(RxWiki News) Many of the pacemakers implanted in the last decade help heart failure patients by prompting both sides of the heart to beat simultaneously, making it more efficient. Now doctors know why, and it could lead to a "pacemaker in a bottle."
Figuring out how that pacemaker works at a biological level could help scientists develop drugs or therapies that work in a fashion similar to a pacemaker.
"Ask your doctor if a CRT pacemaker would be appropriate for you."
Dr. David Kass, study leader, a professor of medicine and biomedical engineering at the Johns Hopkins University School of Medicine and a cardiologist at the Johns Hopkins Heart and Vascular Institute, said heart specialists were able to reveal an important underlying biological mechanism that sheds light on understanding cardiac resynchronization therapy (CRT).
CRT treatment was approved by the U.S. Food and Drug Administration in 2001 to synchronize the heartbeats in both the right and left ventricle and to restore normal heart contractions. Unlike other pacemakers with one wire that to the heart, CRT pacemakers have two wires -- one that goes to each side of the heart, allowing for equal stimulation.
In patients with heart failure, the ventricles are often out of sync with one side contracting but the other remaining relaxed. The reason the CRT pacemaker worked was uncertain.
Dr. Kass said said the recent discovery of why it works could prompt the creation of a "pacemaker in a bottle" that could aid a wide variety of heart failure patients.
Researchers examined the changes that occurred with CRT at a basic level, discovering that when the heart is resynchronized, it makes the heart muscle more responsive to adrenaline, which stimulates its pumping ability.
They found that the modified pacemaker used in CRT increases RGS proteins in the heart. These proteins direct the activity of G proteins, which provide direction to the heart and other organs about what to do by stimulating the heart muscle.
Levels of a particular G protein (a protein that acts as a chemical transmitter inside a cell), called Gi, rise in heart failure patients. This inhibits the heart muscle pumping and prevents G proteins from doing their job. CRT is able to restore the normal balance of the two proteins by inhibiting Gi proteins and helping the heart respond to adrenaline like a healthy heart would.
Most with heart failure do not receive the CRT pacemaker because both sides of their heart are able to beat in sync. Of an estimated six million heart failure patients in the United States, the pacemaker would be appropriate for about one million.
Dr. Kass said that by temporarily forcing a heart out of sync, then letting it return, doctors may be able to trigger the type of biological effect produced by CRT. Such a treatment may be available before development of a drug or gene therapy.
The study was published in the September 14 issue of Science Translational Medicine.