. The use of a cryogenic surface coil in a small animal 9.4T system provided the sensitivity required for detection and quantitative analysis of hemodynamic changes caused by neural activity in the mouse brain in response to electrical forepaw stimulation at different amplitudes. A gradient echo-echo planar imaging (GE-EPI) sequence was used to acquire five coronal brain slices of 0.5mm thickness. BOLD signal changes were observed in primary and secondary somatosensory cortices, the thalamus and the insular cortex, important regions involved in sensory and nociceptive processing. Activation was observed consistently bilateral despite unilateral stimulation of the forepaw. The temporal BOLD profile was segregated into two signal components with different temporal characteristics. The maximum BOLD amplitude of both signal components correlated strongly with the stimulation amplitude. Analysis of the dynamic behavior of the somatosensory 'fast' BOLD component revealed a decreasing signal decay rate constant k(off) with increasing maximum BOLD amplitude (and stimulation amplitude). This study demonstrates the feasibility of a robust BOLD fMRI protocol to study nociceptive processing in isoflurane-anesthetized mice. The reliability of the method allows for detailed analysis of the temporal BOLD profile and for investigation of somatosensory and noxious signal processing in the brain, which is attractive for characterizing genetically engineered mouse models.

Assessment of left ventricular volumes and mass with fast 3D cine steady-state free precession k-t space broad-use linear acquisition speed-up technique (k-t BLAST).

PURPOSE: To compare left ventricular (LV) volume and mass assessment using two-dimensional (2D) cine steady-state free precession (SSFP) and k-t space broad-use linear acquisition speed-up technique (k-t BLAST) accelerated 3D magnetic resonance imaging (MRI). MATERIALS AND METHODS: On a commercially available 1.5T MR scanner, 2D cine SSFP, six- and eight-fold accelerated 3D k-t BLAST were performed to evaluate LV volumes and mass in 17 volunteers. After semiautomatic segmentation of the different MR data sets, the resulting volumes and mass were compared according to the mean difference, 95% confidence interval, standard deviation (SD), Pearson's correlation coefficient, Bland-Altman analysis, and the Pitman-Morgan test. RESULTS: Data acquisition was successful in all subjects. The number of required breathholds was reduced from a maximal of five for the 2D cine SSFP sequence to two for 3D k-t BLAST sequences. Comparing LV volumes, there was excellent agreement between 2D and 3D cine 8x k-t BLAST SSFP volumes (mean difference +/- 2SD end-diastolic volume [EDV] = 5 +/- 8 mL, end-systolic volume [ESV] = 1 +/-12 mL, and stroke volume [SV] = 3 +/- 8 mL), and mass (-1.8 +/- 9 g). CONCLUSION: k-t BLAST-accelerated 3D sequences allow accurate assessment of LV volumes and mass compared to 2D cine SSFP. This method may reduce costs and increase patient comfort due to shortened data acquisition time and reduced number of breathholds.

Quantitative assessment of ventricular function using three-dimensional SSFP magnetic resonance angiography.

PURPOSE: To evaluate three-dimensional (3D), free-breathing, steady-state free precession (SSFP) magnetic resonance angiography (MRA) for volumetric assessment of ventricular function. MATERIALS AND METHODS: In 18 subjects (mean age = 21.5 years) 3D datasets of the heart and great vessels were acquired using an ECG-triggered, free-breathing SSFP technique with a T2-preparation prepulse. Data were acquired during end-systole (ES) and end-diastole (ED) for assessment of stroke volumes (SVs). Through-plane flow measurements of the great arteries were performed as well as 2D-cine SSFP imaging for comparison. For image analysis of the 3D SSFP datasets a simplex mesh model was used. Papillary muscles were excluded from ventricular volumes using thresholds. Intra- and interobserver variability (Bland-Altman analysis) and correlations (Pearson's coefficient) between volumetric and flow measurements were assessed. RESULTS: ES and ED datasets were acquired successfully in all subjects. The best correlation was observed between flow vs. 3D SSFP SV for the LV (r = 0.85, mean difference = -1.0 mL) and the RV (r = 0.89, mean difference = -2.2 mL) with high intra- (LV: r = 0.93; RV: r = 0.94) and interobserver (LV: r = 0.91; RV: r = 0.93) reproducibility. CONCLUSION: 3D SSFP datasets combined with semiautomatic segmentation algorithms allow highly accurate and reproducible assessment of left (LV) and right ventricular (RV) SVs in free-breathing subjects.

Noninvasive MRI assessment of intracranial compliance in idiopathic normal pressure hydrocephalus.

PURPOSE: To assess the state and dynamics of the intracranial system in idiopathic normal-pressure hydrocephalus (I-NPH), we determined intracranial compliance using magnetic resonance imaging (MRI). MATERIALS AND METHODS: The intracranial compliance index (ICCI), which was defined as the ratio of the peak-to-peak intracranial volume change (ICVC(p-p)) to the peak-to-peak cerebrospinal fluid (CSF) pressure gradient (PG(p-p)) during the cardiac cycle, was obtained from the net transcranial blood and CSF flow measured with phase-contrast (PC) cine MRI. ICCI was determined in patients with I-NPH (N = 7), brain atrophy, or asymptomatic ventricular dilation (VD) (N = 6), and in healthy volunteers (control group; N = 11). The changes in ICCI indices were also analyzed after a CSF tap test (N = 2). RESULTS: The ICCI in the I-NPH group was significantly lower than in the control and VD groups, whereas no difference was found between the control and VD groups. The ICVC(p-p) was also lower than in the control and VD groups. However, no significant difference was found in the PG(p-p) between groups. The ICCI increased after the tap test. CONCLUSION: Intracranial compliance analysis with MRI makes it possible to noninvasively obtain more detailed information of intracranial biomechanics in the I-NPH and to assist in the diagnosis of I-NPH.