Archive for October 2020

Post-infarction Cardiac Rupture

Why is it important to have clear diagnostic criteria to use when assessing cardiac rupture in the mouse model of permanent occlusion myocardial infarction? Listen as Deputy Editor Merry L. Lindsey (University of Nebraska Medical Center) interviews lead author Nikolaos Frangogiannis (Albert Einstein College of Medicine) and expert Kristine DeLeon-Pennell (Medical University of South Carolina) about the new study by Hanna et al which compared results from their in-depth histopathological examination with visual inspection of cardiac rupture. Frangogiannis and co-authors found that identifying the rupture site had high specificity but low sensitivity, with a low rate of false positives. Conversely, identifying hemothorax had high sensitivity yet low specificity. Hanna et al. observed key sex differences in their non-reperfusion mouse model of MI. In addition, differences in macrophages and fibroblasts in mice of both sexes which died of cardiac rupture indicated that a perturbed balance of inflammatory mediators may be a factor in the pathogenesis of cardiac rupture. What is the key take-away? When evaluating the cause of death in infarcted mice, look for the rupture site. Listen now.


Anis Hanna, Arti V Shinde, and Nikolaos G. Frangogiannis Validation of diagnostic criteria and histopathological characterization of cardiac rupture in the mouse model of non-reperfused myocardial infarction Am J Physiol Heart Circ Physiol, published October 15, 2020. DOI: ajpheart.00318.2020

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DCM Mutations Alter Intracellular Ca2+ and Signaling

What can three mutations in thin filament regulatory proteins associated with dilated cardiomyopathy tell us about the highly variable phenotypes of DCM? Listen as Associate Editor Crystal Ripplinger (University of California Davis) interviews lead author Paul Robinson (University of Oxford) and expert Michael Greenberg (Washington University in St. Louis) about the latest work by Robinson and co-authors. By studying functional changes in cardiomyocyte contraction, calcium handling and signaling, Robinson and co-authors hoped to identify common pathway activations in troponin T, troponin I and tropomyosin mutations. Why did the authors opt to study DCM mutations in guinea pig cardiomyocytes rather than in a mouse model? Given the substantial number of mutations in both pediatric and adult-onset DCM, what are the implications here for precision medicine in the treatment of this disease? Listen to learn more.


Paul Robinson, Alexander J. Sparrow, Suketu Patel, Marta Malinowska, Svetlana N. Reilly, Yin-Hua Zhang, Barbara Casadei, Hugh Watkins, Charles Redwood Dilated cardiomyopathy mutations in thin-filament regulatory proteins reduce contractility, suppress systolic Ca2+, and activate NFAT and Akt signaling Am J Physiol Heart Circ Physiol, published July 21, 2020. DOI:

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