Cerebral hyperperfusion syndrome is a rare, serious complication of carotid revascularization either after carotid endarterectomy or carotid stent placement. Impaired cerebral autoregulation and post-revascularization changes in cerebral hemodynamics are the main mechanisms involved in the development of the syndrome. Hyperperfusion syndrome may be fatal once an intracranial hemorrhage occurs. This article reviews the literature, intending to make a synthesis of all new data concerning the clinical manifestations of hyperperfusion syndrome, the pathophysiologic pathways involved in its development, the prediction, and the appropriate management. Also, a review of the most recent series of hyperperfusion syndrome following carotid revascularization, both with classic open endarterectomy and carotid artery stenting has been performed.

The most frequent location of visceral venous aneurysms is the portal venous system. They are often associated with cirrhosis and portal hypertension. They may be asymptomatic or present with abdominal pain and other symptoms. Watchful waiting is an appropriate treatment, except when complications occur. Most common complications are aneurysm thrombosis and rupture. Other visceral venous aneurysms are extremely rare.

Initial clinical experience with the use of FDSs in the treatment of visceral and peripheral aneurysms yielded satisfactory results in technical success, aneurysm thrombosis and shrinkage, and in patency of branch vessels. The results in aortic aneurysms are still under investigation. No aneurysm rupture has yet been described. There is a significant incidence of FDS thrombosis. Volume reduction of the aneurysm is a clearer evidence of the clinical success after treatment with FDSs than aneurysm thrombosis.