Eric Aliotta

Convex optimized diffusion encoding (CODE) gradient waveforms for minimum echo time and bulk motion-compensated diffusion-weighted MRI.

To evaluate convex optimized diffusion encoding (CODE) gradient waveforms for minimum echo time and bulk motion–compensated diffusion‐weighted imaging (DWI).

Sympathetic Modulation of Electrical Activation In Normal and Infarcted Myocardium: Implications for Arrhythmogenesis

The influence of cardiac sympathetic innervation on electrical activation in normal and chronically infarcted ventricular myocardium is not understood. Yorkshire pigs with normal hearts (NL, n = 12) or anterior myocardial infarction (MI, n = 9) underwent high-resolution mapping of the anteroapical left ventricle at baseline and during left and right stellate ganglion stimulation (LSGS and RSGS, respectively). Conduction velocity (CV), activation times (ATs), and directionality of propagation were measured. Myocardial fiber orientation was determined using diffusion tensor imaging and histology. Longitudinal CV (CVL) was increased by RSGS (0.98 ± 0.11 vs. 1.2 ± 0.14m/s, P < 0.001) but not transverse CV (CVT). This increase was abrogated by β-adrenergic receptor and gap junction (GJ) blockade. Neither CVL nor CVT was increased by LSGS. In the peri-infarct region, both RSGS and LSGS shortened ARIs in sinus rhythm (423 ± 37 vs. 322 ± 30 ms, P < 0.001, and 423 ± 36 vs. 398 ± 36 ms, P = 0.035, respectively) and altered activation patterns in all animals. CV, as estimated by mean ATs, increased in a directionally dependent manner by RSGS (14.6 ± 1.2 vs. 17.3 ± 1.6 ms, P = 0.015), associated with GJ lateralization. RSGS and LSGS inhomogeneously modulated AT and induced relative or absolute functional activation delay in parts of the mapped regions in 75 and 67%, respectively, in MI animals, and in 0 and 15%, respectively, in control animals (P < 0.001 for both). In conclusion, sympathoexcitation increases CV in normal myocardium and modulates activation propagation in peri-infarcted ventricular myocardium. These data demonstrate functional control of arrhythmogenic peri-infarct substrates by sympathetic nerves and in part explain the temporal nature of arrhythmogenesis.NEW & NOTEWORTHY This study demonstrates regional control of conduction velocity in normal hearts by sympathetic nerves. In infarcted hearts, however, not only is modulation of propagation heterogeneous, some regions showed paradoxical conduction slowing. Sympathoexcitation altered propagation in all infarcted hearts studied, and we describe the temporal arrhythmogenic potential of these findings.Listen to this articles corresponding podcast at http://ajpheart.podbean.com/e/sympathetic-nerves-and-cardiac-propagation/.

Pathological effects of chronic myocardial infarction on peripheral neurons mediating cardiac neurotransmission.

OBJECTIVE To determine whether chronic myocardial infarction (MI) induces structural and neurochemical changes in neurons within afferent and efferent ganglia mediating cardiac neurotransmission. METHODS Neuronal somata in i) right atrial (RAGP) and ii) ventral interventricular ganglionated plexi (VIVGP), iii) stellate ganglia (SG) and iv) T1-2 dorsal root ganglia (DRG) bilaterally derived from normal (n=8) vs. chronic MI (n=8) porcine subjects were studied. We examined whether the morphology and neuronal nitric oxide synthase (nNOS) expression in soma of RAGP, VIVGP, DRG and SG neurons were altered as a consequence of chronic MI. In DRG, we also examined immunoreactivity of calcitonin gene related peptide (CGRP), a marker of afferent neurons. Chronic MI increased neuronal size and nNOS immunoreactivity in VIVGP (but not RAGP), as well as in the SG bilaterally. Across these ganglia, the increase in neuronal size was more pronounced in nNOS immunoreactive neurons. In the DRG, chronic MI also caused neuronal enlargement, and increased CGRP immunoreactivity. Further, DRG neurons expressing both nNOS and CGRP were increased in MI animals compared to controls, and represented a shift from double negative neurons. CONCLUSIONS Chronic MI impacts diverse elements within the peripheral cardiac neuraxis. That chronic MI imposes such widespread, diverse remodeling of the peripheral cardiac neuraxis must be taken into consideration when contemplating neuronal regulation of the ischemic heart.

