A newly discovered heart-specific protein may help experts predict heart failure.
The condition, which occurs when the heart fails to pump a sufficient amount of blood and oxygen to other organs, affects roughly 5.7 million people in the United States. It is a serious disease that claims approximately 300,000 lives every year.
While there’s currently no cure for heart failure, researchers at Cedars-Sinai Heart Institute have discovered a protein that appears to shield the heart from arrhythmias (irregular electrical impulses that cause an abnormal heartbeat). Arrhythmias can lead to heart failure and sudden cardiac death.
The newly discovered heart protein, called BIN1, appears to sculpt small folds within pockets that are on heart muscle cells. These microfolds are critical in that they trap the chemicals that regulate heart rhythm. Decreased levels of BIN1 may actually predict heart rhythm disturbances.
“It turns out that these folds are protective,” said cardiologist Dr. Robin Shaw, an expert in heart failure and rhythm abnormalities at the Cedars-Sinai Heart Institute.
According to Shaw, we have three to four billion heart muscle cells that have to beat in synchrony to create an effective squeeze. When they don’t, dangerous arrhythmias like sudden cardiac death can occur. BIN1 seems to protect against the arrhythmias of sudden cardiac death, keeping the heart in rhythm.
“In most types of heart failure, this protein decreases about 50 percent,” said Shaw. “Our results suggest that one of the reasons that the heart can stop from an arrhythmia is not because of any real structural problem. It’s because the diseased hearts have less of the protein.”
From a diagnostic perspective, the protein could potentially be used as an indicator for heart failure, especially since it can be detected in the bloodstream. Shaw says that he and his team are looking at testing cardiac BIN1 in patient cohorts to identify whose hearts are at risk for failing.
So if BIN1 levels are down, is there any way to restore them? According to Shaw, gene therapy may be able to do this.
“But my personal opinion is that there are pathways that may turn this endogenous production of this protein back on,” he said. “The dream is, in heart failure patients, to restore this protein with drugs that can activate these pathways.”
By Marianne Hayes