T2 and T2⁎ mapping and weighted imaging in cardiac MRI

Cardiac imaging is progressing from simple imaging of heart structure and function to techniques visualizing and measuring underlying tissue biological changes that can potentially define disease and therapeutic options. These techniques exploit underlying tissue magnetic relaxation times: T1, T2 and T2*. Initial weighting methods showed myocardial heterogeneity, detecting regional disease. Current methods are now fully quantitative generating intuitive color maps that do not only expose regionality, but also diffuse changes – meaning that between-scan comparisons can be made to define disease (compared to normal) and to monitor interval change (compared to old scans). T1 is now familiar and used clinically in multiple scenarios, yet some technical challenges remain. T2 is elevated with increased tissue water – edema. Should there also be blood troponin elevation, this edema likely reflects inflammation, a key biological process. T2* falls in the presence of magnetic/paramagnetic materials – practically, this means it measures tissue iron, either after myocardial hemorrhage or in myocardial iron overload. This review discusses how T2 and T2⁎ imaging work (underlying physics, innovations, dependencies, performance), current and emerging use cases, quality assurance processes for global delivery and future research directions

The atrial and ventricular myocardial proteome of endstage lamin heart disease

Lamins A/C (encoded by LMNA gene) can lead to dilated cardiomyopathy (DCM). This pilot study sought to explore the postgenomic phenotype of end-stage lamin heart disease. Consecutive patients with end-stage lamin heart disease (LMNA-group, n = 7) and ischaemic DCM (ICM-group, n = 7) undergoing heart transplantation were prospectively enrolled. Samples were obtained from left atrium (LA), left ventricle (LV), right atrium (RA), right ventricle (RV) and interventricular septum (IVS), avoiding the infarcted myocardial segments in the ICM-group. Samples were analysed using a discovery 'shotgun' proteomics approach. We found that 990 proteins were differentially abundant between LMNA and ICM samples with the LA being most perturbed (16-fold more than the LV). Abundance of lamin A/C protein was reduced, but lamin B increased in LMNA LA/RA tissue compared to ICM, but not in LV/RV. Carbonic anhydrase 3 (CA3) was over-abundant across all LMNA tissue samples (LA, LV, RA, RV, and IVS) when compared to ICM. Transthyretin was more abundant in the LV/RV of LMNA compared to ICM, while sarcomeric proteins such as titin and cardiac alpha-cardiac myosin heavy chain were generally less abundant in RA/LA of LMNA. Protein expression profiling and enrichment analysis pointed towards sarcopenia, extracellular matrix remodeling, deficient myocardial energetics, redox imbalances, and abnormal calcium handling in LMNA samples. Compared to ICM, end-stage lamin heart disease is a biventricular but especially a biatrial disease appearing to have an abundance of lamin B, CA3 and transthyretin, potentially hinting to compensatory responses