Periprocedural drug therapy in carotid artery stenting: the need for more evidence.

Carotid artery stenting (CAS) is a widely accepted alternative for patients at high risk for carotid endarterectomy (CEA). However, the role, indications, and evidence for many pharmacologic agents that are used adjunctively in the periprocedural setting have not been established. Several drugs are commonly used before, during, and after CAS, but their uses have not been standardized.

Control of blood vessel identity: from embryo to adult.

Arteries and veins have been historically defined by the direction of blood flow and oxygen tension within the vessel, in addition to their functional, hemodynamic, and anatomical differences. It is now known that the molecular identity of these vessels is genetically predetermined, with specific molecular pathways activated during the development of arteries and veins. Eph-B4 is a determinant of venous differentiation and Ephrin-B2 is a determinant of arterial differentiation.

Adjunctive pharmacologic use in carotid endarterectomy: a review.

Although carotid endarterectomy (CEA) is now widely accepted as the surgical therapy for carotid stenosis, the role of and indications and evidence for many pharmacologic agents that are used adjunctively in the perioperative setting have not been conclusively established. Aspirin (acetylsalicylic acid) is the pharmaceutical agent that has been studied most extensively in conjunction with CEA; other than aspirin and dextran, the use of many agents before, during, and after CEA has not been standardized. Prospective randomized trials are still needed to demonstrate efficacy, predict outcome, and determine the optimal use of these medications in their adjunctive use during CEA to improve patient care and obtain optimal surgical outcomes.

Shear stress and cyclic strain may suppress apoptosis in endothelial cells by different pathways.

Endothelial cells (ECs) are exposed to hemodynamic forces such as shear stress (SS) and cyclic strain (CS) in vivo. Alterations in these forces may stimulate EC growth and intimal hyperplasia, possibly by promotion of cell survival through inhibition of apoptosis. The authors examined the effect of SS and CS on inhibition of apoptosis and phosphorylation of Akt and its downstream target Bad in bovine aortic ECs in vitro.