Geometric remodeling in atherosclerosis and restenosis comprises a change of the total arterial circumference that, together with plaque growth or neointima formation, determine the lumen of the artery. The change in total arterial circumference relative to a reference cross section ranges from excessive enlargement with an actual increase in lumen to a shrinkage contributing to lumen narrowing. The forces that determine whether an artery shrinks or is able to enlarge as a consequence of atherosclerotic lesions or of post-interventional intimal hyperplasia are unknown but are likely to affect matrix and specifically collagen redistribution. Identifying these forces is of importance because they might be used to promote favorable remodeling. The cellular and humoral triggers of collagen degradation and synthesis, as well as conformation changes of collagen matrices after their deposition, need to be investigated. As with injury-induced intimal hyperplasia and plaque growth in de novo atherosclerosis, injury models may serve as a paradigm for geometric remodeling in atherosclerosis.