The mechanism of transluminal angioplasty

Normal coronary arteries in dogs, atherosclerotic human coronary arteries at autopsy, and rabbit iliac arteries with experimental atherosclerosis were subjected to angioplasty and studied histologically or by electron microscopy. The studies showed desquamation of endothelium, deposition of platelets in the area of angioplasty, and splitting of atheromatous plaques frequently down to the internal elastic membrane. Human coronary arteries studied at post-mortem after successful angioplasty also have demonstrated splitting of the atheromatous plaque at its weakest point. Compression of atheromatous material from the plaque has not been demonstrated experimentally. The mechanism of angioplasty is complex. As the angioplasty balloon expands, splitting of the atheromatous plaque occurs at its weakest, thinnest point. The media and adventitia of the artery are then stretched, producing an enlarged lumen and increased blood flow. Splitting of the atherosclerotic plaque explains the angiographic appearance frequently seen after angioplasty--a separate column of angiographic dye or a small radiolucent filling defect in the area of successful angioplasty.