Jaco J.M. Zwanenburg

Interventricular Mechanical Asynchrony in Pulmonary Arterial Hypertension Left-to-Right Delay in Peak Shortening Is Related to Right Ventricular Overload and Left Ventricular Underfilling

OBJECTIVES The purpose of this study was to explore in pulmonary arterial hypertension (PAH) whether the cause of interventricular asynchrony lies in onset of shortening or duration of shortening. BACKGROUND In PAH, leftward ventricular septal bowing (LVSB) is probably caused by a left-to-right (L-R) delay in myocardial shortening. METHODS In 21 PAH patients (mean pulmonary arterial pressure 55 +/- 13 mm Hg and electrocardiogram-QRS width 100 +/- 16 ms), magnetic resonance imaging myocardial tagging (14 ms temporal resolution) was applied. For the left ventricular (LV) free wall, septum, and right ventricular (RV) free wall, the onset time (T(onset)) and peak time (T(peak)) of circumferential shortening were calculated. The RV wall tension was estimated by the Laplace law. RESULTS The T(onset) was 51 +/- 23 ms, 65 +/- 4 ms, and 52 +/- 22 ms for LV, septum, and RV, respectively. The T(peak) was 293 +/- 58 ms, 267 +/- 22 ms, and 387 +/- 50 ms for LV, septum, and RV, respectively. Maximum LVSB was at 395 +/- 45 ms, coinciding with septal overstretch and RV T(peak). The L-R delay in T(onset) was -1 +/- 16 ms (p = 0.84), and the L-R delay in T(peak) was 94 +/- 41 ms (p < 0.001). The L-R delay in T(peak) was not related to the QRS width but was associated with RV wall tension (p < 0.05). The L-R delay in T(peak) correlated with leftward septal curvature (p < 0.05) and correlated negatively with LV end-diastolic volume (p < 0.05) and stroke volume (p < 0.05). CONCLUSIONS In PAH, the L-R delay in myocardial peak shortening is caused by lengthening of the duration of RV shortening. This L-R delay is related to LVSB, decreased LV filling, and decreased stroke volume.

Subfields of the hippocampal formation at 7 T MRI: In vivo volumetric assessment

Animal and human autopsy studies suggest that subfields of the hippocampal formation are differentially affected by neuropsychiatric diseases. Therefore, subfield volumes may be more sensitive to effects of disease processes. The few human studies that segmented subfields of the hippocampal formation in vivo either assessed the subfields only in the body of the hippocampus, assessed only three subfields, or did not take the differential angulation of the head of the hippocampus into account. We developed a protocol using 7 Tesla MRI with isotropic voxels to reliably delineate the entorhinal cortex (ERC), subiculum (SUB), CA1, CA2, CA3, dentate gyrus (DG)&CA4 along the full-length of the hippocampus. Fourteen subjects (aged 54-74 years, 2 men and 12 women) were scanned with a 3D turbo spin echo (TSE) sequence with isotropic voxels of 0.7 × 0.7 × 0.7 mm(3) on a 7 T MRI whole body scanner. Based on previous protocols and extensive anatomic atlases, a new protocol for segmentation of subfields of the hippocampal formation was formulated. ERC, SUB, CA1, CA2, CA3 and DG&CA4 were manually segmented twice by one rater from coronal MR images. Good-to-excellent consistency was found for all subfields (Intraclass Correlation Coefficients (ICC) varying from 0.74 to 0.98). Accuracy as measured with the Dice Similarity Index (DSI) was above 0.82 for all subfields, with the exception of the smaller subfield CA3 (0.68-0.70). In conclusion, this study shows that it is possible to delineate the main subfields of the hippocampal formation along its full-length in vivo at 7 T MRI. Our data give evidence that this can be done in a reliable manner. Segmentation of subfields in the full-length of the hippocampus may bolster the study of the etiology neuropsychiatric diseases.

Clinical applications of 7 T MRI in the brain

This review illustrates current applications and possible future directions of 7 Tesla (7 T) Magnetic Resonance Imaging (MRI) in the field of brain MRI, in clinical studies as well as clinical practice. With its higher signal-to-noise (SNR) and contrast-to-noise ratio (CNR) compared to lower field strengths, high resolution, contrast-rich images can be obtained of diverse pathologies, like multiple sclerosis (MS), brain tumours, aging-related changes and cerebrovascular diseases. In some of these diseases, additional pathophysiological information can be gained compared to lower field strengths. Because of clear depiction of small anatomical details, and higher lesion conspicuousness, earlier diagnosis and start of treatment of brain diseases may become possible. Furthermore, additional insight into the pathogenesis of brain diseases obtained with 7 T MRI could be the basis for new treatment developments. However, imaging at high field comes with several limitations, like inhomogeneous transmit fields, a higher specific absorption rate (SAR) and, currently, extensive contraindications for patient scanning. Future studies will be aimed at assessing the advantages and disadvantages of 7 T MRI over lower field strengths in light of clinical applications, specifically the additional diagnostic and prognostic value of 7 T MRI.

