The force exerted by the angioplasty balloon mainly enhances the lumen by fracturing the plaque and changing its shape and the shape of the vessel. Very little lumen gain comes from plaque compression. The radial force of the angioplasty balloon causes plaque fracture and dissection where the heterogeneous plaque forms a circumferential ring or at locations in the plaque where there is a junction between softer plaque and harder plaque ( Figure 17.1 ). The pressure within the balloon is increased until it overwhelms the tolerance of the plaque that is being treated. This tolerance depends on the amount of calcium. When the plaque gives way to overwhelming pressure, the energy is propagated along the plaque and tends to create dissections. There is usually evidence of dissection on completion images immediately following the angioplasty, and the more thorough the investigation, the more dissections that can be found. Contrast fills cracks in the plaque, most of which are longitudinal. Oblique angiographic views or cross-sectional imaging with IVUS or optical coherence tomography (OCT) generally show significant disruption of the surface. Experience with balloon angioplasty before the development of stents indicates that some of these dissections heal without treatment. However, they do represent tissue hanging into the flow lumen and may lead to acute occlusion or serve as a nidus for restenosis. The availability of stents has made it possible to treat most dissections safely and quickly but has prompted a dilemma. How aggressively should mild-to-moderate postangioplasty dissections be stented? This will gradually be solved in each vascular bed. However, there are downsides to stent placement since they are permanent implants and have continuous interaction with the vessel wall.