NORA ECCLES HARRISON
CARDIOVASCULAR RESEARCH &
TRAINING INSTITUTE

ADVANCING CARDIOVASCULAR RESEARCH SINCE 1969

CUTTING EDGE CARDIOVASCULAR RESEARCH

Nora Eccles Harrison Cardiovascular Research and Training Institute (CVRTI) delivers cutting-edge cell-to-bedside research and education of cardiovascular disease, which is one of the leading causes of death worldwide. At the CVRTI, we are both developing new insights into the biology of heart muscle cells, and developing novel therapeutics for patients with heart failure and cardiac arrhythmias such as sudden cardiac death.

Located at the University of Utah, the CVRTI nucleates a campus wide, multidisciplinary team of fourteen individual investigator laboratories who are both scientists and physician scientists. The research of the laboratories spans from basic muscle biology and channel electrophysiology to metabolism and genetics. Founded in 1969, the CVRTI is one of the oldest cardiovascular institutes in the country, and its research has already impacted clinical care from development of the first artificial heart, to the genetic basis of long QT arrhythmias, to using electricity to map heart dimensions for arrhythmia ablation, to myocardial recovery.

Nora Eccles Harrison Cardiovascular Research & Training Institute building

CVRTI Seminar Series -RIPS

Thursday, July 23, 2025
12:00 PM – 1:00 PM MT

Yoram Rudy headshot

Principles of Action Potential Conduction in Cardiac Tissue

Yoram Rudy, PhD


Distinguished Professor Emeritus
Washington University in Saint Louis
Member, US National Academy of Engineering
Fellow, US National Academy of Inventors


Join us in person only at
Eccles Health Sciences Education Building, EHSEB, Bldg. 575, Room 2600, 25 S. 2000 E. (Lunch Provided)

Heart failure is a complex condition that affects millions worldwide. While it may sound like the heart has stopped working entirely, it really means that the heart can’t pump blood as effectively as it should. There are several types of heart failure, each with unique causes, symptoms, and treatment strategies. Two of the most discussed types are heart failure with reduced ejection fraction (HFrEF) and heart failure with preserved ejection fraction (HFpEF).

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Latest Publications

<h3>Enhancing mitochondrial pyruvate metabolism ameliorates ischemic reperfusion injury in the heart</h3>

Enhancing mitochondrial pyruvate metabolism ameliorates ischemic reperfusion injury in the heart

In this publication, we explored boosting mitochondrial metabolism to reduce heart damage after blood flow was restored following a heart attack, to prevent ischemic-reperfusion injury. We found that inhibiting the lactate exporter in heart cells, using both cell and animal approaches, that we could decrease the harmful effects to the heart during re-oxygenation. Our results suggest that this approach may help prevent further injury to the heart during a myocardial infarction. In summary, normalizing pyruvate and lactate metabolism by using MCT4 inhibition represents a promising pharmacological strategy to mitigate cardiovascular injury.
Drakos Labs, JCI-Insig, 2024
<h3>Familial Associations of Prevalence and Cause-Specific Mortality for Thoracic Aortic Disease and Bicuspid Aortic Valve in a Large-Population Database</h3>

Familial Associations of Prevalence and Cause-Specific Mortality for Thoracic Aortic Disease and Bicuspid Aortic Valve in a Large-Population Database

Researchers at the University of Utah led by Dr. Jason Glotzbach, used the Utah Population Database to investigate the likelihood that family members of people with bicuspid aortic valve or thoracic aortic disease also have these conditions. Bicuspid aortic valve is the most common congenital cardiovascular abnormality, when the aortic valve has two leaflets rather than the usual three. This can cause a heart murmur and can lead to valve dysfunction, which may require valve replacement. In addition, people with a bicuspid aortic valve have an increased risk of developing dilation of the aortic wall, called an aortic aneurysm, and aortic dissection, which is a life-threatening emergency caused when blood flow creates a tear in the lining of the aortic wall and splits the layers of the aorta.
Selzman Lab, Circulation, 2023
<h3>Cardiac Gene Therapy Treats Diabetic Cardiomyopathy and Lowers  Blood Glucose</h3>

Cardiac Gene Therapy Treats Diabetic Cardiomyopathy and Lowers  Blood Glucose

In this publication (JCI Insight, 2023, PMID: 37639557), our team reported that a cardiac gene therapy can rescue not only the heart function but also systemic glucose control and insulin sensitivity in a mouse model of obesity and type 2 diabetes. We previously found that a heart muscle cell membrane protein, known as cardiac bridging integrator 1 (cBIN1), is critical to normal heart contraction and relaxation, and that cBIN1 expression is decreased in failing hearts from animals and humans with acquired heart failure. Importantly, our prior research also identified that cBIN1 gene therapy mediated by an adeno-associated virus (AAV)-based approach can rescue heart failure in rodents. In this study, we revealed a novel function of the cBIN1-organized structure in heart muscle cells: mobilization of the cellular machinery required for insulin-stimulated glucose utilization (see below for the Graphic Abstract, JCI Insight, 2023).
Hong Lab, JCI Insight, 2023

CAREERS AT CVRTI

We’re Hiring!
Openings for graduate students, postdoctoral fellows, and laboratory staff at the CVRTI.

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