ATHEROSCLEROTIC plaques in the subclavian artery proximal to the origin of the vertebral artery have been found in 14% to 35% of patients with cerebrovascular insufficiency evaluated by aortocranial arteriography.1,2 If these plaques cause symptoms, they might do so by serving as a source for emboli which are carried through the vertebral artery to the brain, by reducing flow and pressure in the vertebral basilar system, or by changing the pressure gradient so that blood flows from its cephalic end toward its origin from the subclavian artery, a situation dubbed the subclavian steal. Which of these mechanisms precipitates symptoms in patients with subclavian steal has been the subject of much discussion.
In order to ascertain whether disturbed hemodynamics per se would result in reduced cephalic flow in animals with otherwise normal aortocranial arteries, the effect of reversed flow in the vertebral artery has been studied in acute3 and