As in the short story “The Strange Case of Dr. Jekyll and Mr. Hyde ”, inflammation has a good side, which is the protection against pathogens, and helps in the process of cellular and tissue repair after an injury; on the other hand, it may also perpetuate and worsen the injury and, in the case of acute myocardial infarction (AMI), it may be the trigger of coronary occlusion. In the acute phase of AMI, the immune system is activated in the process of myocardial repair, in which the necrotic tissue is replaced by the scar tissue (fibrosis). From anatomopathological studies, we know that in the first hours after coronary occlusion, neutrophils are mainly recruited to the injury site. The local neutrophil population peaks around the third day, then a progressive decline is observed. From the fifth day, they are replaced by macrophages and both are responsible for clearing non-viable myocytes. In addition to this role, together with smooth muscle cells macrophages are responsible for angiogenesis and collagen production. The scarring process begins at the periphery of the infarcted area and extends to the nucleus, and this repair mechanism is completed in about 4–8 weeks, depending on the infarction size.
展开▼
