13.1 POJA-L4548+4549+4550
Title: Acute myocardial infarction (human)
Description:
(A, B): Heart, different areas of margin of acute myocardial infarction (about 2-3 days old), Haematoxylin-eosin and (C) Kluver-Barrera stained.
(A, B): (1) Normal stained myocardium fibres, at (2) increased eosinophilia due to coagulative necrosis (ischaemic necrosis). Note wavy pattern of narrowed myocardium fibres and there are almost no central nuclei. The interstitial spaces are dilated due to oedema fluid. There is moderate to heavy infiltration by neutrophils (= neutrophilic granulocytes or PMN), some show signs of karyorrhexis.
(C): Stained with Kluver-Barrera (C) demonstrates clearly the coagulative necrosis of wavy fibres and the dense PMN infiltrate (*). Note dense-stained contraction bands (arrows) i.e. transverse bands composed of closely packed hypercontracted sarcomeres. Exposure to high concentration of calcium ions from the plasma is the causative factor because the sarcolemmae of the myocardium cells are damaged by ischaemia.
Background: Summary of sequelae during infarction. Myocardial infarctions show ischaemic coagulation necrosis due to lack of oxygen i.e. obstruction of the coronary arteries (e.g. arteriosclerosis, thrombosis). Within 4-12 hours there is occurrence of oedema, haemorrhage and beginning coagulation necrosis. At the periphery of the infarction wavy fibres are located close to contractile vital cells. As a result of systolic forces on the viable fibres the non-contractile dead cells deform and become wavy. In the margins of infarctions myocytolysis (so-called vacuolar degeneration) comprising large vacuolar spaces with water in the cells. Followed by progressive coagulation necrosis, nuclear pyknosis and cardiomyocyte hypereosinophilia. Coincident marginal contraction band necrosis and begin of infiltration of neutrophils (12-24 hours) start . After 1-3 days coagulation necrosis with loss of nuclei including striations and interstitial infiltrate of neutrophils are present. Prominent at 2-3 days necrotic muscle cells with acute inflammation followed and eventually in 3- 7 days beginning disintegration of necrotic myofibres, dying neutrophils and early phagocytosis of dead cells by macrophages at the infarct border.
Keywords/Mesh: cardiovascular system, heart, ventricle, infarction, myocardial infarction, coagulative necrosis, contraction band, pyknosis, myocytolysis, hypereosinophilia, karyorrhexis, histology, POJA collection
Title: Acute myocardial infarction (human)
Description:
(A, B): Heart, different areas of margin of acute myocardial infarction (about 2-3 days old), Haematoxylin-eosin and (C) Kluver-Barrera stained.
(A, B): (1) Normal stained myocardium fibres, at (2) increased eosinophilia due to coagulative necrosis (ischaemic necrosis). Note wavy pattern of narrowed myocardium fibres and there are almost no central nuclei. The interstitial spaces are dilated due to oedema fluid. There is moderate to heavy infiltration by neutrophils (= neutrophilic granulocytes or PMN), some show signs of karyorrhexis.
(C): Stained with Kluver-Barrera (C) demonstrates clearly the coagulative necrosis of wavy fibres and the dense PMN infiltrate (*). Note dense-stained contraction bands (arrows) i.e. transverse bands composed of closely packed hypercontracted sarcomeres. Exposure to high concentration of calcium ions from the plasma is the causative factor because the sarcolemmae of the myocardium cells are damaged by ischaemia.
Background: Summary of sequelae during infarction. Myocardial infarctions show ischaemic coagulation necrosis due to lack of oxygen i.e. obstruction of the coronary arteries (e.g. arteriosclerosis, thrombosis). Within 4-12 hours there is occurrence of oedema, haemorrhage and beginning coagulation necrosis. At the periphery of the infarction wavy fibres are located close to contractile vital cells. As a result of systolic forces on the viable fibres the non-contractile dead cells deform and become wavy. In the margins of infarctions myocytolysis (so-called vacuolar degeneration) comprising large vacuolar spaces with water in the cells. Followed by progressive coagulation necrosis, nuclear pyknosis and cardiomyocyte hypereosinophilia. Coincident marginal contraction band necrosis and begin of infiltration of neutrophils (12-24 hours) start . After 1-3 days coagulation necrosis with loss of nuclei including striations and interstitial infiltrate of neutrophils are present. Prominent at 2-3 days necrotic muscle cells with acute inflammation followed and eventually in 3- 7 days beginning disintegration of necrotic myofibres, dying neutrophils and early phagocytosis of dead cells by macrophages at the infarct border.
Keywords/Mesh: cardiovascular system, heart, ventricle, infarction, myocardial infarction, coagulative necrosis, contraction band, pyknosis, myocytolysis, hypereosinophilia, karyorrhexis, histology, POJA collection