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

 October Seminar Series


Eleni Tseliou profile

 University of Utah Speaker

Thursday, October 5, 2023

12:00pm – 1:00pm (MT)

 Sphingolipids in Heart Failure and Myocardial Recovery


Eleni Tseliou, MD, PhD
Assistant Professor of Medicine
The University of Utah

 University of Utah Speaker

Thursday, October 12, 2023

12:00pm – 1:00pm (MT)

 CTRP1 as A Novel Regulator of Renin-Angiotensin System


 Fei Wang, PhD
 Assistant Professor, Internal Medicine
The University of Utah

Fei wang profile
Bram and Jake profile

 RIPs (Research in Progress)  In-Person Only

Thursday, October 19, 2023

12:00pm – 1:00pm (MT)

Transfer Learning for Improved Classification of Drivers in Atrial Fibrillation
 Bram Hunt, Doctoral Student
 Department of Biomedical Engineering
 The Ranjan Lab, University of Utah


 Uncertainty Quantification in the Context of Ventricular Tachycardia Simulations

 Jake Bergquist, PhD, T32 Postdoctoral Fellow
 Department of Internal Medicine
The Ranjan Lab, University of Utah

Join us for a hybrid meeting via Zoom or at  Eccles Health Sciences Education Building, EHSEB, Bldg. 575, Room 1700, 25 S. 2000 E. (Lunch Provided)

 Email Diane Ragan, diane.ragan@utah.edu for Zoom Link



Cardiac ischemia, also known as myocardial ischemia, is a serious condition that often occurs with little to no warning. Some people don’t even experience symptoms, hence the reference to this being a “silent” threat.

3d illustration human body heart

Latest Publications

<h3>Distinct transcriptomic and proteomic profile specifies patients who have heart failure with potential of myocardial recovery on mechanical unloading and circulatory support</h3>

Distinct transcriptomic and proteomic profile specifies patients who have heart failure with potential of myocardial recovery on mechanical unloading and circulatory support

As a last resort for people with end-stage heart failure, doctors can implant a device called a left ventricular assist device (LVAD), a mechanical pump that takes the load off the heart muscle. While the device is intended to stay in the body permanently, doctors noticed that, in some patients, the assistance provided by the LVAD allowed the patient’s own heart to regain strength and function.
<h3>GJA1-20k rescues Cx43 localization and arrhythmias in arrhythmogenic cardiomyopathy</h3>

GJA1-20k rescues Cx43 localization and arrhythmias in arrhythmogenic cardiomyopathy

This report established a new paradigm for arrhythmia treatment: improving Connexin 43 trafficking with gene therapy in arrhythmogenic cardiomyopathy. Here Connexin43 (Cx43} hemichannels (green) exit the Golgi apparatus and utilize the cytoskeleton (yellow} to traffic to cardiac intercalated discs. In healthy hearts, GJA1-20k (red} organizes the cytoskeleton delivery highway for efficient Cx43 hemichannel trafficking and healthy cardiac rhythm. In mice and humans with Arrhythmogenic Cardiomyopathy, GJA1-20k is diminished, resulting in impaired trafficking highways, limited Cx43 localization to intercalated discs, and ventricular arrhythmia. In a mouse model of Arrhythmogenic Cardiomyopathy, gene therapy with transduction of exogenous GJA1-20k limits cardiac arrhythmia. (Created with Biorender.com}

CAREERS AT CVRTI

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

Learn More

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