Clinical and radiographic examinations indicate preliminarily indicati
ons that transluminal angioplasty may be effective in overall manageme
nt of the patient with vasospasm. Many questions remain, including: Ho
w does it work?; Are the effects persistent!; Is the arterial wall inj
ured by the process? Recent studies in several patients who died after
angioplasty allow us to provide some answers. Undilated spastic arter
ies show proliferation of both cellular and connective tissue elements
. There is good evidence that myofibroblasts have reorganized the coll
agen framework, increasing fibril density and thus thickness. Dilated
vessels show thinning of the arterial wall without disruption but with
compaction of the new collagen fibrils. Cellular nests are also compr
essed and stretched. The endothelial layers are undisturbed. The succe
ss of dilatation depends on the amount and location of proliferation p
resent. The effect is usually permanent. Because our protocols call fo
r dilatation no greater than 10% above normal diameter, the muscle lay
ers have not been torn or stretched although focal areas of necrosis a
re sometimes seen. Understanding the constrictive process and its reli
ef through dilatation, allows us to formulate a therapeutic plan. Our
experience in treating 89 patients with vasospasm after SAH suggests t
hat, for best results, angioplasty should be performed before the angi
opathic features become florid. This helps to preserve flow through th
e short arteries to the brain stem and deep brain nuclei, which may be
involved indirectly in the vasospastic process.