Christian H. Ziener

Comparison of Susceptibility Weighted Imaging and TOF-Angiography for the Detection of Thrombi in Acute Stroke

Background and Purpose Time-of-flight (TOF) angiography detects embolic occlusion of arteries in patients with acute ischemic stroke due to the absence of blood flow in the occluded vessel. In contrast, susceptibility weighted imaging (SWI) directly enables intravascular clot visualization due to hypointense susceptibility vessel signs (SVS) in the occluded vessel. The aim of this study was to compare the diagnostic accuracy of both methods to determine vessel occlusion in patients with acute stroke. Methods 94 patients were included who presented with clinical symptoms for acute stroke and displayed a delay on the time-to-peak perfusion map in the territory of the anterior (ACA), middle (M1, M1/M2, M2/M3) or posterior (PCA) cerebral artery. The frequency of SVS on SWI and vessel occlusion or stenosis on TOF-angiography was compared using the McNemar-Test. Results 87 of 94 patients displayed a clearly definable SVS on SWI. In 72 patients the SVS was associated with occlusion or stenosis on TOF-angiography. Fifteen patients exclusively displayed SVS on SWI (14 M2/M3, 1 M1), whereas no patient revealed exclusively occlusion or stenosis on TOF-angiography. Sensitivity for detection of embolic occlusion within major vessel segments (M1, M1/M2, ACA, and PCA) did not show any significant difference between both techniques (97% for SWI versus 96% for TOF-angiography) while the sensitivity for detection of embolic occlusion within M2/M3 was significantly different (84% for SWI versus 39% for TOF-angiography, p<0.00012). Conclusions SWI and TOF-angiography provide similar sensitivity for central thrombi while SWI is superior for the detection of peripheral thrombi in small arterial vessel segments.

Intracellular and extracellular T1 and T2 relaxivities of magneto‐optical nanoparticles at experimental high fields

This study reports the T1 and T2 relaxation rates of rhodamine‐labeled anionic magnetic nanoparticles determined at 7, 11.7, and 17.6 T both in solution and after cellular internalization. Therefore cells were incubated with rhodamine‐labeled anionic magnetic nanoparticles and were prepared at decreasing concentrations. Additionally, rhodamine‐labeled anionic magnetic nanoparticles in solution were used for extracellular measurements. T1 and T2 were determined at 7, 11.7, and 17.6 T. T1 times were determined with an inversion‐recovery snapshot‐flash sequence. T2 times were obtained from a multispin‐echo sequence. Inductively coupled plasma‐mass spectrometry was used to determine the iron content in all samples, and r1 and r2 were subsequently calculated. The results were then compared with cells labeled with AMI‐25 and VSOP C‐200. In solution, the r1 and r2 of rhodamine‐labeled anionic magnetic nanoparticles were 4.78/379 (7 T), 3.28/389 (11.7 T), and 2.00/354 (17.6 T). In cells, the r1 and r2 were 0.21/56 (7 T), 0.19/37 (11.7 T), and 0.1/23 (17.6 T). This corresponded to an 11‐ to 23‐fold decrease in r1 and an 8‐ to 15‐fold decrease in r2. A decrease in r1 was observed for AMI‐25 and VSOP C‐200. AMI‐25 and VSOP exhibited a 2‐ to 8‐fold decrease in r2. In conclusion, cellular internalization of iron oxide nanoparticles strongly decreased their T1 and T2 potency. Magn Reson Med, 2010.

In vivo measurement of local aortic pulse-wave velocity in mice with MR microscopy at 17.6 tesla

Transgenic mouse models of human diseases have gained increasing importance in the pathophysiology of cardiovascular diseases (CVD). As an indirect measure of vascular stiffness, aortic pulse‐wave velocity (PWV) is an important predictor of cardiovascular risk. This study presents an MRI approach that uses a flow area method to estimate local aortic pulse‐wave velocity at different sites in the murine aorta. By simultaneously measuring the cross‐sectional area and the through‐plane velocity with a phase‐contrast CINE method, it was possible to measure average values for the PWV in the ascending and descending aorta within the range of 2.4–4.3 m/s for C57BL/6J mice (ages 2 and 8 months) and apoE‐knockout mice (age 8 months). Statistically significant differences of the mean values of the PWV of both groups could be determined. By repeating CINE measurements with a time delay of 1 ms between two subsequent data sets, an effective temporal resolution of 1000 frames/s (fps) could be achieved. Magn Reson Med, 2009.

