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Coagulative necrosis is a type of accidental cell death typically caused by ischemia or infarction. In coagulative necrosis, the architectures of dead tissue are preserved for at least a couple of days. [1] It is believed that the injury denatures structural proteins as well as lysosomal enzymes, thus blocking the proteolysis of the damaged cells.
Myocardial infarction complications may occur immediately following a myocardial infarction (heart attack) (in the acute phase), or may need time to develop (a chronic problem). After an infarction, an obvious complication is a second infarction, which may occur in the domain of another atherosclerotic coronary artery, or in the same zone if ...
In particular, acute myocardial infarction in the distribution of the circumflex artery is likely to produce a nondiagnostic ECG. [10] The use of additional ECG leads like right-sided leads V3R and V4R and posterior leads V7, V8, and V9 may improve sensitivity for right ventricular and posterior myocardial infarction. [citation needed]
Contraction band necrosis is a type of uncontrolled cell death unique to cardiac myocytes and thought to arise in reperfusion from hypercontraction, which results in sarcolemmal rupture. [ 1 ] It is a characteristic histologic finding of a recent myocardial infarction (heart attack) that was partially reperfused.
It was first described in medical literature by Schlesinger and Reiner in 1955. [1] It is considered a type of cellular necrosis. [1] Two types of myocytolysis have been defined: coagulative and colliquative. [1] [2] [3] Coagulative myocytolysis appears in the myocardium near areas of coagulative necrosis or areas affected by myocardial ...
The only possible sign the first 4 hours is waviness of fibres at border. Later, however, a coagulation necrosis is initiated, with edema and hemorrhage. After 12 hours, there can be seen karyopyknosis and hypereosinophilia of myocytes with contraction band necrosis in margins, as well as beginning of neutrophil infiltration. At 1 – 3 days ...
[1] The condition can be caused by full-thickness necrosis (death) of the myocardium (heart muscle) after myocardial infarction, chest trauma, [2] and by over-prescription of anticoagulants. [3] [4] Other causes include ruptured aneurysm of sinus of Valsalva and other aneurysms of the aortic arch. [5]
Fibrinoid necrosis is a pathological lesion that affects blood vessels, and is characterized by the occurrence of endothelial damage, followed by leakage of plasma proteins, including fibrinogen, from the vessel lumen; these proteins infiltrate and deposit within the vessel walls, where fibrin polymerization subsequently ensues. [1] [2] [3] [4]