A new theory of the mechanism of percutaneous arterial angioplasty is advanced. For this study, abdominal aortas and coronary, renal, superior mesenteric, and iliac arteries were obtained from cadavers. In addition, the iliac arteries of dogs were dilated and studied. No evidence of significant compression or redistribution of plaques could be found, supporting the theory that atheromatous material is incompressible. Cracking of the intima and separation of it from the media were histologically demonstrated following angioplasty. It is proposed that the stretched media distends following dilatation, carrying with the intima and atheromatous material. Once the media is freed from the encasing effect of the intima, it adapts to the circulatory needs of the body. Beyond a certain point, the arterial widening becomes permanent, due to an overstretching of the muscle fibers, which is demonstrated by a corkscrew deformity of the muscle cell nuclei.