The Steven M. Gootter Foundation has supported a study at the Stanford Cardiovascular Institute to engineer human heart cells from human pluripotent stem cells and determine how and why arrhythmias occur.  A common case of arrhythmia is ventricular fibrillation, or irregular heartbeats in the ventricles of the heart. One known trigger is fibrosis, or scar tissue.  Dr. Oscar Abilez and his team are generating the tissue in his lab and stimulating various patterns of fibrosis to see how the distribution of fibrosis may affect heart rhythms. One of the main goals of this research is to identify the parameters of fibrosis in the dish that make it more or less likely to cause an arrhythmia.  With this new information in hand, they will then examine existing patterns of fibrosis from magnetic resonance imaging (MRI) of the hearts in patients that have had known arrhythmias.

Their goal is to uncover the patterns of fibrosis that correlate with the onset and severity of the patients’ known arrhythmic events.  When that is accomplished, their hope is that a clinician will be able to prospectively look at a patient’s MRI and say with confidence that the pattern or size of fibrosis would suggest that the patient is at a higher risk of developing a fatal arrhythmia.  They can then assess appropriate treatment options that are more precise, and perhaps even preventive.

The Foundation has granted an Investigator Award to Jared Churko, University of Arizona Assistant Professor of Cellular and Molecular Medicine, Genetics-GIDP, Physiological Sciences GIDP, and is the Director, iPS Cell Core.  Arrhythmogenic cardiomyopathy (ACM) is a heart disease involving arrhythmias and higher rates of sudden cardiac death. ACM mice models support the role that exercise exacerbates ACM pathology. However, a human model is required to determine if exercise is pathological to ACM patients. With funding support from the Steven M. Gootter Foundation, the Churko lab is generating stems cells from ACM patients and studying how human ACM cells lead to pathophysiology and sudden cardiac death. Specifically, his lab is converting ACM stem cells into cardiomyocytes (the contractile beating heart cells) and studying how the patient’s own heart cells respond to stress and exercise conditions. Furthermore, the Churko lab is developing molecular tools to identify undiagnosed patients and developing therapies to mitigate ACM pathology.