Hemorragia subaracnoidea, isquemia cerebral y endotelina-1

SUBARACHNOID HEMORRHAGE,CEREBRAL ISCHEMIA AND ENDOTHELIN-1Summary. Introduction. Cerebral vasospasm is involved in the development of delayed ischemic lesions in patients with subarach-noid hemorrhage. We developed an integral theoretical model to explain the pathophysiology of cerebral vasospasm, in whichendothelin-1 has a pivotal role in the development of both cerebral vasospasm and delayed ischemic neurological deficits (DIND) .Objective. The objective of this study is to analyze the relationship between temporal profile of plasma endothelin-1 levels and thedevelopment of cerebral vasospasm and DIND. Patients and methods. We analyzed sequentially plasma endothelin-1 levels in17 patients with aneurysmatic subarachnoid hemorrhage. All the patients had complete clinical and neuroradiological studies.Patients were classified according to Fisher’s score. Results. Patients (4 males and 13 females, aged 48.1 ± 20.3 years) had a goodclinical condition (Hunt-Hess 10). Two weeks after bleeding, patients had higher plasma endothelin-1 levels than healt hyvolunteers (p= 0.024). Patients who developed DIND had higher plasma endothelin-1 levels (p= 0,034) and a different evolution(p= 0.0146) than patients without DIND. There is a significant correlation (p= 0,02) between basal plasma endothelin-1 levels a ndGOS score. Multiple regression analysis shows a significant dependence between plasma endothelin-1 levels and Fisher’s score(p= 0.0195), development of DIND (p= 0.0095), and GOS score (p= 0,0319). Logistic regression analysis finds a predictiverelation between Fisher’s score and plasma endothelin-1 levels for the development of DIND (overall predicted= 74.24%; p= 0.014 8).Conclusions. Plasma endothelin-1 levels are increased in patients after subarachnoid hemorrhage and are associated with thedevelopment of cerebral vasospasm and DIND. [REV NEUROL 2000; 30: 27-34] [http://www.revneurol.com/3001/i010027.pdf]Key words. Cerebral vasospasm. Delayed ischemic neurological deficit. Endothelin-1. Pathophysiology. Subarachnoid hemorrhage.