Vascular remodeling represents a spectrum of structural changes whereby the
vascular wall responds to changes in its hemodynamic environment. Such cha
nges may be classified as vessel enlargement (outward remodeling), diminuti
on (inward remodeling), alternatively as adaptive (compensatory, appropriat
e to the hemodynamic stimulus), or maladaptive (dysfunctional, inappropriat
e). The direction and scale of remodeling are coordinated by endothelial pr
oduction of growth factors, proteases, and cellular adhesion molecules in r
esponse to sensed changes in blood how. In early atherosclerosis, outward r
emodeling preserves lumen size. Although protective in the long-term, the m
atrix degradation involved in this process may predispose atherosclerotic p
laques to rupture, hence increasing the risks of acute coronary syndromes.
Inward remodeling also occurs in advanced atherosclerotic lesions, whereby
the vessel shrinks rather than enlarging, exacerbating rather than ameliora
ting stenosis. In transplant coronary artery disease, early inward remodeli
ng may be a more important component of vessel stenosis than intimal thicke
ning, while inappropriate inward remodeling appears to be as' least as impo
rtant as excessive intimal growth in the development of restenosis after an
gioplasty. Increased awareness of vascular remodeling, and in particular it
s malaptive forms, may provide new therapeutic insights for the future.