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Fetal magnetic resonance imaging (MRI) is an important adjunct modality for the evaluation of fetal abnormalities. Recently, low-field MRI systems at 0.55 Tesla have become available which can produce images on par with 1.5 Tesla systems but with lower power deposition, acoustic noise, and artifact. In this article, we describe a technical innovation using low-field MRI to perform diagnostic quality fetal MRI.

To determine RExperiments were performed in 3 healthy adult volunteers on a prototype whole-body 0.55T MRI, using a custom free-breathing electrocardiogram-triggered, single-slice echo-shifted multi-echo spin echo (ES-MCSE) pulse sequence with respiratory navigation. Transverse relaxation rates RThe mean RJoint estimation of transverse relaxation rates and off-resonance is feasible at 0.55 T with a free-breathing electrocardiogram-gated and navigator-gated ES-MCSE sequence. At 0.55 T, the mean R

Speech production MRI benefits from lower magnetic fields due to reduced off-resonance effects at air-tissue interfaces and from the use of dedicated receiver coils due to higher SNR and parallel imaging capability. Here we present a custom designed upper airway coil forFour adult volunteers were scanned with both custom speech and prototype head-neck coils. We evaluated SNR gains of each of the coils over eleven upper airway volumes-of-interest measured relative to the integrated body coil. We evaluated parallel imaging performance of both coils by computing g-factors for SENSE reconstruction of uniform and variable density Cartesian sampling schemes with R = 2, 3, and 4.The dedicated coil shows approximately 3.5-fold SNR efficiency compared to the head-neck coil. For R = 2 and 3, both uniform and variable density samplings have g-factor values below 1.1 in the upper airway region. For R = 4, g-factor values are higher for both trajectories.The dedicated coil configuration allows for a significant SNR gain over the head-neck coil in the articulators. This, along with favorable g values, makes the coil useful in speech production MRI.

BACKGROUND: In vivo imaging of oxidative stress can facilitate the understanding and treatment of cardiovascular diseases. We evaluated nitroxide-enhanced MRI with 3-carbamoyl-proxyl (3CP) for the detection of myocardial oxidative stress. METHODS: Three mouse models of cardiac oxidative stress were imaged, namely angiotensin II (Ang II) infusion, myocardial infarction (MI), and high-fat high-sucrose (HFHS) diet-induced obesity (DIO). For the Ang II model, mice underwent MRI at baseline and after 7 days of Ang II (n = 8) or saline infusion (n = 8). For the MI model, mice underwent MRI at baseline (n = 10) and at 1 (n = 8), 4 (n = 9), and 21 (n = 8) days after MI. For the HFHS-DIO model, mice underwent MRI at baseline (n = 20) and 18 weeks (n = 13) after diet initiation. The 3CP reduction rate, K(red), computed using a tracer kinetic model, was used as a metric of oxidative stress. Dihydroethidium (DHE) staining of tissue sections was performed on Day 1 after MI. RESULTS: For the Ang II model, K(red) was higher after 7 days of Ang II versus other groups (p < 0.05). For the MI model, K(red), in the infarct region was significantly elevated on Days 1 and 4 after MI (p < 0.05), whereas K(red) in the noninfarcted region did not change after MI. DHE confirmed elevated oxidative stress in the infarct zone on Day 1 after MI. After 18 weeks of HFHS diet, K(red) was higher in mice after diet versus baseline (p < 0.05). CONCLUSIONS: Nitroxide-enhanced MRI noninvasively quantifies tissue oxidative stress as one component of a multiparametric preclinical MRI examination. These methods may facilitate investigations of oxidative stress in cardiovascular disease and related therapies.

Purpose Endothelial nitric oxide synthase (eNOS) plays a central role in regulating vascular tone, blood flow, and microvascular permeability. Endothelial dysfunction, including eNOS dysfunction, is an early biomarker of vascular disease. This study aimed to show that myocardial T1 mapping during nitric oxide synthase (NOS) inhibition could assess coronary microvascular eNOS function. Methods Wild-type mice, eNOS−/− mice, and wild-type mice fed a high-fat diet underwent T1 mapping at baseline and for 20 min after injection of NG-nitro-L-arginine methyl ester (LNAME), a NOS inhibitor. First-pass perfusion MRI was performed in wild-type mice at baseline and 5 min after LNAME injection. Results T1 mapping detected an increase in myocardial T1 5 min after an injection of 4 mg/kg LNAME compared with baseline in control mice (T1 = 1515 ± 30 ms with LNAME versus T1 = 1402 ± 30 ms at baseline, P

PURPOSE To image late mechanical activation and identify effective left-ventricular (LV) pacing sites for cardiac resynchronization therapy (CRT). There is variability in defining mechanical activation time, with some studies using the time to peak strain (TPS) and some using the time to the onset of circumferential shortening (TOS). We developed improved methods for imaging mechanical activation and evaluated them in heart failure (HF) patients undergoing CRT. MATERIALS AND METHODS We applied active contours to cine displacement encoding with stimulated echoes (DENSE) strain images to detect TOS. Six healthy volunteers underwent magnetic resonance imaging (MRI) at 1.5T, and 50 patients underwent pre-CRT MRI (strain, scar, volumes) and echocardiography, assessment of the electrical activation time (Q-LV) at the LV pacing site, and echocardiography assessment of LV reverse remodeling 6 months after CRT. TPS at the LV pacing site was also measured by DENSE. RESULTS The latest TOS was greater in HF patients vs. healthy subjects (112 ± 28 msec vs. 61 ± 7 msec, P 0.75; P

Background Conditions such as obesity and diabetes lead to coronary microvascular disease and, subsequently, an increased risk of adverse cardiac events. Increased microvascular permeability is thought to be an early biomarker of coronary microvascular disease. While prior studies have used MRI with gadolinium-labeled albumin, a macromolecular contrast agent, to detect myocardial infarction, we hypothesized that MRI T1 mapping with gadolinium-labeled albumin could detect more subtle changes in coronary microvascular permeability such as those induced by noninjurious pharmacological methods.

