infarct

An infarct is an area of tissue necrosis caused by ischemia from loss or severe reduction of blood supply. It typically results from arterial occlusion due to thrombus or embolus, but can also arise from sustained hypoperfusion or vessel compression. The extent of infarction depends on the tissue’s susceptibility to ischemia, the presence of collateral circulation, and the duration of reduced blood flow.

In solid organs, infarcts are often classified by color. Pale (anemic) infarcts occur in tissues with end-arterial blood supply, such as the heart, kidney, and spleen, where a sudden occlusion leads to a mostly avascular necrotic area. Red (hemorrhagic) infarcts occur in tissues with dual blood supply or a loose parenchyma, such as the lung, intestine, or brain, and may also follow reperfusion.

Common clinical examples include myocardial infarction, caused by coronary artery occlusion; cerebral infarction, or ischemic stroke, due to arterial blockage in the brain; and infarcts of the kidney, spleen, or intestine. Pulmonary infarction can occur after pulmonary embolism and is often hemorrhagic.

Pathologically, infarcts typically show tissue necrosis with loss of normal architecture. In most organs, the necrosis is coagulative and is followed by infiltration with inflammatory cells; in the brain, infarcts commonly evolve to liquefactive necrosis with cystic cavitation over time.

Diagnosis and management focus on identifying the site and cause of ischemia, using imaging and laboratory studies, and restoring perfusion when possible. Risk-factor modification and addressing the underlying source of occlusion are central to prevention.