The Gene Therapy Lab

Discovering novel treatments for an old arrhythmia…

Rishi Arora, MD, Director of Experimental Electrophysiology, Northwestern University Feinberg School of Medicine


The Gene Therapy Lab

Northwestern University Feinberg School of Medicine is playing a leadership role in the field of heart medicine by offering hope to today’s patients with AF as well as those diagnosed in the future. 

Gene Therapy Research, conducted in the laboratory of Dr. Rishi Arora, is discovering new ways to treat an old arrhythmia and identifying novel treatments for AF. Current treatments for AF, such as medications, ablations, and surgical procedures like the MAZE, are being proven effective, but there are still limitations with these methods. To further improve upon current treatment options for AF, Dr. Arora’s lab is working to develop new, gene-based approaches to treat AF. Gene therapy has been used to treat other diseases, including coronary artery disease and congestive heart failure. Dr. Arora and his collaborators hope to do the same with AF.

What is Gene Therapy and how does it work?

All of the body’s functions are ultimately regulated by its genetic makeup, with each cell having its own genetic code. Most diseases are associated with a disordered functioning of one or more genes. Some of these gene disorders can be corrected by replacing the abnormal or “bad” gene with a more normal or “good” gene. This is Gene Therapy. Recent research suggests that the malfunction of certain types of genes can contribute to AF. For example, nerves within the autonomic nervous system that supply the heart muscle can become hyperactive in AF. This hyperactivity is controlled by certain types of genes. Hyperactivity of the autonomic nervous system may predispose a patient to AF. Dr. Arora and his team have recently attempted to “turn off” hyperactive nerves by injecting a special gene into the left atrium of the heart.

By placing electrodes on the heart, Dr. Arora and his team have been able to record electrical activity in the atrium model. Using sensitive recording equipment to acquire electrical signals from the heart, they interpret and examine those signals and pathways to discover the culprit genes that are contributing to AF. Dr. Arora and his team have also developed new catheters through which they can externally administer “good” genes into the heart to replace or overcome “bad” genes. In this way, the gene delivered to the heart prevents the patient from experiencing AF. While this is a significant discovery, there is much more research needed in the area of gene therapy for AF. For example, it is yet unknown the role that some genes may play in causing AF in certain types of patients compared to others. Many patients with high blood pressure may have a certain type of gene that causes AF, while patients with congestive heart failure may possess other genes responsible for AF. Ongoing work in Dr. Arora’s laboratory is focused on growing understanding of which genes are specifically responsible for AF in patients with congestive heart failure, how these genes can be delivered into the heart using a minimally invasive approach, and then controlled, or “turned on and off” at will.