In vivo detection of cerebral cortical microinfarcts with high-resolution 7T MRI

Cerebrovascular disease has an important role in cognitive decline and dementia. In this context, cerebral microinfarcts are attracting increasing attention, but these lesions could thus far not be detected in vivo. The aim of this study was to try to identify possible cortical microinfarcts on high-resolution 7T in vivo magnetic resonance imaging (MRI) and to perform a histopathologic validation study on similar appearing lesions on 7T ex vivo MRI of postmortem brain tissue. The study population consisted of 22 elderly subjects, who underwent 7T MRI. The fluid attenuated inversion recovery, T2, and T1 weighted scans of these subjects were examined for possible cortical microinfarcts. In the ex vivo MRI study, 15 formalin-fixed coronal brain slices of 6 subjects with Alzheimer and vascular pathology were examined and subjected to histopathologic verification. On the in vivo scans, 15 cortical lesions could be identified that were likely to be microinfarcts in 6 subjects. In the postmortem tissue, 6 similar appearing lesions were identified of which 5 were verified as cortical microinfarcts on histopathology. This study provides strong evidence that cortical microinfarcts can be detected in vivo, which will be of great value in further studies into the role of vascular disease in cognitive decline and dementia.

Intracranial Vessel Wall Imaging at 7.0-T MRI

Background and Purpose— Conventional imaging methods cannot depict the vessel wall of intracranial arteries at sufficient resolutions. This hampers the evaluation of intracranial arterial disease. The aim of the present study was to develop a high-resolution MRI method to image intracranial vessel wall. Methods— We developed a volumetric (3-dimensional) turbo spin-echo (TSE) sequence for intracranial vessel wall imaging at 7.0-T MRI. Inversion recovery was used to null cerebrospinal fluid to increase contrast with the vessel wall. Magnetization preparation was applied before inversion to improve signal-to-noise ratio. Seven healthy volunteers and 35 patients with ischemic stroke or transient ischemic attack underwent imaging to test the magnetization preparation inversion recovery TSE sequence. Gadolinium-based contrast agent (Gadobutrol, 0.1 mL/kg) was administered to assess possible lesion enhancement in the patients. Results— The walls of intracranial arterial vessels could be visualized in all volunteers and patients with good contrast between wall, blood, and cerebrospinal fluid. The quality of the vessel wall depiction was independent of the vessel orientation relative to the plane of acquisition. In 21 of the 35 patients, a total number of 52 intracranial vessel wall lesions were identified. Eleven of the 52 lesions showed enhancement after contrast administration. Only 14 of the 52 lesions resulted in stenosis of the arterial lumen. Conclusions— Intracranial vessel wall and its pathology can be depicted with the magnetization preparation inversion recovery TSE sequence at 7.0 T. The magnetization preparation inversion recovery TSE sequence will make it possible to study the role of intracranial arterial wall pathology in ischemic stroke. Clinical Trial Registration Information— URL: http://www.trialregister.nl/trialreg/index.asp. Unique identifier: NTR2119.

Steady-state free precession with myocardial tagging: CSPAMM in a single breathhold

A method is presented that combines steady‐state free precession (SSFP) cine imaging with myocardial tagging. Before the tagging preparation at each ECG‐R wave, the steady‐state magnetization is stored as longitudinal magnetization by an α/2 flip‐back pulse. Imaging is continued immediately after tagging preparation, using linearly increasing startup angles (LISA) with a rampup over 10 pulses. Interleaved segmented k‐space ordering is used to prevent artifacts from the increasing signal during the LISA rampup. First, this LISA‐SSFP method was evaluated regarding ghost artifacts from the steady‐state interruption by comparing LISA with an α/2 startup method. Next, LISA‐SSFP was compared with spoiled gradient echo (SGRE) imaging, regarding tag contrast‐to‐noise ratio and tag persistence. The measurements were performed in phantoms and in six subjects applying breathhold cine imaging with tagging (temporal resolution 51 ms). The results show that ghost artifacts are negligible for the LISA method. Compared to the SGRE reference, LISA‐SSFP was two times faster, with a slightly better tag contrast‐to‐noise. Additionally, the tags persisted 126 ms longer with LISA‐SSFP than with SGRE imaging. The high efficiency of LISA‐SSFP enables the acquisition of complementary tagged (CSPAMM) images in a single breathhold. Magn Reson Med 49:722–730, 2003.

High-resolution magnetization-prepared 3D-FLAIR imaging at 7.0 Tesla.

