Our results demonstrated a significant improvement in EF with a trend toward correlation between the improvement in OSA severity and that in EF. This is in accordance with previous reports on nCPAP treatment.8,10,21 The present findings on ED in sleep apnea measured at approximately 10:00 am complement our previous findings that were obtained immediately after patients awoke, suggesting that those findings reflected a stable state rather than overnight effects.,12 ED, which is a documented subclinical condition that precedes atherosclerosis,51 improved to normal levels during the 1 year of treatment with MAS, and TBARS levels decreased to near-normal levels. Therefore, we speculate that, despite the substantial residual apnea, treatment with the MAS may have a positive protective effect from future cardiovascular complications, although this has to be further investigated. Only two studies3,33 so far have addressed the potential favorable effects of MAS treatment on cardiovascular risk factors, exhibiting a significant reduction in diastolic BP after treatment. Since cardiovascular complications tend to develop in untreated patients with OSA, even if the OSA does not worsen,47 we believe that the current results support offering treatment with the MAS to patients who do not respond to nCPAP treatment, with the hope that further cardiovascular damage will be reduced or slowed. This is supported by the similar RH-PAT findings of patients with MAS at 1 year and those of the reference group, although the remnant OSA had a bearing on TBARS levels, which had decreased significantly but did not reach the levels of the reference group. In the untreated control group, on the other hand, the initial EF of 1.9 ± 0.4 deteriorated to 1.7 ± 0.4 following 9 month without treatment (Table 1). The lipid levels (ie, low-density lipoprotein [LDL], high-density lipoprotein [HDL], and triglycerides) were significantly reduced in the study group at the 1-year evaluation. This drop cannot be readily explained as there were no changes in medical status or interventions performed during this year, although we did not monitor patient lifestyles, which could have changed following MAS treatment. While lowering lipid levels can potentially benefit EF, we believe that this is less likely in the current study due to several reasons. First, HDL levels decreased similarly to LDL levels. Second, EF increased significantly in the treatment group at the 3-month evaluations, before the significant changes in lipid levels occurred. Finally, the lipid levels in the reference group were similar to the baseline levels of the treatment group (total cholesterol level, p = 0.74; triglycerides, p = 0.9), yet their EF was higher.