Researchers have found that a protein produced by immune cells that cause holes in the heart cells after a heart attack, indicating that immune cells play a decisive role in sudden death and irregular heartbeat.
The study was conducted by researchers from the Harvard University Faculty of Medicine in the United States, and its results were published in the “Science” magazine on September 4, and the Yorik Alert website was written about.
Myocardial Infarction and sudden cardiac death are the most deadly complications of coronary artery.
A blockage of one of the arteries of the heart muscle infarction leads to a lack of supply of myocardial cells with oxygen, and this weakens its ability to maintain a fixed rhythm, and it may cause irregular heart rhythm (heart rhythm) and is called ventricular tachycardia and ventricular fibrilllation.
In wrestling ventricular heart, the heart beats very quickly, but with a coordinated rhythm, while in ventricular fibrillation, the rhythm is chaotic and unaccodeible.
Immune cell infiltration
Both wrestling ventricular heart and ventricular fibrillation are serious heart rhythm disorders that may lead to sudden heart attack and death within minutes.
Most arrhythmias occur within 48 hours after myocardial infarction, coinciding with thick infiltration of immune cells into heart tissue.
The researchers were interested in how to enhance these immune cells of the heart rhythm disorder, and they found in the laboratory mice that the neutrophils that come to the infarction area (the dead tissue area resulting from the interruption of oxygen supply) in large numbers organized the “Ritnlg” gene, encrypted by the gamma molecule protein. Pormy, which is part of the family of pore formation that defends the host against bacteria by hole its membranes.
When the researchers removed this protein from the neutral cells in mice, the burden of arrhythmias decreased 12 times after the heart muscle infarction.
The researchers found Jenna, which is “Retn”, in human heart tissue with myocardial infarction.