Background Cardiac resynchronization therapy (CRT) benefits selected heart failure patients; however, CRT has a nonresponse rate of approximately 30-40%. Important factors that contribute to lead placement decisions and overall CRT success include determination of mechanical dyssynchrony, presence and location of scar, and the identification of late-activated segments. Recent imaging studies have reported progress in the first two areas. Previously, myocardial tagging showed promise for mapping mechanical activation time [1], but analysis of tagged images is time consuming. We investigated the use of cine DENSE to detect regions of late mechanical activation. Methods Cine DENSE at a temporal resolution of 17 ms, in-plane pixel size of 1.4 mm × 1.4 mm to 2.2 mm × 2.2 mm, and slice thickness of 8 mm was performed in standard short-axis planes in 4 canines with pacing-induced heart failure and left bundle branch block (LBBB) induced by catheter ablation. Using semi-automatic analysis methods [2,3], regional circumferential strain (Ecc) was determined from the mid-cavity short-axis DENSE images. The time to the onset of contraction (mechanical activation time) was defined as the time at which the slope of each Ecc curve first became negative, as shown in Figure 1. The mechanical activation time was computed for regions that were 5 × 5 pixels in size. Results Cine DENSE showed that the septum underwent early activation, while the late-activated regions were consistently located in the anterolateral and inferolateral segments. These patterns were visualized using time-to

Background In clinical patients undergoing cardiac resynchronization therapy (CRT), myocardial properties (mechanical, electrical, and scar-mediated) at the left ventricular (LV) lead position (LVLP) and overall LV dyssynchrony (circumferential uniformity ratio estimate [CURE, 0-1]) are of interest with respect to CRT outcomes. We sought to define the relative importance of these factors for CRT response in a clinical CMR study with longitudinal follow-up.

Animal models have become a popular platform for the investigation of the molecular and systemic mechanisms of pathological cardiovascular physiology. Chronic pacing studies with implantable pacemakers in large animals have led to useful models of heart failure and atrial fibrillation. Unfortunately, molecular and genetic studies in these large animal models are often prohibitively expensive or not available. Conversely, the mouse is an excellent species for studying molecular mechanisms of cardiovascular disease through genetic engineering. However, the large size of available pacemakers does not lend itself to chronic pacing in mice. Here, we present the design for a novel, fully implantable wireless-powered pacemaker for mice capable of long-term (>30 days) pacing. This design is compared to a traditional battery-powered pacemaker to demonstrate critical advantages achieved through wireless inductive power transfer and control. Battery-powered and wireless-powered pacemakers were fabricated from standard electronic components in our laboratory. Mice (n = 24) were implanted with endocardial, battery-powered devices (n = 14) and epicardial, wireless-powered devices (n = 10). Wireless-powered devices were associated with reduced implant mortality and more reliable device function compared to battery-powered devices. Eight of 14 (57.1%) mice implanted with battery-powered pacemakers died following device implantation compared to 1 of 10 (10%) mice implanted with wireless-powered pacemakers. Moreover, device function was achieved for 30 days with the wireless-powered device compared to 6 days with the battery-powered device. The wireless-powered pacemaker system presented herein will allow electrophysiology studies in numerous genetically engineered mouse models as well as rapid pacing-induced heart failure and atrial arrhythmia in mice.

Background Cardiac resynchronization therapy (CRT) is an effective treatment for selected patients with heart failure (HF) and left bundle branch block (LBBB). However, an ongoing major issue with CRT is that 30-50% of treated patients are non-responders. One potential cause of a poor response is implantation of the CRT left-ventricular (LV) pacing lead at a suboptimal location, i.e., a location with scar or where mechanical activation is not delayed [1,2]. This study developed and applied cine DENSE strain imaging [3] to map mechanical activation and detect late-activated segments. Methods Cine DENSE was performed on a 1.5T MRI system in standard short-axis planes in 6 healthy subjects and 16 HF patients with LBBB and nonischemic cardiomyopathy referred to CRT. Circumferential strain (Ecc) was computed using previously described semiautomatic methods [4,5]. Midwall Ecc was arranged into a matrix with 18 rows representing spatial segments of the LV and 30-45 columns representing cardiac phases (Fig 1a). Singular value decomposition (SVD) was applied to denoise the spatiotemporal Ecc matrix, and an active contour method was used to automatically estimate the

Background Right ventricular (RV) dysfunction occurs in many cardiovascular conditions including pulmonary hypertension, congenital heart disease, and left-sided heart failure (HF), and its presence often alters patient management. Myocardial strain imaging has been used to assess left ventricular (LV) dysfunction; however, due to its thin wall, complex shape, and eccentric motion, strain analysis of the RV is more challenging and typically relies on manual delineation of tissue. Cine