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Sleep apnea is strongly associated with HF, & could worsen HF through sympathetic activity, hypoxia, & hemodynamic & oxidative stress. If apneic activity causes acute stress in HF, it should increase BNP. We hypothesized that BNP changes are associated with the frequency & severity of apneic episodes, intermittent arousals, & hypoxia. 64 NYHA class II-III HF pts with EF <40% underwent a baseline sleep study. 5 pts with no sleep apnea & 12 with severe sleep apnea underwent repeat studies, during which blood was collected every 20 minutes to measure BNP. Pts with severe sleep apnea also underwent a 3rd study while they were administered oxygen. This provided 643 observations with which to relate apnea to BNP. The association of log BNP with each of 6 markers of apnea severity was evaluated with fixed effects panel regressions. There was no relationship between BNP & number of apneic episodes or number of arousals. However, severity of hypoxia (time spent with oxygen saturation below 90%) significantly predicted BNP; each 10% increase in duration of hypoxia increased BNP by 9.6% [95% CI 1.5-17.7, p=0.02]. Figure 1 shows, for each time point through the night, the difference from the mean for BNP and % of time with pO2 < 90%. BNP appears to fluctuate with the extent of hypoxia. In contrast, figure 2 shows the same BNP data & frequency of sleep disordered breathing episodes (dashed line). BNP does not fluctuate with frequency of sleep disordered breathing episodes. Hypoxia appears to be an important factor that underlies the impact of sleep abnormalities on hemodynamic stress in HF. Prevention of hypoxia might be especially important in these patients.