Cardiovascular health is vital to human well-being, and cardiac magnetic resonance (CMR) imaging is considered the clinical reference standard for diagnosing cardiovascular disease. However, its adoption is hindered by long scan times, complex contrasts, and inconsistent quality. While deep learning methods perform well on specific CMR imaging sequences, they often fail to generalize across modalities and sampling schemes. The lack of benchmarks for high-quality, fast CMR image reconstruction further limits technology comparison and adoption. The CMRxRecon2024 challenge, attracting over 200 teams from 18 countries, addressed these issues with two tasks: generalization to unseen modalities and robustness to diverse undersampling patterns. We introduced the largest public multi-modality CMR raw dataset, an open benchmarking platform, and shared code. Analysis of the best-performing solutions revealed that prompt-based adaptation and enhanced physics-driven consistency enabled strong cross-scenario performance. These findings establish principles for generalizable reconstruction models and advance clinically translatable AI in cardiovascular imaging.

In atrial fibrillation (AF), atrial biomechanics are altered, reducing atrial movement. It remains unclear whether these changes are due to altered anatomy, myocardial stiffness, or constraints from surrounding structures. Understanding the causes of changed atrial deformation in AF could enhance tissue characterization and inform AF diagnosis, stratification, and treatment. We created patient-specific anatomical models of the left atrium (LA) from CT images. Passive LA biomechanics were simulated using finite deformation continuum mechanics equations. LA stiffness was represented by the Guccione material law, where α scaled the anisotropic stiffness parameters. Regional passive stiffness parameters were calibrated to peak regional deformation during the reservoir phase and validated against deformation transients derived from retrospective gated CT images during the reservoir and conduit phase. Physiological LA deformation varies regionally, with the roof deforming significantly less than other regions during the reservoir phase. The fitted model matched peak patient deformations globally and regionally with an average error of [Formula: see text] mm over our cohort. We compared deformation transients through the reservoir and conduit phases and found that the simulated deformation transients were within an average of [Formula: see text] mm per unit time of the CT-derived deformation transients. Regional stiffness varied across the atria with average α values of 1.8, 1.6, 2.2, 1.6 and 2.1 across the cohort in the anterior, posterior, septum, lateral and roof regions respectively. Using mixed effect models, we found no correlation between regional patient LA deformation and regional estimates of wall thickness or regional volumes of epicardial adipose tissue. We found a significant correlation between regionally calibrated stiffness and CT-derived LA biomechanics (p = 0.023). We have shown that regional heterogeneity in stiffness contributes to regional LA biomechanics, while anatomical features appeared less important. These findings provide insight into the underlying causes of altered LA biomechanics in AF.

Changes in left ventricular (LV) aggregate cardiomyocyte orientation and deformation underlie cardiac function and dysfunction. As such, in vivo aggregate cardiomyocyte "myofiber" strain ( [Formula: see text]) has mechanistic significance, but currently there exists no established technique to measure in vivo [Formula: see text]. The objective of this work is to describe and validate a pipeline to compute in vivo [Formula: see text] from magnetic resonance imaging (MRI) data. Our pipeline integrates LV motion from multi-slice Displacement ENcoding with Stimulated Echoes (DENSE) MRI with in vivo LV microstructure from cardiac Diffusion Tensor Imaging (cDTI) data. The proposed pipeline is validated using an analytical deforming heart-like phantom. The phantom is used to evaluate 3D cardiac strains computed from a widely available, open-source DENSE Image Analysis Tool. Phantom evaluation showed that a DENSE MRI signal-to-noise ratio (SNR) ≥20 is required to compute [Formula: see text] with near-zero median strain bias and within a strain tolerance of 0.06. Circumferential and longitudinal strains are also accurately measured under the same SNR requirements, however, radial strain exhibits a median epicardial bias of -0.10 even in noise-free DENSE data. The validated framework is applied to experimental DENSE MRI and cDTI data acquired in eight ( N=8 ) healthy swine. The experimental study demonstrated that [Formula: see text] has decreased transmural variability compared to radial and circumferential strains. The spatial uniformity and mechanistic significance of in vivo [Formula: see text] make it a compelling candidate for characterization and early detection of cardiac dysfunction.