The aim of the present study is to develop a submillimeter volumetric (three‐dimensional) fluid‐attenuated inversion recovery sequence at 7T. Implementation of the fluid‐attenuated inversion recovery sequence is difficult as increased T1 weighting from prolonged T1 constants at 7T dominate the desired T2 contrast and yield suboptimal signal‐to‐noise ratio. Magnetization preparation was used to reduce T1 weighting and improve the T2 weighting. Also, practical challenges limit the implementation. Long refocusing trains with low flip angles were used to mitigate the specific absorption rate constraints. This resulted in a three‐dimensional magnetization preparation fluid‐attenuated inversion recovery sequence with 0.8 × 0.8 × 0.8 = 0.5 mm3 resolution in a clinically acceptable scan time. The contrast‐to‐noise ratio between gray matter and white matter (contrast‐to‐noise ratio = signal‐to‐noise ratio [gray matter] − signal‐to‐noise ratio [white matter]) increased from 12 ± 9 without magnetization preparation to 28 ± 8 with magnetization preparation (n = 12). The signal‐to‐noise ratio increased for white matter by 13 ± 6% and for gray matter by 48 ± 15%. In conclusion, three‐dimensional fluid‐attenuated inversion recovery with high resolution and full brain coverage is feasible at 7T. Magnetization preparation reduces the T1 weighting, thereby improving the T2 weighted contrast and signal‐to‐noise ratio. Magn Reson Med, 2010.

Imaging Intracranial Vessel Wall Pathology With Magnetic Resonance Imaging Current Prospects and Future Directions

To date, the probable cause of ischemic stroke is often inferred from the size and location of the infarct, in combination with an evaluation of the heart and the presence of extracranial arterial occlusion or high-grade stenosis.1 Currently used conventional lumenography-based methods such as digital subtraction angiography, computed tomography angiography, and magnetic resonance (MR) angiography are used to determine the presence of such an acute occlusion or high-grade arterial stenosis. From extracranial studies, it is known that luminal narrowing may be absent in patients with severe atherosclerosis owing to arterial remodeling.2–4 Therefore, these methods do not provide information about the underlying pathological processes, which most often involve the vessel wall.5 Vessel wall changes such as vessel wall thickening, enhancement, or the presence of vulnerable atherosclerotic plaques without luminal stenosis are therefore often missed but might be of importance for a better understanding of ischemic stroke.6 Furthermore, intracranial atherosclerosis is an important cause of ischemic stroke7 and often involves the vessel wall. Patients with intracranial atherosclerosis have high recurrent stroke rates,8 and increasingly more attention is being directed to the assessment of the intracranial vessel wall, necessitating an imaging technique directly assessing the intracranial vessel wall. MR imaging (MRI) seems the most promising technique to reliably image intracranial vessel wall pathologies because of its superior soft tissue contrast. Recent advances in MRI9 have made it possible to obtain information about these abnormalities within the intracranial vessel wall, which provides an imaging tool to investigate the role of intracranial vessel wall abnormalities in the diagnosis of stroke. In this review, we discuss the current status of intracranial vessel wall MRI and its potential to identify different intracranial vessel wall pathologies. First, we present the state-of-the-art MRI methods to visualize the intracranial vessel wall …

Correction of phase offset errors in main pulmonary artery flow quantification

To investigate whether an existing method for correction of phase offset errors in phase‐contrast velocity quantification is applicable for assessment of main pulmonary artery flow with an MR scanner equipped with a high‐power gradient system.

Cerebral Microbleeds on MR Imaging: Comparison between 1.5 and 7T

BACKGROUND AND PURPOSE: The detection of microbleeds differs strongly between studies, due to differences in scan protocol. This study aims to compare the visualization of microbleeds with 3D T2*-weighted imaging at 1.5T with 3D dual-echo T2*-weighted imaging at 7T. MATERIALS AND METHODS: Thirty-four patients (29 male; mean age, 58 ± 12 years) with atherosclerotic disease from the Second Manifestations of ARTerial Disease study were included. 3D T2*-weighted imaging at 1.5T and dual-echo T2*-weighted imaging at 7T were done in all patients. The presence and number of definite microbleeds were recorded on minimal intensity projections. Inter- and intraobserver reliability was assessed with Cohen κ test and the ICC. The difference in presence and number of microbleeds was tested with the McNemar test and Wilcoxon signed rank test. RESULTS: The interobserver ICC at 7T was 0.61 and the intraobserver ICC was 0.94, whereas at 1.5T the interobserver ICC was 0.50 and the intraobserver ICC was 0.59. Microbleeds were detected in significantly more patients on 7T (50%) than on 1.5T scans (21%) (P = .001). The number of microbleeds was also higher at 7T (median, 0.5; range, 0–5) than on 1.5T (median, 0.0; range, 0–6) (P = .002). CONCLUSIONS: 3D dual-echo T2*-weighted imaging at 7T results in better and more reliable detection of microbleeds compared with 3D T2*-weighted imaging at 1.5T.