TY - JOUR
T1 - Oxidative stress in obstructive sleep apnoea
AU - Svatikova, Anna
AU - Wolk, Robert
AU - Lerman, Lilach O.
AU - Juncos, Luis A.
AU - Greene, Eddie L.
AU - McConnell, Joseph P.
AU - Somers, Virend K.
N1 - Funding Information:
This work was supported by grants NIH HL-65176, HL-61560, HL-70602, and M01-RR00585.
PY - 2005/11
Y1 - 2005/11
N2 - Aims: Any sustained elevation of oxidative stress in patients with obstructive sleep apnoea (OSA) might help explain their increased risk for cardiovascular diseases. We tested the hypothesis that measures of oxidative stress are increased in otherwise healthy subjects with OSA when compared to closely matched OSA-free control subjects. Methods and results: Plasma indices of oxidative stress and lipid peroxidation [thiobarbituric acid-reactive substances (TBARS), oxidized LDL (oxLDL), isoprostanes] were measured in 41 moderate-severe OSA males without other diseases and in 35 matched controls first before sleep, then after 4 h of untreated OSA, and again in the morning after 4 h of effective treatment with continuous positive airway pressure (CPAP). Plasma levels of oxLDL, TBARS, and isoprostanes in OSA patients (n = 34, 26, 17, respectively) were comparable to the controls (n = 28, 27, 15 for the three markers, respectively). Neither untreated OSA nor CPAP treatment nor normal sleep affected levels of any of the three measures of oxidative stress. There was no association between the severity of sleep apnoea and any measure of oxidative stress. Conclusion: Otherwise healthy OSA patients, without any other co-morbidities, do not manifest evidence for higher oxidative stress and lipid peroxidation. Thus, oxidative stress and lipid peroxidation do not appear to be key mediators of increased cardiovascular disease in OSA patients.
AB - Aims: Any sustained elevation of oxidative stress in patients with obstructive sleep apnoea (OSA) might help explain their increased risk for cardiovascular diseases. We tested the hypothesis that measures of oxidative stress are increased in otherwise healthy subjects with OSA when compared to closely matched OSA-free control subjects. Methods and results: Plasma indices of oxidative stress and lipid peroxidation [thiobarbituric acid-reactive substances (TBARS), oxidized LDL (oxLDL), isoprostanes] were measured in 41 moderate-severe OSA males without other diseases and in 35 matched controls first before sleep, then after 4 h of untreated OSA, and again in the morning after 4 h of effective treatment with continuous positive airway pressure (CPAP). Plasma levels of oxLDL, TBARS, and isoprostanes in OSA patients (n = 34, 26, 17, respectively) were comparable to the controls (n = 28, 27, 15 for the three markers, respectively). Neither untreated OSA nor CPAP treatment nor normal sleep affected levels of any of the three measures of oxidative stress. There was no association between the severity of sleep apnoea and any measure of oxidative stress. Conclusion: Otherwise healthy OSA patients, without any other co-morbidities, do not manifest evidence for higher oxidative stress and lipid peroxidation. Thus, oxidative stress and lipid peroxidation do not appear to be key mediators of increased cardiovascular disease in OSA patients.
KW - Cardiovascular diseases
KW - Isoprostanes
KW - Obstructive sleep apnoea
KW - Oxidative stress
KW - TBARS
KW - oxLDL
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U2 - 10.1093/eurheartj/ehi440
DO - 10.1093/eurheartj/ehi440
M3 - Article
C2 - 16105851
AN - SCOPUS:27644451715
SN - 0195-668X
VL - 26
SP - 2435
EP - 2439
JO - European heart journal
JF - European heart journal
IS - 22
ER -