Congenital Heart Disease - Diagnosis, Treatment and Prevention
The Strategic Research Area is chaired by Jeff Feinstein, MD and David Rosenthal, MD.
| Al-Ahmad, Amin MD |
| Chang, Ching-Pin MD, PhD |
| Conrad, Carol K MD |
| Dubin, Anne MD |
| Feinstein, Jeff MD |
| Haddad, Francois MD |
| Mochly-Rosen, Daria PhD |
| Ramamoorthy, Chandra MBBS, FRCA |
| Riemer, R. Kirk PhD |
| Rosenthal, David MD |
| Roth, Stephen J. MD, MPH |
| Tsuda, Shoichi, MD |
| Taylor, Charles PhD |
| Van Hare, George MD |
| Wu, Joe MD, PhD |
| Wise, Paul H. MD, MPH |
With 2007 Institute seed funding, the Congenital Heart Disease group has begun a research study: Evaluation of Ischemia in Patients with Congenital Heart Disease: A Possible Mechanism for Cardiac Dysfunction. Dr. Rosenthal is the prinicpal investigator.
This work engages investigators from pediatric Cardiology, adult Cardiology, Radiology and from the programs of Molecular Imaging, and the adult Congenital Heart Disease program. It utilizes Stanford's strength in advanced imaging to answer questions about ischemia as a possible pathogenic mechanism of potential significance as a therapeutic target.
Ischemia has been recognized for many years as an important cause of cardiomyopathy in adult patients with heart failure due to systolic dysfunction. The diagnosis of ischemic cardiomyopathy can be made using multiple imaging techniques including stress echocardiograpy, SPECT imaging, and more recently, PET imaging. In particular, PET imaging offers the opportunity to measure in both qualitative and quantitative manners, regional myocardial blood flow, and the metabolic changes in glucose metabolism which indicate relative ischemia.
We believe the PET scans will demonstrate regions of inducible ischemia, which may be detectable using MRI imaging as well. If ischemia is implicated as a possible pathogenic mechanism in this disease, it would be of potential significance as a therapeutic target. At present, there are no therapies demonstrated to have efficacy in prevention of myocardial dysfunction in this disease.
Proposed follow-up would seek further to delineate the prevalence and cardiac distribution of ischemia, and to evaluate the role of ventricular morphology in predisposing to ischemic injury.