Increased maximum gradient amplitude improves robustness of spin-echo cardiac diffusion-weighted MRI

Background Cardiac motion presents a major challenge in diffusion weighted MRI (DWI), often leading to large signal dropouts that necessitate repeated measurements (Pai, V.M., MRM 2011). While cardiac DWI is generally ECG gated to apply diffusion weighting during peak-systole or enddiastole, these intervals can be short and difficult to pinpoint, resulting in poor sequence reproducibility. Recent improvements in gradient hardware provide larger maximum gradients than current systems (Gmax=80mT/m), which can substantially reduce the temporal footprint of diffusion preparation and make cardiac DWI more robust to bulk motion.

Eddy current-nulled convex optimized diffusion encoding (EN-CODE) for distortion-free diffusion tensor imaging with short echo times

To design and evaluate eddy current–nulled convex optimized diffusion encoding (EN‐CODE) gradient waveforms for efficient diffusion tensor imaging (DTI) that is free of eddy current–induced image distortions.

Quantifying precision in cardiac diffusion tensor imaging with second-order motion-compensated convex optimized diffusion encoding.

To quantify the precision of in vivo cardiac DTI (cDTI) acquired with a spin echo, first‐ and second‐order motion‐compensated (M1M2), convex optimized diffusion encoding (CODE) sequence.

Simultaneous measurement of T2 and apparent diffusion coefficient (T2+ADC) in the heart with motion-compensated spin echo diffusion-weighted imaging

To evaluate a technique for simultaneous quantitative T2 and apparent diffusion coefficient (ADC) mapping in the heart (T2+ADC) using spin echo (SE) diffusion‐weighted imaging (DWI).

High-resolution spin-echo Cardiac Diffusion-Weighted MRI with motion compensated Convex Optimized Diffusion Encoding (CODE)

Background Cardiac Diffusion Weighted MRI (cDWI) has the potential to characterize myocardial infarction (MI) without contrast. However, the clinical utility of cDWI has been limited by severe sensitivity to cardiac motion that manifests as signal dropouts which corrupt measures of myocardial diffusivity. This can be managed by carefully timing the diffusion encoding gradients (GDiff) to a quiescent diastolic phase, but this approach is burdensome and highly sensitive to heart-rate changes. More recently, motion compensated (MOCO) diffusion encoding gradients with nulled first (M1) and second (M2) moments have demonstrated good robustness to cardiac motion (Stoeck, MRM 2015, Nguyen, MRM 2013) but they necessarily increase the echo time (TE) compared to monopolar encoding (MONO), which reduces SNR and/or limits spatial resolution. We have developed a MOCO cDWI sequence that employs Convex Optimized Diffusion Encoding (CODE) to reduce bulk motion sensitivity and shorten TE compared to existing MOCO schemes.

Effect of flow-encoding strength on intravoxel incoherent motion in the liver

To study the impact of variable flow‐encoding strength on intravoxel incoherent motion (IVIM) liver imaging of diffusion and perfusion.

Effect of intra-myocardial Algisyl-LVR™ injectates on fibre structure in porcine heart failure

Recent preclinical trials have shown that alginate injections are a promising treatment for ischemic heart disease. Although improvements in heart function and global structure have been reported following alginate implants, the underlying structure is poorly understood. Using high resolution ex vivo MRI and DT-MRI of the hearts of normal control swine (n = 8), swine with induced heart failure (n = 5), and swine with heart failure and alginate injection treatment (n = 6), we visualized and quantified the fibre distribution and implant material geometry. Our findings show that the alginate injectates form solid ellipsoids with a retention rate of 68.7% ± 21.3% (mean ± SD) and a sphericity index of 0.37 ± 0.03. These ellipsoidal shapes solidified predominantly at the mid-wall position with an inclination of -4.9° ± 31.4° relative to the local circumferential direction. Overall, the change to left ventricular wall thickness and myofiber orientation was minor and was associated with heart failure and not the presence of injectates. These results show that alginate injectates conform to the pre-existing tissue structure, likely expanding along directions of least resistance as mass is added to the injection sites. The alginate displaces the myocardial tissue predominantly in the longitudinal direction, causing minimal disruption to the surrounding myofiber orientations.