News | Heart Failure | February 10, 2016

Study Details Molecular Mechanism That Regulates How the Heart Pumps Blood

Findings could lead to new heart failure drugs

new study, titin protein, blood pumping, heart failure

February 10, 2016 — In a finding that could lead to new drugs to treat heart failure, researchers have uncovered the molecular mechanism that regulates how the heart pumps blood.

The key molecular player in this mechanism is a giant protein called titin, according to a study led by senior author Pieter de Tombe, Ph.D., of Loyola University Chicago Stritch School of Medicine. The study was published Feb. 8, 2016, in Proceedings of the National Academy of Sciences.

De Tombe is interim vice dean for research and chair of the Department of Cell and Molecular Physiology at Loyola University Chicago Stritch School of Medicine.

A healthy heart regulates itself so that with each beat, it pumps out as much blood as it receives. When blood enters the heart, it stretches the wall of the pumping chamber, triggering muscle to contract and pump blood out. This regulatory-control mechanism is known as the Frank-Starling law, named after physiologists Otto Frank and Ernest Starling.

In heart failure patients, the Frank-Starling law breaks down. Heart muscle becomes too weak to pump out of the heart the same amount of blood that flows into the heart. To compensate, the heart enlarges, develops more muscle mass and beats faster. But eventually these compensatory measures fall short. The heart cannot pump enough blood to meet the body’s needs for blood and oxygen, leading to shortness of breath, fatigue, weakness, swelling in legs, fluid retention and other symptoms.

The study by de Tombe and colleagues found the titin protein is key to understanding the Frank-Starling mechanism and therefore how much blood the heart is able to pump out with each beat. Titin is an essential component of muscle. It’s the largest protein in the body, weighing about 15 times as much as an average protein. In the heart, it acts like a spring, affecting the heart’s ability to contract and relax. Normally when people age, the titin protein gets shorter. But in heart failure patients, the protein grows longer and becomes less effective.

“Our findings provide insights into the molecular basis of the Frank-Starling regulatory mechanism,” de Tombe said. “This will help clarify the field and could point the way to new medications to more effectively treat heart failure. We were able to eliminate a number of other competing theories, including some of our own.”

About 5.1 million people in the United States have heart failure, and heart failure is listed as a contributing cause in one out of nine deaths, according to the Centers for Disease Control and Prevention. About half of heart failure patients die within five years of diagnosis. Heart failure costs the nation about $32 billion each year, including healthcare costs and missed days of work.

The study is titled “Titin strain contributes to the Frank-Starling law of the heart by structural rearrangements of both thin-and thick-filament proteins.” It was funded in part by grants from the National Institutes of Health.

De Tombe’s co-authors are Younss Ait-Mou, Karen Hsu, Gerrie Farman and Mohit Kumar of Loyola University Chicago Stritch School of Medicine; Thomas Irving of the Illinois Institute of Technology; and Marion Greaser of the University of Wisconsin.

For more information: www.pnas.org

Related Content

Biotronik Studies Demonstrate Efficacy of Minimizing Metal Burden in SFA Therapy
News | Stents Bare Metal| September 22, 2017
Physicians demonstrated that reducing metal burden in superficial femoral artery (SFA) therapy could effectively reduce...
Edwards Inspiris Resilia Valve Receives FDA Approval
News | Heart Valve Technology| September 21, 2017
Edwards Lifesciences Corp. recently received U.S. Food and Drug Administration (FDA) approval for its Inspiris Resilia...
MyoKardia Presents Additional Positive Data From Phase 2 PIONEER-HCM Study at HFSA 2017
News | Heart Failure| September 21, 2017
MyoKardia Inc. announced that additional positive data from the first patient cohort of its Phase 2 PIONEER-HCM study...
DISRUPT BTK Study Shows Positive Results With Lithoplasty in Calcified Lesions Below the Knee
News | Peripheral Artery Disease (PAD)| September 20, 2017
Shockwave Medical reported positive results from the DISRUPT BTK Study, which were presented at the annual...
Heart Failure Market to Surpass $16 Billion by 2026
News | Heart Failure| September 19, 2017
The heart failure space across the seven key markets of the U.S., France, Germany, Italy, Spain, the U.K. and Japan is...
Corindus Announces First Patient Enrolled in PRECISION GRX Registry
News | Robotic Systems| September 18, 2017
September 18, 2017 — Corindus Vascular Robotics Inc.
Two-Year ILLUMENATE Trial Data Demonstrate Efficacy of Stellarex Drug-Coated Balloon
News | Drug-Eluting Balloons| September 18, 2017
Philips announced the two-year results from the ILLUMENATE European randomized clinical trial (EU RCT) demonstrating...
Sentinel Cerebral Protection System Significantly Reduces Stroke and Mortality in TAVR
News | Embolic Protection Devices| September 18, 2017
September 18, 2017 – Claret Medical announced publication of a new study in the...
Marijuana Associated With Three-Fold Risk of Death From Hypertension
News | Hypertension| September 14, 2017
Marijuana use is associated with a three-fold risk of death from hypertension, according to research published recently...
Peter Schneider, M.D. presents late breaking clinical trial results at VIVA 17 in Las Vegas. Panelists (l to r) Krishna Rocha-Singh, M.D., Sean Lyden, M.D., John Kaufman, M.D., Donna Buckley, M.D.

Peter Schneider, M.D. presents late breaking clinical trial results at VIVA 17 in Las Vegas. Panelists (l to r) Krishna Rocha-Singh, M.D., Sean Lyden, M.D., John Kaufman, M.D., Donna Buckley, M.D.

Feature | Cath Lab| September 14, 2017
September 14, 2017 — Here are quick summaries for all the key late-breaking vascular and endovascular clinical trials
Overlay Init