Heart failure is a leading cause of death, yet its underlying electrophysiological (EP) mechanisms are not well understood. In this study, we use a multiscale approach to analyze a model of heart failure and connect its results to features of the electrocardiogram (ECG). The heart failure model is derived by modifying a previously validated electrophysiology model for a healthy rabbit heart. Specifically, in accordance with the heart failure literature, we modified the cell EP by changing both membrane currents and calcium handling. At the tissue level, we modeled the increased gap junction lateralization and lower conduction velocity due to downregulation of Connexin 43. At the biventricular level, we reduced the apex-to-base and transmural gradients of action potential duration (APD). The failing cell model was first validated by reproducing the longer action potential, slower and lower calcium transient, and earlier alternans characteristic of heart failure EP. Subsequently, we compared the electrical wave propagation in one dimensional cables of healthy and failing cells. The validated cell model was then used to simulate the EP of heart failure in an anatomically accurate biventricular rabbit model. As pacing cycle length decreases, both the normal and failing heart develop T-wave alternans, but only the failing heart shows QRS alternans (although moderate) at rapid pacing. Moreover, T-wave alternans is significantly more pronounced in the failing heart. At rapid pacing, APD maps show areas of conduction block in the failing heart. Finally, accelerated pacing initiated wave reentry and breakup in the failing heart. Further, the onset of VF was not observed with an upregulation of SERCA, a potential drug therapy, using the same protocol. The changes introduced at the cell and tissue level have increased the failing heart's susceptibility to dynamic instabilities and arrhythmias under rapid pacing. However, the observed increase in arrhythmogenic potential is not due to a steepening of the restitution curve (not present in our model), but rather to a novel blocking mechanism.

Scientists have long sought to understand how vascular networks supply blood and oxygen to cells throughout the body. Recent work focuses on principles that constrain how vessel size changes through branching generations from the aorta to capillaries and uses scaling exponents to quantify these changes. Prominent scaling theories predict that combinations of these exponents explain how metabolic, growth, and other biological rates vary with body size. Nevertheless, direct measurements of individual vessel segments have been limited because existing techniques for measuring vasculature are invasive, time consuming, and technically difficult. We developed software that extracts the length, radius, and connectivity of in vivo vessels from contrast-enhanced 3D Magnetic Resonance Angiography. Using data from 20 human subjects, we calculated scaling exponents by four methods-two derived from local properties of branching junctions and two from whole-network properties. Although these methods are often used interchangeably in the literature, we do not find general agreement between these methods, particularly for vessel lengths. Measurements for length of vessels also diverge from theoretical values, but those for radius show stronger agreement. Our results demonstrate that vascular network models cannot ignore certain complexities of real vascular systems and indicate the need to discover new principles regarding vessel lengths.

Guided by empirically established connections between clinically important tissue properties and diffusion tensor parameters, we introduce a framework for decomposing variations in diffusion tensors into changes in shape and orientation. Tensor shape and orientation both have three degrees-of-freedom, spanned by invariant gradients and rotation tangents, respectively. As an initial demonstration of the framework, we create a tunable measure of tensor difference that can selectively respond to shape and orientation. Second, to analyze the spatial gradient in a tensor volume (a third-order tensor), our framework generates edge strength measures that can discriminate between different neuroanatomical boundaries, as well as creating a novel detector of white matter tracts that are adjacent yet distinctly oriented. Finally, we apply the framework to decompose the fourth-order diffusion covariance tensor into individual and aggregate measures of shape and orientation covariance, including a direct approximation for the variance of tensor invariants such as fractional anisotropy.