29/09/2011

The World Heart Day is an opportunity to increase the awareness of the population and of the administrations, politicians, productive sector and social agents of the enormous medical and economical burden of heart diseases in our society and in the world. A single heart disease, coronary artery disease, is the leading cause of death in Europe and in the world, and is expected to remain so in 2025.Reducing the burden of heart diseases is a complex task that requires the coordinated execution of many actions involving many players, from sanitary education and promotion of healthy life stiles to innovation in diagnostic and therapeutic tools or care delivery systems. While the complexity of this task is as overwhelming as its importance, a point is very clear: heart units in large public, tertiary, university hospitals must play a leading role. This role is now jeopardized in many places by an adverse economical scenario that prompt the implementation of policies aimed to obtain the maximal immediate economical efficiency in university hospitals with a low priority for research and teaching.VHIR's Heart Area (Area del Cor) fights to minimize the impact of heart diseases based on equilibrated care, research and teaching. The research program involves different research areas that cover the most relevant heart diseases form a multidisciplinary approach, involving prevention, diagnosis, and treatment, with an emphasis in translation and innovation, and a with an unique premise: prosecution of excellence. During 2010, ACOR published 75 scientific articles in peer reviewed journals (more than an article per week), with a total impact factor of 419, including many basic, clinical and epidemiological papers in the very top scientific journals. In the fist nine months of 2011 we have surpassed those figures. This places ACOR in a leading position in our media, but is far from being enough. We need to increase the rate of generation of high value knowledge, and, even more urgently, to accelerate the translation of this knowledge to our patients and the society. This is an essential part of our mission, and our commitment with the public funds we are receiving, and we will make every effort to keep it.Dr. David García DoradoHead of VHIR's Heart AreaAt the same time of the World Heart Day, the Laboratory of Experimental Cardiology at VHIR has published on Basic Res Cardiol. the article 'The role of mitochondrial permeability transition in reperfusion-induced cardiomyocyte death depends on the duration of ischemia'.Mitochondrial permeability transition (MPT) is critical in cardiomyocyte death during reperfusion but it is not the only mechanism responsible for cell injury. The objectives of the study is to investigate the role of the duration of myocardial ischemia on mitochondrial integrity and cardiomyocyte death. Mitochondrial membrane potential (??m, JC-1) and MPT (calcein) were studied in cardiomyocytes from wild-type and cyclophilin D (CyD) KO mice refractory to MPT, submitted to simulated ischemia and 10 min reperfusion. Reperfusion after 15 min simulated ischemia induced a rapid recovery of ??m, extreme cell shortening (contracture) and mitochondrial calcein release, and CyD ablation did not affect these changes or cell death. However, when reperfusion was performed after 25 min simulated ischemia, CyD ablation improved ??m recovery and reduced calcein release and cell death (57.8 ± 4.9% vs. 77.3 ± 4.8%, P &lt, 0.01). In a Langendorff system, CyD ablation increased infarct size after 30 min of ischemia (61.3 ± 6.4% vs. 45.3 ± 4.0%, P = 0.02) but reduced it when ischemia was prolonged to 60 min (52.8 ± 8.1% vs. 87.6 ± 3.7%, P &lt, 0.01). NMR spectroscopy in rat hearts showed a rapid recovery of phosphocreatine after 30 min ischemia followed by a marked decay associated with contracture and LDH release, that were preventable with contractile blockade but not with cyclosporine A. In contrast, after 50 min ischemia, phosphocreatine recovery was impaired even with contractile blockade (65.2 ± 4% at 2 min), and cyclosporine A reduced contracture, LDH release and infarct size (52.1 ± 4.2% vs. 82.8 ± 3.6%, P &lt, 0.01). In conclusion, the duration of ischemia critically determines the importance of MPT on reperfusion injury. Mechanisms other than MPT may play an important role in cell death after less severe ischemia.Ruiz-Meana M, Inserte J, Fernandez-Sanz C, Hernando V, Miro-Casas E, Barba I, Garcia-Dorado D. "http://www.ncbi.nlm.nih.gov/pubmed/21959501" More information