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Localized death of tissue that is caused by obstructed inflow of arterial blood. Also known as infarction.



a focus of organ or tissue necrosis resulting from an interruption of the blood supply to the area. The direct causes of infarcts are thrombosis, embolism, or spasm of the arteries feeding this tissue. Hypoxia is a decisive factor in the development of the tissue changes associated with an infarct.

There are three types: white, or ischemic, infarct, which is a zone of necrosis lacking in blood; red, or hemorrhagic, infarct, in which the zone of necrosis is saturated with excessive blood; and ischemic infarct with a hemorrhagic zone. The first and third types of infarct are generally formed in the heart, kidneys, and spleen, and the second in the lungs and intestine. An infarct may be conical (kidney, lungs) or irregular (heart, brain) in shape. Its consistency varies with the nature of the necrosis, which may be dry (myocardial infarct) or moist (cerebral infarct).

Infarcts cause profound changes in the organs affected. The dead areas are resorbed or organized, resulting in the formation of a cyst (in the brain) or a scar (in the heart muscle), or they may suppurate and liquefy (septic infarct). The size, location, and properties of an infarct determine whether the affected organ becomes weakened or loses its functions.


References in periodicals archive ?
After an acute MI, infarcted myocardium can be better characterized by distinguishing between the microvascular obstruction zone, the infarction core necrosis, the peripheral infarction zone, and the ischemic zone with delineation of the myocyte area at risk.
improved angiogenesis with an increased number of new blood vessels in the infarcted tissue.
p-Coumaric acid attenuates apoptosis in isoproterenol induced myocardial infarcted rats by inhibiting oxidative stress.
The brain tissues of the sham group exhibited no positive expression of VEGF, while the expressions of VEGF protein and mRNA in the brain tissues of the model control group and the NBP treatment group reached their peaks 1 day after CIR, The expressions of VEGF protein and mRNA in the NBP treatment group were significantly greater than what occurred in the model control group (p < 0,05) (Table 2), The VEGF protein expressions at different time points were mainly concentrated around the infarcted lesions, while only a small amount of positive expressions were in the center of infarcted lesions, The expressions were mainly inside the neurons and glial cells, followed by the VEC (Figures 1 and 2),
Prince, "A biochemical, electrocardiographic, electrophoretic, histopathological and in vitro study on the protective effects of (-)epicatechin in isoproterenol-induced myocardial infarcted rats," European Journal of Pharmacology, vol.
The timing of implementation of anti-remodeling strategies is important, as the prevention of topographic LV alterations by early treatment appears more effective, as opposed to their reversal in established chronic heart failure; for example, higher efficacy was demonstrated after early (7 days), compared to delayed (2 months) alginate implantation in infarcted rat hearts [3].
The team showed that the creatine CEST method can map changes in creatine levels, and pinpoint infarcted areas in heart muscle tissue, just as MRS methods can.
The cardioprotective effects of a combination of quercetin and alpha-tocopherol on isoproterenol-induced myocardial infarcted rats.
The presence of depressive behavior in infarcted rats was associated with an increase of Bax and Bcl-2 expression, proteins used as an index of vulnerability for apoptosis within prefrontal cortex and hypothalamus compared to control animals [29].
Still further, Waters suggests that both cardiomegaly and HTN increase the risk for acute PMI since 42% of hearts weighing more than 500 gm, and >1/3 of hypertensive patients had an acutely infarcted papillary muscle.