Treatment of inflammation in the heart
Researchers from the Washington University School of Medicine in St. Louis have found a factor that provokes inflammation in the heart after a myocardial infarction. These are immune cells that try to repair damage, but instead cause inflammation, which leads to even greater disorders. In addition, the researchers found that the drug Pirfenidone, already approved for the treatment of idiopathic pulmonary fibrosis, effectively suppresses such inflammation in mice, protecting the heart from progressive damage.
With a heart attack, blood stops flowing to the heart muscle, cells in this area die. If a person survives, his body tries to restore the myocardium, forming scar tissue, but it reduces the contractility of the heart. Another wave of damage can begin when immune cells try to repair cardiomyocytes, but instead increase inflammation. According to the researchers, finding ways to prevent inflammation in the infarction zone will help prevent the progression of heart failure.
Pirfenidone has demonstrated cardioprotective effects in a number of animal models of myocardial infarction. The authors suggested that the effect of pirfenidone on the heart will be similar to how it helps with lung fibrosis: it will slow down the formation of scar tissue.
Mice with a model of myocardial infarction lived longer if they received pirfenidone. But it did not reduce the percentage of scar tissue in the heart. To clarify the mechanisms of heart recovery, the researchers assessed the state of local immunity. The number of macrophages, T-lymphocytes, neutrophils and monocytes remained unchanged before and after treatment. A significant difference in the number of B-lymphocytes was found.
B is a lymphocyte (blue with a red rim) in the heart tissue.
As it turned out, B cells play an important role in inflammatory damage to the heart. In addition, scientists have discovered that there are a number of different B-lymphocytes in the heart that are closely related to each other. Pirfenidone modulates these cells and thereby has a protective effect on the heart muscle after a heart attack.
Complete removal of B-lymphocytes led to the disappearance of the positive effect of the drug.
It is possible that pirfenidone triggers other mechanisms of protection of the heart, both directly and indirectly – through immune cells. The authors continue to investigate these details. They also launched the process of developing a modified version of pirfenidone to treat the effects of myocardial infarction and prevent heart failure with fewer side effects.
Article by L. Adamo et al. Modulation of subsets of cardiac B lymphocytes improves cardiac function after acute injury is published in the journal JCI Insight.
Aminat Adzhieva, portal "Eternal Youth" http://vechnayamolodost.ru based on the materials of WUSTL: Scientists ID source of damaging inflammation after heart attack.