Plasma homocysteine in obstructive sleep apnoea

Abstract

Aims Whether increased homocysteine is one mechanism linking obstructive sleep apnoea (OSA) to cardiovascular abnormalities is unclear. We hypothesised that plasma homocysteine would be higher in OSA patients than in control subjects, would increase further during sleep, and decrease after treatment with continuous positive airway pressure (CPAP). Methods and ResultsFor study A, homocysteine was measured in 22 OSA patients and 20 controls first before sleep, then after 5 h of untreated OSA, and then in the morning after CPAP treatment. Homocysteine was similar in the OSA and control subjects at all three time points, and declined overnight in both groups (P ¼ 0:0017, P ¼ 0:036, respectively). To further assess this diurnal variation, we studied plasma homocysteine under a full-night protocol in 10 OSA patients and 12 controls (study B). Homocysteine was measured before sleep, in the morning after sleep, and at noon. Results in both OSA and control groups showed an overnight decline in homocysteine which was reversed by noon (repeated measures ANOVA: OSA, P ¼ 0:04; controls, P ¼ 0:02). Study C showed that disturbed sleep did not affect homocysteine levels in normal subjects. Conclusion There is a significant diurnal variation in plasma homocysteine, so that homocysteine is lower in the morning after waking. Neither OSA nor disturbed sleep elicit acute or chronic changes in homocysteine.

Oxidative stress and oxidant signaling in obstructive sleep apnea and associated cardiovascular diseases

“…Together these results suggest that increased homocysteine levels are associated with the occurrence of ischemic heart disease in OSA patients, but OSA alone does not appear to be an inducer of increased plasma homocysteine. More rigorous time course studies by Svatikova et al [64] also showed that having OSA per se did not change homocysteine levels, and CPAP treatment was not effective in lowering homocysteine in patients with OSA [65]. In contrast, Jordan et al [66] reported that 7 of 16 untreated OSA patients showed homocysteine levels > 11.7 μM, and that the level of homocysteine was effectively lowered by CPAP treatment.…”

Homocysteine Levels and Echocardiographic Findings in Obstructive Sleep Apnea Syndrome

“…It is oxidized in the plasma during hydrogen peroxide production to form free radicals which are toxic to endothelial cells. Due to the damaged endothelium, high homocysteine levels also limit NO production, and recent studies have shown that circulating NO levels are decreased in OSAS patients [3,4,6]. …”

“…Consequently, homocysteine causes oxidative stress in the endothelium, and decreases NO levels and the production of antioxidants. Thus homocysteine may increase the extent of oxidative stress induced by hypoxia episodes in OSAS [3,4,6]. Normally endothelial cells detoxify homocysteine by releasing NO, which forms S-nitroso-homocysteine adducts by binding to homocysteine [3].…”

“…Surges in sympathetic activity, blood pressure, ventricular wall tension and afterload adversely affect ventricular function [9]. Many studies have shown that OSAS patients have an increased risk of cardiovascular mortality [1,2,3,4,6,7]. Clinical and epidemiological studies have shown that there is a clear association between elevated blood homocysteine levels and coronary heart, peripheral artery and cerebrovascular diseases, stroke and venous thrombosis [3,4,6,7].…”

“…atherosclerosis. OSAS is associated with endothelial dysfunction, increased CRP and cytokine expression, elevated fibrinogen levels and decreased fibrinolytic activity [2,3,6,7,8]. …”