infarcts

An infarct is an area of tissue that undergoes necrosis due to an abrupt loss of blood supply, typically from occlusion of an artery or venous drainage. Infarcts can occur in virtually any organ but are most commonly described in the heart, brain, kidneys, spleen, and lungs. They result from reduction or interruption of arterial inflow or venous outflow, leading to ischemia and cell death. The pattern of infarction depends on the tissue architecture and the availability of collateral circulation. In solid organs with a single end artery supply, infarcts are typically wedge-shaped and pale (white infarcts). In organs with a dual blood supply or venous occlusion, infarcts may be hemorrhagic (red infarcts). Cerebral infarcts often produce liquefactive necrosis due to the brain’s enzyme-rich environment.

Pathologically, most infarcts show coagulative necrosis with loss of nuclei and preservation of tissue architecture early on, followed by inflammation and eventual repair and scar formation. In the brain, necrosis progresses toward liquefaction and gliosis. Clinically, infarcts present according to the organ affected: myocardial infarction causes chest pain and biomarker elevation; cerebral infarction presents with focal neurological deficits; renal or splenic infarcts may be flank pain or abdominal signs. Diagnosis relies on imaging and clinical context.

Management aims to restore blood flow when possible, treat the underlying cause, and reduce recurrent risk through antithrombotic therapy, revascularization procedures, and cardiovascular risk management. Prognosis depends on infarct size, location, and the presence of collateral circulation or comorbid disease.