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HowToPreventHeartDisease.com |
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Is There A Way To Cut Sudden Heart Attack Deaths? Even if heart attack victims were saved, it is very likely that 1 in 7 of them would die abruptly within 3 years, mostly from arrhythmia. Arrhythmia is a condition in which the heart beats irregularly and in most cases overly rapid. In fact, this kind of sudden cardiac death happens to some 60,000 to 80,000 people every year in Germany. Is there a way to cut down the number of sudden cardiac death? This might be possible, provided if gene-altered cells could be grafted onto cardiac tissue damaged by a heart attack in a human. Researchers from University of Bonn have employed a new technique to virtually eliminate the additional risk of arrhythmia in mice that had experienced heart attacks as compared to those which had not. The technique involves implanting genetically-modified tissue directly into a damaged heart. The findings of their study appeared in the British journal Nature on December 5, 2007. Doctors usually implant pacemakers for patients who suffered heart attack. The function of the pacemaker is to deliver electrical impulse that can help restore normal rhythm if the heart begins to beat irregularly. However, there is no cellular basis for correcting the vulnerability to arrhythmia.
In the study, mouse embryo heart cells (known as cardiomyocytes) were transplanted into the hearts of the mice that had been induced to have cardiac failure. A catheter was then directly introduced into the heart of the mouse to see if arrhythmia could be provoked. The rate of irregular heart activity was found to be just over 30 percent, which was the same as with the healthy ones. On the other hand, almost 100 percent of a control group of mice which had heart attacks died when subjected to the same test.Taking heart cells from embryos was feasible in laboratory mice, but could this also work for humans with heart disease? In order to look for a substitute that might work in people, the researchers performed the same heart operation by grafting skeletal muscular cells taken from the leg of the same animal. The new cells not only fail to protect the heart but also made the arrhythmia worse. This is because heart muscle electrically couples (with the heart tissue) but the skeletal muscle does not. It is a protein called connexin 43 found only in heart cells that makes the electrical coupling happening. Based on the discovery, the researchers created a group of mice that over expressed connexin 43 in skeletal muscle. Then, they repeated the experiment. The results found was as well as with the embryo heart muscle. The researchers believed this could pave the way to laboratory production of muscle tissue containing connexin 43. Nevertheless, they also concerned that there were still too many key steps to be taken before such technique could be applied on humans. The very first step they need to do is to test the technique in large animals with hearts that were significantly different from those of mice.
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