Myocardial microstructure dynamics can be characterized by in vivo DT-CMR. Sheetlet function was abnormal in DCM with altered systolic conformation and reduced mobility, contrasting with HCM, which showed reduced mobility with altered diastolic conformation. These novel insights significantly improve understanding of contractile dysfunction at a level of noninvasive interrogation not previously available in humans.

CODE significantly improved SNR for ADC mapping in the brain, liver and heart, and significantly improved DWI bulk motion robustness in the liver and heart. Magn Reson Med 77:717-729, 2017. © 2016 International Society for Magnetic Resonance in Medicine.

Predictive computational modeling has revolutionized classical engineering disciplines and is in the process of transforming cardiovascular research. This is particularly relevant for investigating emergent therapies for heart failure, which remains a leading cause of death globally. The creation of subject-specific biventricular computational cardiac models has been a long-term endeavor within the biomedical engineering community. Using high resolution (0.3 × 0.3 × 0.8 mm) ex vivo data, we constructed a precise fully subject-specific biventricular finite-element model of healthy and failing swine hearts. Each model includes fully subject-specific geometries, myofiber architecture and, in the case of the failing heart, fibrotic tissue distribution. Passive and active material properties are prescribed using hyperelastic strain energy functions that define a nearly incompressible, orthotropic material capable of contractile function. These materials were calibrated using a sophisticated multistep approach to match orthotropic tri-axial shear data as well as subject-specific hemodynamic ventricular targets for pressure and volume to ensure realistic cardiac function. Each mechanically beating heart is coupled with a lumped-parameter representation of the circulatory system, allowing for a closed-loop definition of cardiovascular flow. The circulatory model incorporates unidirectional fluid exchanges driven by pressure gradients of the model, which in turn are driven by the mechanically beating heart. This creates a computationally meaningful representation of the dynamic beating of the heart coupled with the circulatory system. Each model was calibrated using subject-specific experimental data and compared with independent in vivo strain data obtained from echocardiography. Our methods produced highly detailed representations of swine hearts that function mechanically in a remarkably similar manner to the in vivo subject-specific strains on a global and regional comparison. The degree of subject-specificity included in the models represents a milestone for modeling efforts that captures realism of the whole heart. This study establishes a foundation for future computational studies that can apply these validated methods to advance cardiac mechanics research.

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 ϭ 12) or anterior myocardial infarction (MI, n ϭ 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 (CV L) was increased by RSGS (0.98 Ϯ 0.11 vs. 1.2 Ϯ 0.14m/s, P Ͻ 0.001) but not transverse CV (CV T). This increase was abrogated by ␤-adrenergic receptor and gap junction (GJ) blockade. Neither CV L nor CVT was increased by LSGS. In the peri-infarct region, both RSGS and LSGS shortened ARIs in sinus rhythm (423 Ϯ 37 vs. 322 Ϯ 30 ms, P Ͻ 0.001, and 423 Ϯ 36 vs. 398 Ϯ 36 ms, P ϭ 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 Ϯ 1.2 vs. 17.3 Ϯ 1.6 ms, P ϭ 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 Ͻ 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 periinfarct substrates by sympathetic nerves and in part explain the temporal nature of arrhythmogenesis.

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