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Basic Science Research
In laboratories throughout the NYU Langone Medical Center, basic science research is under way to better understand the pathogenesis of cardiovascular disease, to analyze how current treatments work, and to develop potential new therapies.
Investigators at the Cardiac Electrophysiology/Heart Rhythm Center conduct laboratory research to decipher the cellular mechanisms that initiate and sustain cardiac arrhythmias, especially atrial fibrillation. The scientists use a rabbit model of myocardial infarction to study the cellular changes induced by pressure overload atrial dilation.
Cardiac Catheterization Laboratory
Continued involvement in cutting edge cardiovascular research allows us to provide the most up to date treatment options for maximized beneficial outcomes in patients needing percutaneous coronary intervention.
Cardiac Rehabilitation Research
Basic scientific research is under way at the Cardiac Rehabilitation Center to study the process of disease and healing of the heart. Research is carried out in conjunction with other departments and divisions of the medical center.
NYU Cardiothoracic Surgeons focus their basic research on the molecular and cellular mechanisms of blood vessel formation (angiogenesis) and remodeling of injured vessels, the pathogenesis of aortic valve calcification adn the analysis of gene expression in mitral valve prolapse. By understanding these processes, the team aims to develop novel diagnostic, prognostic adn therapeutic tools to improve the treatment of patients with cardiovascular diseases.
Basic science research in pediatric cardiology takes place in the division's Molecular and Cellular Research Laboratories. The group's overall objective is to study the role of ion-translocating mechanisms in cardiac function, particularly as it relates to heart rhythm and development. The team utilizes state-of-the art multidisciplinary approaches that take advantage of several complementary methodologies.
The Division of Vascular Surgery founded the Vascular Surgery Basic Science Laboratory at New York University School of Medicine in 1999. Since its formation, the laboratory has been extremely successful in expanding the understanding of the mechanisms involved in vascular disease. Particular attention has focused on the role of matrix metalloproteinases during vascular remodeling following ischemic heart injury.
In addition to clinical trials, investigators at NYU's Heart Rhythm Center also conduct laboratory research to decipher the cellular mechanisms that initiate and sustain cardiac arrhythmias, especially atrial fibrillation (AF). Led by Dr. Douglas Holmes, the scientists use a rabbit model of myocardial infarction to study the cellular changes induced by pressure overload atrial dilation. They accomplish their work by scrutinizing myocytes with a new confocal microscope generously donated by Leon Charney.
The most common variety of atrial fibrillation develops in patients with abnormally large atrial dimensions associated with hypertensive, atherosclerotic, and valvular heart disease. These atria have electrophysiological changes that promote fibrillation, such as conduction velocity slowing and refractory period lengthening. While atria are hypokinetic after AF, it is not known to what extent these dilated cardiac structures are hypokinetic prior to AF. Histological evidence, however, does suggest dysfunction. The electrical changes could be the consequence of compensatory mechanisms in the face of atrial contractile failure. NYU investigators propose that atrial fibrillation is most closely related to atrial contractile failure, that this failure is slowly progressive until a threshold level is reached beyond which AF is inevitable, and that this contractile failure will be manifest both clinically and at the cellular level.
At the cellular level, the researchers are investigating the electrophysiologic alterations underlying abnormal automaticity and triggered activity. Failing cardiac tissues undergo remodeling of their ion handling proteins, characterized by up or down regulation of protein expression. In general, these changes tend to amplify subthreshold electrical events into triggered activity. While the mechanisms behind ventricular ectopy have become well characterized, those of the atrium are less well understood.
Among the differences between atrial and ventricular cells is the presence of IP3 receptors in atrial tissue. These calcium-releasing receptors are up-regulated in failing atrium, and may play a role in both triggered activity within the atrial free wall and abnormal automaticity from spontaneously firing cells within the pulmonary veins. Using confocal microscopy and patch clamp techniques, in a collaboration with the laboratory of Drs. William Coetzee and Michael Artman, the investigators simultaneously measure subcellular calcium transients and sarcolemmal membrane currents. Interactions between excitation-contraction mechanisms and IP3 calcium release could form the basis of new atrial specific therapeutic targeting.
Cardiac Electrophysiology/Heart Rhythm Center
403 East 34th Street, RIV-2nd Floor
New York, NY 10016
Larry A. Chinitz, M.D.
Director, The Heart Rhythm Center
Associate Professor of Medicine
Neil E. Bernstein, M.D.
Assistant Director, The Heart Rhythm Center
Assistant Professor of Medicine
Douglas S. Holmes, M.D.
Assistant Professor of Medicine
Anthony Aizer, M.D.
Instructor of Medicine