NORA ECCLES HARRISON
CARDIOVASCULAR RESEARCH &
TRAINING INSTITUTE

ADVANCING CARDIOVASCULAR RESEARCH SINCE 1969

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.

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The heart’s primary function is to pump blood throughout the body. This is done by an electrical connection that originates from the sinoatrial node (SA node). The electrical impulse begins at the SA node travels throughout the heart. The electrical impulse travels along a pathway through the heart to create the heart’s movement.
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Latest Publications

<h3>eLife publication from the Shaw Lab</h3>

eLife publication from the Shaw Lab

After 30 years of worldwide research in ischemic-preconditioning, Shimura et al have identified the mediator molecule. Stress responsive GJA1-20k works with actin to cause a newly identified protective mitochondrial fission, providing a therapeutic option to protect organs against anticipated ischemia.
<h3>Nature Communications publication from the Drakos Lab</h3>

Nature Communications publication from the Drakos Lab

Our findings demonstrate that VDAC2 plays a crucial role in cardiac function by influencing cellular calcium signaling. Through this unique role in cellular calcium dynamics and excitation-contraction coupling VDAC2 emerges as a plausible therapeutic target for heart failure (HF)
<h3>JACC Clinical Electrophysiology publication from the Ranjan Lab</h3>

JACC Clinical Electrophysiology publication from the Ranjan Lab

This data provides mechanistic insights into atrial fibrillation (AF) recurrence, suggesting that post-ablation scar pattern dividing the atria into smaller regions is an important and better predictor than left atrium (LA) volume and total scar, with improved long-term outcomes in persistent AF.

CAREERS AT CVRTI

We’re Hiring!
Openings for graduate students, postdoctoral fellows, and grants/contracts officer at the CVRTI.

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