ABSTRACT
Physicians now take for granted the concept that infarction is due to lack of blood supply and nutrition caused by obstruction of arteries that supply regions of ischemia. Early observers referred to focal necrotic regions using nonspecific descriptive terms such as softenings, ramollissements, and encephalomalacia. These softenings were not clearly attributed to ischemia until the middle of the 19th century.1
Physicians had known for centuries that coagulation occurred within the vascular system. Vesalius, in the middle of the 16th century, described ‘unnatural deposits’ within the left atrium in patients with gangrene of the extremities.2 Diseased vessels were also well described. Thomas Willis, writing in the middle years of the 17th century, noted instances in which ‘both carotid arteries were choked up so that not the least drop of blood could pass through either of them’.3 Others also found thrombi and coagula in the vascular system at necropsy, but debated whether or not these formed postmortem or during life. During the late 18th and early 19th centuries, two major figures, John Hunter in England and Cruveilhier in France, thought that coagula were caused by inflammation in the veins.1 Hunter, writing at the end of the 18th century, noted the frequency of vein inflammation after surgery and after phlebotomies and postulated that venous thrombi formed as exudates from the walls of blood vessels.4 Cruveilhier, in 1829, wrote that coagulation in veins was the earliest sign of phlebitis.1 Thrombi within arteries and the heart were attributed at that time to similar inflammatory conditions.
