Carotid endarterectomy open. In several clinical trials, the 30-day incidence of heart attack, stroke, or death was significantly higher with stenting than with endarterectomy (9.6% vs. 3.9%). The Carotid Revascularization Endarterectomy versus Stenting Trial (CREST) funded by the National Institutes of Health (NIH) reported that the results of stents and endarterectomy were comparable. However, the European International Carotid Stenting Study (ICSS) found that stents had almost double the rate of complications. The aim of CEA is to prevent the adverse sequelae of carotid artery stenosis secondary to atherosclerotic disease, i.e. ischemic stroke. As with any prophylactic operation, careful evaluation of the relative
Carotid body acid-base transporters (e.g. Na-H) which raise intracellular pH, and activates transporters (e.g. Cl-HCO) which decrease it. Changes in proton concentration caused by acidosis (or the opposite from alkalosis) inside the cell stimulates the same pathways involved in P sensing. Another mechanism is through oxygen sensitive potassium channels. A drop in dissolved oxygen lead to closing of these channels which results in depolarization. This leads to release of the neurotransmitter dopamine in the glossopharyngeal and vagus afferente to the vasomotor area. The type I (glomus) cells in the carotid (and aortic bodies) are derived from neuroectoderm and are thus electrically excitable.