13.1 POJA-L4552+4553.
Myocardial fibrosis (after infarction, human).
13.1 POJA-L4552+4553
Title: Myocardial fibrosis (after infarction, human)
Description:
(A, B): Hypertrophic heart, myocardial fibrosis, HE. After a myocardial infarction within 5-10 days macrophages remove necrotic cardiomyocytes and the damaged area is progressively replaced by the ingrowth of vascularized granulation tissue (2-4 weeks). The vital myocytes close to the infarction area show vacuolar dystrophy due to damage by hypoxia. Vacuolization of myocytes can result in myolysis and will be repaired by reactive connective tissue proliferation. The fibrosis process progresses and the myocytes are gradually replaced by hyalinized connective tissue (1). In most instances scarring is well advanced by the end of the 6th week. Within the scar small groups of dystrophic vacuolized myocardial cells (2) remain. Additional findings are the presence of accumulated adipocytes (so-called lipomatosis) (3) which can be detected in obese and in elderly people. Hypertrophic myocytes with conspicuous nuclei are also detectable (arrows).
Background: Summary of sequelae during infarction. Myocardial infarctions show ischemic coagulation necrosis due to lack of oxygen i.e. obstruction of the coronary arteries (e.g. arteriosclerosis, thrombosis). After 1-3 days coagulation necrosis with loss of nuclei including striations and interstitial infiltrate of neutrophils. Prominent at 2-3 days necrotic muscle cells with acute inflammation. In 3- 7 days beginning disintegration of necrotic myofibers, dying neutrophils and early phagocytosis of dead cells by macrophages at the infarct border. After 7- 10 days macrophages removed the necrotic myocytes and the damaged zone is progressively replaced by the ingrowth of fibrovascular granulation tissue at the margins of the infarction. In 10-14 days well-established granulation tissue with new blood vessels and collagen deposition. After 2-8 weeks increased collagen deposition with decreased vascularity and cellularity. At the end of the 6th week scarring is well advanced. After more than 2 months a dense collagenous scar. One a lesion is completely healed it is hardly possible to distinguish between an eight-week-old lesion and a ten-year-old lesion. (Partly adapted from ref. Robbins & Cotran Pathological Base of Disease, 8th ed. 2014, W.B. Saunders Company, ISBN 978-1-4160-3121-5). (http://www.us.elsevierhealth.com/robbins-pathology/robbins-cotran-pathologic-basis-of-disease-hardcover/9781416031215/
Keywords/Mesh: heart, ventricle, fibrosis, necrosis, lipomatosis, infarction, myocardial infarction, myolysis, histology, POJA collection
Title: Myocardial fibrosis (after infarction, human)
Description:
(A, B): Hypertrophic heart, myocardial fibrosis, HE. After a myocardial infarction within 5-10 days macrophages remove necrotic cardiomyocytes and the damaged area is progressively replaced by the ingrowth of vascularized granulation tissue (2-4 weeks). The vital myocytes close to the infarction area show vacuolar dystrophy due to damage by hypoxia. Vacuolization of myocytes can result in myolysis and will be repaired by reactive connective tissue proliferation. The fibrosis process progresses and the myocytes are gradually replaced by hyalinized connective tissue (1). In most instances scarring is well advanced by the end of the 6th week. Within the scar small groups of dystrophic vacuolized myocardial cells (2) remain. Additional findings are the presence of accumulated adipocytes (so-called lipomatosis) (3) which can be detected in obese and in elderly people. Hypertrophic myocytes with conspicuous nuclei are also detectable (arrows).
Background: Summary of sequelae during infarction. Myocardial infarctions show ischemic coagulation necrosis due to lack of oxygen i.e. obstruction of the coronary arteries (e.g. arteriosclerosis, thrombosis). After 1-3 days coagulation necrosis with loss of nuclei including striations and interstitial infiltrate of neutrophils. Prominent at 2-3 days necrotic muscle cells with acute inflammation. In 3- 7 days beginning disintegration of necrotic myofibers, dying neutrophils and early phagocytosis of dead cells by macrophages at the infarct border. After 7- 10 days macrophages removed the necrotic myocytes and the damaged zone is progressively replaced by the ingrowth of fibrovascular granulation tissue at the margins of the infarction. In 10-14 days well-established granulation tissue with new blood vessels and collagen deposition. After 2-8 weeks increased collagen deposition with decreased vascularity and cellularity. At the end of the 6th week scarring is well advanced. After more than 2 months a dense collagenous scar. One a lesion is completely healed it is hardly possible to distinguish between an eight-week-old lesion and a ten-year-old lesion. (Partly adapted from ref. Robbins & Cotran Pathological Base of Disease, 8th ed. 2014, W.B. Saunders Company, ISBN 978-1-4160-3121-5). (http://www.us.elsevierhealth.com/robbins-pathology/robbins-cotran-pathologic-basis-of-disease-hardcover/9781416031215/
Keywords/Mesh: heart, ventricle, fibrosis, necrosis, lipomatosis, infarction, myocardial infarction, myolysis, histology, POJA collection