In vivo comparison of atherosclerotic plaque progression with vessel wall strain and blood flow velocity in apoE −/− mice with MR microscopy at 17.6 T

ObjectAt present, in vivo plaque characterization in mice by MRI is typically limited to the visualization of vascular lesions with no accompanying analysis of vessel wall function. The aim of this study was to analyze the influence of atherosclerotic plaque development on the morphological and mechanical characteristics of the aortic vessel wall in a pre-clinical murine model of atherosclerosis.Materials and methodsGroups of apolipoprotein E-deficient (apoE−/−) and C57BL/6J control mice fed a high-fat diet were monitored over a 12-week time period by high-field MRI. Multi-Slice-Multi-Spin-Echo and Phase-Contrast MRI sequences were employed to track changes to aortic vessel wall area, blood flow velocity and distensibility.ResultsAfter 6- and 12-weeks, significant changes in vessel wall area and circumferential strain were detected in the apoE−/− mice relative to the control animals. Blood flow velocity and intravascular lumen remained unchanged in both groups, findings that are in agreement with the theory of positive remodeling of the ascending aorta during plaque progression.ConclusionThis study has demonstrated the application of high-field MRI for characterizing the temporal progression of morphological and mechanical changes to murine aortic vasculature associated with atherosclerotic lesion development.

Frequency distribution and signal formation around a vessel

We describe the NMR signal formation properties of a single vessel. Instead of assuming the frequency distribution to be a simple Lorentzian or Gaussian one, we take into account that the frequency distribution around the vessel is a complex function. Considering the static dephasing regime we find a relationship between signal formation and frequency distribution. Analytical expressions for the frequency distribution in a voxel and the magnetization decay are obtained. In the case of small volume fractions of blood and week magnetic fields the results can be used for describing signal formation processes in a vascular network. A relationship between the frequency distribution and the properties of the vascular network is derived. The magnetization decay in different time regimes is discussed. The result is relevant for describing signal formation processes around a vessel for arbitrary pulse sequences.

Murine atherosclerotic plaque imaging with the USPIO Ferumoxtran-10

In this study we intended to image plaque inflammation in a murine model of atherosclerosis with MRI and Ferumoxtran-10 (Sinerem, Guerbet, France). 8 apoE-/- mice were injected 500 micromol Fe/kg or 1000 micromol Fe/kg Ferumoxtran-10. 2 apoE-/- mice were injected NaCl. After a post-contrast time of 24 to 336 hours the mice were scarificed and the aortas were imaged ex vivo. All measurements were performed on a 17.6 Tesla Bruker AVANCE 750WB MR scanner (Bruker, Germany). Spin-echo sequences and gradient-echo sequences with variable TE were performed and T2* maps were generated. Prussian-blue and hematoxilin-eosin histology were obtained afterwards and iron-uptake was quantified by counting iron positive areas. 2 apoE-/- mice were imaged in vivo before and 48 hours after 1000 micromol Fe/kg. Atheroma iron uptake was not elevated after 24 hours compared to controls. 48 hours after 1000 micromol Fe/kg but not 500 micromol Fe/kg histology revealed a 1.3- fold increase in plaque iron content compared to NaCl injected mice. Normalized T2*-times decreased from 0.86+/-0.02 in controls to 0.66+/-0.15 after a dose of 500 micromol Fe/ml and 0.59+/-0.14 in mice injected with 1000 micromol Fe/Kg (p=0.038). These results translated into a mean of 122% increase in CNR, as measured by in vivo MRI. We have demonstrated that Ferumoxtran-10 is taken up by atherosclerotic plaques in untreated apoE-/- mice and this alters plaque signal properties.

Suitable reference tissues for quantitative susceptibility mapping of the brain

Since quantitative susceptibility mapping (QSM) quantifies magnetic susceptibility relative to a reference value, a suitable reference tissue has to be available to compare different subjects and stages of disease.

Potential of quantitative susceptibility mapping for detection of prostatic calcifications

To evaluate whether quantitative susceptibility (QSM) may be used as an alternative to computed tomography (CT) to detect calcification in prostate cancer patients.

Signal evolution in the local magnetic field of a capillary - analogy to the damped driven harmonic oscillator

The temporal behavior of the magnetization decay caused by the local inhomogeneous magnetic field of a capillary is analyzed. Respecting the diffusion of the spins surrounding the capillary and the strength of the susceptibility difference between the capillary and the surrounding medium, it is possible to distinguish different dephasing regimes. Each dephasing regime can be related to a certain characteristic form of the magnetization decay. If the influence of the diffusion dominates, the magnetization exhibits a monotonic decay. In the opposite case of dominating influence of the susceptibility effects, the magnetization shows an oscillating behavior. It can be shown that the dephasing process is closely related to the behavior of a damped driven harmonic oscillator.

Theoretical model of the single spin-echo relaxation time for spherical magnetic perturbers

Magnetically labeled cells and tissue iron deposits provide qualitative means to detect and monitor cardiovascular and cerebrovascular diseases with magnetic resonance imaging. However, to quantitatively examine the extent of pathological micromorphological changes, detailed knowledge about microstructural parameters and relaxation times is required.