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Heart specialists at Johns Hopkins University have figured out how to use a large pacemaker for heart failure, which makes both sides of the heartbeat together for effective pumping, functioning at the biological level. Their findings, published in the September 14 issue of Movement Medicine Science, may open the door to drugs or genetic therapies that mimic the effect of a pacemaker, and new ways to use a pacemaker for a wider range of patients with heart failure.
All sides of the left ventricle of the heart (main pumping chamber) need to win coordination with each other for the heart to effectively pump blood to the rest of the body. In many people suffering from heart failure, the right and left sides of the ventricle synchronized with contraction of one side while loosening the other.
Several years ago, Johns Hopkins helped researchers develop a pacemaker that synchronizes heartbeat adjustments and restores normal contractions. This treatment, called heart resynchronization therapy (CRT), was approved by the Food and Drug Administration in 2001 and is widely used today to improve symptoms and enable people to live longer. However, the reasons that have worked at the biological level are not yet known.
David Cass, Ph.D., is the professor of medicine and biomedical engineering at the Johns Hopkins University School of Medicine, who led the development of the CRT, a senior author of this new study. "We have revealed our main mechanism and basic biological mission that helps us understand how the CRT works." With this information, we can work on developing entirely new therapies, such as drugs or gene therapy, to be essentially a type of 'pacemaker in a bottle' to help a wide range Of patients with heart failure, "says Cass, who is also a cardiologist at the Johns Hopkins University Heart and Vascular Institute.
When investigating the changes that were occurring with CRT at the basic science level, Kass and his colleagues found that resynchronizing the heart makes the heart muscle more responsive to adrenaline, which stimulates the heart's ability to pump.
"What we learned," says Cass, "is that the CRT is used to adjust the levels of the regulator of G-protein signals (RGS) proteins in the heart.RGS proteins guide the activity of G proteins, which are messengers that tell the heart and other organs what Must be done.
In heart failure, certain protein levels G, known as GI, rise. The GI prevents myocardial infarction, getting in the way of another protein, GS - which stimulates myocardium, thus preventing GS from doing its job. CRT restores the natural balance of the Gaza Strip and the Gaza Strip.
Cass uses a car likeness to explain the process. GS proteins represent accelerator. Proteins represent Guy brakes. In heart failure, it's like driving with one foot on the gas, the other on the brake. CRT says that the foot takes off the brake, inhibiting the GI proteins so that the entire left ventricle is not confined in a coordinated manner, but the heart muscle now responds to hormones, such as adrenaline, more like a healthy heart.
While the typical pacemaker is only one wire that goes to the right side of the heart, the CRT transducer is transformed by Cass and his colleagues first helped develop two wires. The second lead goes to the surface of the left ventricle so that both sides of the heart are stimulated at the same time.
Typically, translational research begins on the lab bench, in molecular cellular or animal models, and then discoveries are tested in people. However, with CRT, first modified pacemakers were developed and offered to patients with acute heart failure. The most important results: help hearts become stronger and healthier. In published studies, most patients receiving CRT were less tired and short of breath, better survival long term.
"This was fantastic," notes Cass. "Since CRT has also made the heart do more work, we have never treated heart failure that has made the heart more work, while death rates are also decreasing." The next step for Kas and his colleagues was to go into the basic science lab in an attempt to understand why and how the CRT worked.
Do not offer the majority of people with CRT heart failure because the sides of their hearts are beating in sync. Of the six million patients with heart failure in the United States, estimated at 1 million, they have a type of disease that is designed to treat CRT. However, in another part of the study, researchers discovered in animal models that if the temporarily forced heartbeat the compatibility to beat the synchronized, then resynchronized, improved myocardium, the response was to have better adrenaline.
"This gives us yet to find another way to explore," says Cass. "By temporarily placing the heart synchronously and then allowing it to return, we may be able to trigger the type of biological effect that produces the CRT, which in theory can be applied to patients sooner than the drug or gene therapy." Cass and his colleagues are actively seeking either Gene therapy and rapid curriculum modification.
Source: Johns Hopkins University
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