Neurovascular compression syndromes at the thoracic outlet generally present with predominantly arterial, venous, or neurogenic symptoms. The arterial abnormalities produce unique problems in diagnosis and management, and usually affect young, otherwise healthy, active individuals. Between 1984 and 1995 23 patients presented to our facility, with acute symptoms of arterial occlusion or embolization, found to be originating from the axillosubclavian arterial segment. The group comprised 14 females and nine males, ranging from 15 to 74 years, with an average age of 37 years. There were seven competitive athletes, three industrial workers, and 13 home, office, or service workers. The most severe presenting symptoms, occurring alone or in combination, and ranked in order of frequency observed, were: arm 'claudication' (74%), hand ischemia (48%), and digital gangrene (44%). Transaxillary thoracic outlet decompression was undertaken in 22 cases. This was combined with arterial reconstruction in 11 cases and sympathectomy for ischemic causalgia in seven cases. Transaxillary resection of a cervical rib was accomplished in 8 cases. There was one postoperative graft occlusion (PTFE), corrected by thrombectomy, with cumulative secondary patency (to 64 months), and one secondary embolic occlusion. Excepting the two secondary procedures, no patient had recurrent symptoms at a mean follow-up of 61 months. Effective and durable correction of the axillosubclavian arterial compressive abnormalities requires adequate thoracic outlet decompression, and anatomic vascular reconstruction when necessary. Failed prior procedures were a consequence of inaccurate diagnosis, failure to identify and correct the proximal embolizing arterial lesion, or inadequate decompression. Unilateral Raynaud's symptoms require meticulous investigation for arterial compression at the thoracic outlet with careful interpretation of subtle angiographic findings.