Cerebral hemodynamics play a pivotal role in stroke pathogenesis. Transcranial Doppler (TCD) studies demonstrated the importance of cerebral vasomotor reactivity (VMR) on the outcome of carotid artery occlusion (CAO). So far, positron emission tomography represents the best technique for detecting both hemodynamic and metabolic aspects of cerebral perfusion adaptive processes in cerebrovascular patients. Near-infrared spectroscopy (NIRS) is a new method allowing for a non-invasive assessment of cerebral blood flow and hemoglobin (Hb) oxygenation parameters.A recent TCD and NIRS study demonstrated that patients with symptomatic CAO had lower VMR values measured by TCD and lower oxygen saturation (oxygen%) increases detected by NIRS than asymptomatic ones. The parameters were obtained simultaneously after CO(2) inhalation. The present study aims to investigate if Hb oxygen % could represent also at rest a marker of hemodynamic status in carotid disease.Thirty-five symptomatic and 17 asymptomatic patients with CAO underwent a simultaneous examination by means of TCD and NIRS at rest condition and during CO(2) reactivity test. Symptomatic patients presented with oxygen% values at rest higher (p = 0.001) and VMR values lower (p < 0.001) than asymptomatic subjects. According to a logistic model, for each unitary VMR increase, the odds of being symptomatic decreases of about 10% (OR = 0.9, p = 0.001); for each unitary increase of oxygen% at baseline, this odd increases of about 23% (OR = 1.23, p = 0.031). In addition to TCD VMR values, oxygen hemoglobin saturation at rest detected by NIRS can discriminate symptomatic from asymptomatic patients with CAO. NIRS can add an important contribution to explain pathophysiological mechanisms of stroke occurrence.

Hemoglobin oxygen saturation as a marker of cerebral hemodynamics in carotid artery occlusion. An integrated Near-Infrared Spectroscopy and Transcranial Doppler study / Vernieri, F; Silvestrini, Mauro; Tibuzzi, M; Pasqualetti, P; Altamura, C; Passarelli, F; Matteis, M; Rossini, P. M.. - In: JOURNAL OF NEUROLOGY. - ISSN 0340-5354. - 253:(2006), pp. 1459-1465.

Hemoglobin oxygen saturation as a marker of cerebral hemodynamics in carotid artery occlusion. An integrated Near-Infrared Spectroscopy and Transcranial Doppler study.

SILVESTRINI, Mauro;
2006-01-01

Abstract

Cerebral hemodynamics play a pivotal role in stroke pathogenesis. Transcranial Doppler (TCD) studies demonstrated the importance of cerebral vasomotor reactivity (VMR) on the outcome of carotid artery occlusion (CAO). So far, positron emission tomography represents the best technique for detecting both hemodynamic and metabolic aspects of cerebral perfusion adaptive processes in cerebrovascular patients. Near-infrared spectroscopy (NIRS) is a new method allowing for a non-invasive assessment of cerebral blood flow and hemoglobin (Hb) oxygenation parameters.A recent TCD and NIRS study demonstrated that patients with symptomatic CAO had lower VMR values measured by TCD and lower oxygen saturation (oxygen%) increases detected by NIRS than asymptomatic ones. The parameters were obtained simultaneously after CO(2) inhalation. The present study aims to investigate if Hb oxygen % could represent also at rest a marker of hemodynamic status in carotid disease.Thirty-five symptomatic and 17 asymptomatic patients with CAO underwent a simultaneous examination by means of TCD and NIRS at rest condition and during CO(2) reactivity test. Symptomatic patients presented with oxygen% values at rest higher (p = 0.001) and VMR values lower (p < 0.001) than asymptomatic subjects. According to a logistic model, for each unitary VMR increase, the odds of being symptomatic decreases of about 10% (OR = 0.9, p = 0.001); for each unitary increase of oxygen% at baseline, this odd increases of about 23% (OR = 1.23, p = 0.031). In addition to TCD VMR values, oxygen hemoglobin saturation at rest detected by NIRS can discriminate symptomatic from asymptomatic patients with CAO. NIRS can add an important contribution to explain pathophysiological mechanisms of stroke occurrence.
2006
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11566/55683
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