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Purpose To evaluate the signal properties of 2D time of flight (TOF), quiescent-interval single-shot (QISS), ECG-gated 3D fast spin-echo (FBI), and ungated 3D fast spin-echo ghost (Ghost) magnetic resonance angiography (MRA) over a range of flow velocities in a pulsatile flow phantom with a 50% diameter stenosis at 1.5T. Materials and Methods Blood-mimicking fluid was pumped at eight peak flow velocities through a stenotic region in triphasic and monophasic waveforms. Vascular signal proximal, within, and distal to the stenosis was measured from the source images of the four MRA methods. Coronal maximum intensity projection images were used to compare image quality. Results TOF and QISS signal trends were similar, but QISS exhibited the most consistent signal across velocities. At high velocities (≥42.4 cm/s), TOF showed post-stenotic signal loss that was not observed with QISS. FBI and Ghost signals peaked at low velocities (3.9–9.7 cm/s) without flow compensation and at high velocities (≥64.6 cm/s) with flow compensation. Conclusion FBI and Ghost demonstrated dependence on blood flow velocity and flow compensation. TOF was sensitive to flow artifacts at high velocities. QISS proved most robust for accurately depicting the normal lumen and stenosis under a wide range of flow conditions. Monophasic and triphasic flow did not appreciably affect the signal performance of any method.

Background: Elevated intracardiac pressure due to heart failure induces electrical and structural remodeling in the left atrium (LA) that begets atrial myopathy and arrhythmias. The underlying molecular pathways that drive atrial remodeling during cardiac pressure overload are poorly defined. The purpose of this study is to characterize the response of the ETV1 signaling axis in the LA during cardiac pressure overload in humans and mouse models and explore the role of ETV1 in atrial electrical and structural remodeling. Methods: We performed gene expression profiling in 265 left atrial samples from patients who underwent cardiac surgery. Comparative gene expression profiling was performed between two murine models of cardiac pressure overload, transverse aortic constriction (TAC) banding and Angiotensin II (AngII) infusion, and a genetic model of Etv1 cardiomyocyte-selective knockout ( Etv1 f/f Mlc2a Cre/+ ). Results: Using the Cleveland Clinic biobank of human LA specimens, we found that ETV1 expression is decreased in patients with reduced ejection fraction. Consistent with its role as an important mediator of the Neuregulin-1 (NRG1) signaling pathway and activator of rapid conduction gene programming, we identified a direct correlation between ETV1 expression level and NRG1, ERBB4, SCN5A , and GJA5 levels in human LA samples. In a similar fashion to heart failure patients, we showed that left atrial ETV1 expression is downregulated at the RNA and protein levels in murine pressure overload models. Comparative analysis of LA RNA-seq datasets from TAC and AngII treated mice showed a high Pearson correlation, reflecting a highly ordered process by which the LA undergoes electrical and structural remodeling. Cardiac pressure overload produced a consistent downregulation of ErbB4, Etv1, Scn5a, and Gja5 and upregulation of profibrotic gene programming, which includes Tgfbr1/2, Igf1, and numerous collagen genes. Etv1 f/f Mlc2a Cre/+ mice displayed atrial conduction disease and arrhythmias. Correspondingly, the LA from Etv1 f/f Mlc2a Cre/+ mice showed downregulation of rapid conduction genes and upregulation of profibrotic gene programming, whereas analysis of a gain-of-function ETV1 RNA-seq dataset from neonatal rat ventricular myocytes transduced with Etv1 showed reciprocal changes. Conclusions: ETV1 is downregulated in the LA during cardiac pressure overload, contributing to both electrical and structural remodeling.

Most nonenhanced MRA techniques for evaluating peripheral artery disease (PAD) require cardiac synchronization through physiological gating. Electrocardiographic (ECG) gating is the most popular method for cardiac synchronization; however, it is subject to interference from switching magnetic field gradients and radiofrequency pulses. A method is described for self-gated nonenhanced MRA that does not require the use of ECG gating. Imaging was prospectively triggered by detecting the acceleration of blood flow during systole with a reference-less phase contrast navigator. The technique was implemented for non-subtractive nonenhanced MRA using quiescent-interval single-shot (QISS) MRA. The lower extremity peripheral arteries of eight healthy subjects were imaged using ECG-, pulse-, and self-gated QISS. Self-gated QISS triggered with 99% accuracy. There were no significant differences in relative contrast, contrast-to-noise ratio, or image quality between self-gated and ECG-gated QISS MRA (p > 0.05). Image quality with pulse gating was inferior.

Background Mesenchymal stem cells (MSC) have immunomodulatory and neuro-protective properties and are being studied for treatment of multiple sclerosis (MS). Tractography-based diffusion tensor imaging (DTI), cortical thickness (Cth) and T2 lesion volume (T2LV) can provide insight into treatment effects. Objective The objective of this study was to analyse the effects of MSC transplantation in MS on exploratory MRI measures. Methods MRIs were obtained from 24 MS patients from a phase 1 open-label study of autologous MSC transplantation. DTI metrics were obtained in lesions and normal-appearing white matter motor tracts (NAWM). T2LV and Cth were derived. Longitudinal evolution of MRI outcomes were modelled using linear mixed effects. Pearson’s correlation was calculated between MRI and clinical measures. Results Lesional radial diffusivity (RD) and axial diffusivity (AD) decreased pre-transplant and showed no changes post-transplant. There were mixed trends in NAWM RD and AD pre/post-transplant. Transplantation stabilized T2LV growth. NAWM RD and AD correlated with Cth, T2LV and with leg and arm function but not with cognition. Lesional DTI demonstrated similar but less robust correlations. Conclusions Microstructural tissue integrity is altered in MS. DTI changes pre-transplant may be influenced by concomitant lesion accrual. Contributor to DTI stabilization post-transplant is multifactorial. DTI of major motor tracts correlated well with clinical measures, highlighting its sensitivity to clinically meaningful changes.