| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
(Stroke. 2007;38:250.)
© 2007 American Heart Association, Inc.
Letters to the Editor |
Department of Neurology, Hospital de Navarra, Pamplona, Spain
Sleep Unit, Department of Pneumology, Hospital Txagorritxu, Vitoria-Gasteiz, Spain
Department of Neurology, Clínica Universitaria de Navarra, Pamplona, Spain
Department of Neurology, Hospital de Navarra, Pamplona, Spain
Sleep Unit, Department of Pneumology, Hospital Txagorritxu, Vitoria-Gasteiz, Spain
Research Unit, Hospital Txagorritxu, Vitoria-Gasteiz, Spain
Sleep Unit, Department of Pneumology, Hospital Txagorritxu, Vitoria-Gasteiz, Spain
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
Response:
We are very grateful to Lavie and Lavie for their polite correction. As they point out, this variable (T90) should be expressed in Table 2 in "percentage of sleep time spent below 90% saturation," not in seconds.
After revising data referring to T90 variable in both groups, we didnt find any mistakes (ischemic stroke: median 14.6, SD 18.44, nonischemic stroke: median 16.12, SD 22.51). We think it could be possible to have some explanations for these findings. First, as you can see in Table 2, differences of AHI between 2 groups are significant (P=0,049) but very small (ischemic stroke: median 28, SD 17, nonischemic stroke median 20.1, SD 17), so T90 could be similar in both groups. Moreover, median AHI is moderate in severity, and for that reason it is not surprising that T90 is not very high. Second, it is important to remind that we have studied old people with many associated medical conditions not considered in exclusion criteria (as for example moderate chronic obstructive pulmonary disease or chronic bronchitis) that could have influence in respiratory function, and for that reason we think that T90 could have been determined not only by AHI.
Even though hypoxia and reoxygenation phenomena are responsible for oxidative stress and endothelial damage, as Lavie and Lavie have demonstrated, this is probably not the single mechanism involved in the increased vascular risk in obstructive sleep apnea hypopnea (OSAH) patients. For example, it is well know that repeated episodes of apnea and hypopnea
Related Article:
Stroke 2007 38: 249.
|
Stroke Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 2007 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |