March 28, 2013
Can an abnormal metaboreflex activation causing coronary constriction help to explain the reduced ability of the heart to increase cardiac performance in heart failure patients during exercise? While the metaboreflex has been studied for decades, new research by Coutsos et al in a chronic dog model of heart failure gives fresh insights on how ventricular function is improved by relieving vasoconstriction and thus enhancing coronary blood flow. Associate Editor Fabio Recchia interviews lead author Donal O’Leary (Wayne State University) and expert Antonio Crisafulli (University of Cagliari, Italy) about this interesting work and its potential clinical impact on heart failure patients.
Matthew Coutsos, Javier A. Sala-Mercado, Masashi Ichinose, ZhenHua Li, Elizabeth J. Dawe, and Donal S. O'Leary Muscle Metaboreflex-Induced Coronary Vasoconstriction Limits Ventricular Contractility During Dynamic Exercise in Heart Failure Am J Physiol Heart Circ Physiol, published online January 25, 2013, doi: 10.1152/ajpheart.00879.2012.
March 26, 2013
How is Ca2+ cycling in the heart altered in cardiomyopathy in Duchenne muscular dystrophy? Does a lack of the cytoskeletal protein dystrophin cause a perturbation in communication between L-type calcium channels and mitochondria? In our latest podcast on the work by Viola et al., Associate Editor Meredith Bond hosts a discussion with lead author Livia Hool (The University of Western Australia) and expert Angela Dulhunty (Australian National University). We examine the effect of disruption of the myocyte cytoskeleton in the mdx mouse model. We address the role of the myocyte cytoskeleton in regulating communication between plasma membrane and mitochondria, and we tackle potential clinical applications for muscular dystrophy patients. Listen now.
Helena M. Viola, Stefan M. K. Davies, Aleksandra Filipovska, and Livia C. Hool L-type Ca2+ channel contributes to alterations in mitochondrial calcium handling in the mdx ventricular myocyte Am J Physiol Heart Circ Physiol, published online January 18, 2013, doi: 10.1152/ajpheart.00700.2012.
March 8, 2013
Our latest podcast explores the newly published article by Kim et al. In this work, lead author Guy Salama (University of Pittsburgh) and colleagues found that by prolonging action-potential duration, bradycardia may destabilize calcium and cause arrhythmia. Associate Editor Igor Efimov leads an engaging discussion with Salama and expert Steven Poelzing (Virginia Tech) about how intracellular calcium can affect cardiac electrophysiology, and through calcium-voltage coupling, can become the original source of arrhythmia. We also take a look at gender differences in remodeling and arrhythmogenesis, and the possible role estrogen may play in the susceptibility of the female heart to bradycardia-mediated arrhythmias.
Jong J. Kim, Jan Nemec, Rita Papp, Robert Strongin, Jonathan J Abramson, and Guy Salama Bradycardia alters Ca2+ dynamics which enhances dispersion of repolarization and arrhythmia risk Am J Physiol Heart Circ Physiol, published online January 11, 2013, doi: 10.1152/ajpheart.00787.2012.
March 6, 2013
What can we learn from the most common enzyme deficiency in the world? Quite a lot, actually. G6PD deficiency has cascading effects on NADPH, reactive oxygen species production, and anti-oxidant reserves, all outlined in a comprehensive new Review article by Hecker et al. Associate Editor Ajay Shah interviews first author Peter Hecker (Washington University in St. Louis) as well as leading expert, and Associate Editor, Ronglih Liao (Brigham and Women's Hospital and Harvard Medical School) about compartmentalization, potential drug therapies, and where the study of G6PD deficiency will lead to next.
Peter A. Hecker, Jane A. Leopold, Sachin A. Gupte, Fabio A. Recchia, and William C. Stanley Impact of glucose-6-phosphate dehydrogenase deficiency on the pathophysiology of cardiovascular disease Am J Physiol Heart Circ Physiol, published online December 15, 2012, doi: 10.1152/ajpheart.00721.2012.