Angioplasty of vasospasm: is it reasonable?

Clinical and radiographic examinations indicate preliminarily indications that transluminal angioplasty may be effective in overall management of the patient with vasospasm. Many questions remain, including: How does it work?; Are the effects persistent?; Is the arterial wall injured by the process? Recent studies in several patients who died after angioplasty allow us to provide some answers. Undilated spastic arteries show proliferation of both cellular and connective tissue elements. There is good evidence that myofibroblasts have reorganized the collagen 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 compressed and stretched. The endothelial layers are undisturbed. The success of dilatation depends on the amount and location of proliferation present. The effect is usually permanent. Because our protocols call for dilatation no greater than 10% above normal diameter, the muscle layers have not been torn or stretched although focal areas of necrosis are sometimes seen. Understanding the constrictive process and its relief through dilatation, allows us to formulate a therapeutic plan. Our experience in treating 89 patients with vasospasm after SAH suggests that, for best results, angioplasty should be performed before the angiopathic features become florid. This helps to preserve flow through the short arteries to the brain stem and deep brain nuclei, which may be involved indirectly in the vasospastic process.