2009 News

Cardiomyopathy, a weakening of the heart muscle often associated with inadequate heart pumping, affects tens of thousands of people in the United States. Researchers have discovered a new molecular pathway controlled by a master-switch protein in the heart muscles called myocardin that may be key to understanding some forms of heart disease. This pathway links heart muscle structure to heart-cell survival.

The discovery, published in the Proceedings of the National Academy of Sciences, provides new insights into the molecular program that controls how heart cells differentiate in a developing embryo and mature, and more importantly, identifies myocardin-activated genes as candidates that may underlie some forms of heart failure and cardiomyopathy.

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Neurofibromatosis type I (NF1), also known as von Recklinghausen disease, is one of the most common inherited genetic disorders in humans. Symptoms include curvature of the spine, skin spots, learning difficulties, epilepsy, as well as cardiovascular problems. Researchers led by Jonathan Epstein, MD, Chairman of Penn’s Department of Cell and Developmental Biology and Scientific Director of the Penn Cardiovascular Institute, developed a zebrafish model for NF1, which will advance the ability to perform high-throughput chemical screening for new compounds that may one day become treatments. They recently published their findings in the Proceedings of the National Academy of Sciences.

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Heart function significantly improved in children and young adults with single ventricle congenital heart disease who have had the Fontan operation following treatment with sildenafil, a drug used to treat erectile dysfunction and pulmonary hypertension, say researchers from The Children's Hospital of Philadelphia (CHOP). Single ventricle defects are a collection of cardiac malformations that impair the heart's ability to pump blood. Examples include: tricuspid atresia, pulmonary atresia/intact ventricular septum and hypoplastic left heart syndrome. The Fontan operation is a procedure that redirects systemic venous blood directly to the pulmonary arteries, bypassing the heart. It is the third surgery in a staged palliation for single ventricle heart defects. Researchers hypothesized that sildenafil may help cardiac performance by directly improving the squeeze of the heart muscle and by allowing for better filling of the heart.

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NEW YORK (Reuters Health) - Higher levels of testosterone in older women are related to insulin resistance, metabolic syndrome and heart disease, new research indicates. In younger women, high testosterone levels are associated with health risks, but their clinical relevance in postmenopausal women has not been well studied, the authors remark in an early release publication of the Journal of Clinical Endocrinology and Metabolism.

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Among eligible Medicare beneficiaries, increased use of carotid arterial stenting (CAS) procedures to treat carotid stenosis - the narrowing of the carotid artery – is associated with higher rates of mortality and adverse clinical outcomes, including heart attack and stroke, according to researchers from the University of Pennsylvania Perelman School of Medicine.

Published in the November 2009 issue of the Journal of Vascular Surgery, the study adds to a growing body of research about the effectiveness of stenting for preventing heart attack, stroke, and death. Findings lend further insight into factors influencing how medical technology performs when integrated as treatment among the general Medicare population as opposed to in a controlled clinical trial setting.

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While studying how the heart is formed, scientists at the University of Pennsylvania Perelman School of Medicine serendipitously found a novel cellular source of atrial fibrillation (AF), the most common type of abnormal heart beat. Researchers have identified a population of cells that are like skin pigment-producing cells (melanocytes) located in the atria of the heart and pulmonary veins of mice and humans, uncovering evidence in mice that the cells contribute to atrial fibrillation. The finding may lead to a more precise way to treat AF, with reduced side effects.

The Penn scientists describe an unusual cell type whose dysfunction can initiate atrial arrhythmia, at least in mice. These cells, referred to as cardiac melanocytes because they express the melanin synthetic enzyme dopachrome tautomerase (DCT), reside in regions associated with atrial arrhythmia (for instance, in the pulmonary veins and atria) and in culture, display action potentials resembling those of atrial myocytes. Further study, the scientists said, showed DCT-expressing cells in the mouse heart were distinct from both heart muscle cells and skin melanocytes, although they could conduct electrical currents that are important for coordinated contraction of the heart.

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Two Penn researchers, along with scientists from the Fred Hutchinson Cancer Research Center, have been awarded $8 million for collaborative stem cell research projects. Edward Morrisey, PhD, Scientific Director of the Institute for Regenerative Medicine at the University of Pennsylvania and Mortimer Poncz, MD, Professor of Pediatrics, Children’s Hospital of Philadelphia received the funding from the National Heart Lung Blood Institute (NHLBI) as part of a $170 million effort to create the NHLBI Progenitor Cell Biology Consortium, which will bring together researchers from the heart, lung, blood, and technology research fields.

Poncz and Fred Hutchinson Cancer Research Center, Seattle (Dr. Beverly Torok-Storb, Ph.D.) will study the specialization of blood-forming cell lines, develop molecular interventions that will drive the formation of blood cells toward desired lines, and establish new, functional platelets that potentially may be used for the targeted delivery of bioactive proteins.

Morrisey and Fred Hutchinson Cancer Research Center (Dr. Irwin Bernstein, M.D.) endeavor to determine how certain signaling pathways - ordered sequences of biochemical reactions inside cells - affect cardiac and blood-forming cell development and cardiac regeneration and repair. The team will also study whether these pathways may be harnessed for therapeutic applications.

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