Infarct

Definition and Etiology

The term originates from the Latin infarcire, meaning "to stuff" or "to cram." Fundamentally, an infarct represents vascular (or circulatory) necrosis. This means that a tissue or part of an organ dies due to acute ischemia.

The main etiological factors causing this condition include:

• Thrombosis;
• Embolism;
• Prolonged arterial spasm.

Morphology and Shape of the Lesion

The gross appearance and shape of the necrotic zone directly depend on the angioarchitecture—the structural features of the vascular system in a specific organ—as well as the presence of anastomoses and collaterals.

1. Triangular (conical, wedge-shaped). Typical for organs with a trunk (master-branch) pattern of vascular branching.
2. Irregular shape. Found in organs with a dispersed or mixed pattern of vascular branching.

Based on the type of necrosis developing, infarcts are divided into coagulative (characteristic of most organs, particularly the kidneys) and colliquative / liquefactive (less common, typical for the brain).

Classification by Gross Appearance

Depending on the macroscopic picture, several types of infarct are distinguished:

• White (ischemic, avascular). Occurs when blood flow in the feeding artery or its branch ceases completely. Most frequently localized in the spleen, brain, and heart.
• Ischemic with a hemorrhagic rim. Typical localization is the myocardium and kidneys. This feature is due to the presence of numerous vascular collaterals and anastomoses. As a result, the demarcation zone occupies a significant area and acquires a prominent red-brown color.
• Red (hemorrhagic). Develops upon obstruction of arteries (less commonly veins) in the lungs, intestines, ovaries, and brain. Two conditions are necessary for its occurrence: a dual blood supply to the organ and the presence of venous congestion.
• Red (venous) splenic infarct. A rare variant (spleen typically develops a white infarct). Occurs due to thrombosis or obstruction of the splenic vein. The necrotic zone becomes engorged with blood, turns dark red or black, and the demarcation zone is poorly defined ("blurred").

Pathogenesis of Pulmonary Hemorrhagic Infarction

The mechanism of red infarction using pulmonary tissue as an example unfolds as follows:

1. Obstruction of a pulmonary artery branch occurs (by a thrombus or thromboembolus).
2. Blood pressure drops sharply within the obstructed vascular bed.
3. Blood rapidly rushes via anastomoses from the bronchial artery system (where high pressure is maintained) into the low-pressure zone.
4. Capillaries of the interalveolar septa rupture, and the tissue becomes hemorrhagic (soaked with blood).

Evolution and Outcomes

After 24 hours, the necrotic zone becomes clearly visible, acquiring a pale-yellowish or pale-brownish color. A demarcation zone forms between it and healthy tissue. Histologically, this zone consists of an inflammatory infiltrate (leukocytes and macrophages), hyperemic vessels, and areas of red blood cell diapedesis (including small hemorrhages).

Outcomes are divided into two groups:

1. Favorable:

• Organization (scarring). In the first days, segmented neutrophils and macrophages partially resorb the necrotic tissue. On days 7–10, granulation tissue begins to grow inward from the demarcation zone. Gradually, it replaces the necrotic zone, matures, and turns into a scar.
• Cyst formation. Formation of a cavity (sometimes fluid-filled) at the site of colliquative necrosis (frequently observed in the brain).
• Glial scar. Replacement of the defect with glial tissue. This outcome is characteristic of small ischemic brain infarctions.

2. Unfavorable:

• Suppuration. Purulent melting of the infarct zone occurs (septic disintegration).