Does the altered cardiovascular variability associated with obstructive sleep apnea contribute to development of cardiovascular disease in patients with obstructive sleep apnea syndrome?

Associated With Obstructive Sleep Apnea Contribute to Development of Cardiovascular Disease in Patients With Obstructive Sleep Apnea Syndrome? To the Editor: In a recent issue of Circulation, Narkiewicz et al1 demonstrated that cardiovascular variability is altered in patients with obstructive sleep apnea (OSA). The authors concluded that abnormalities in cardiovascular variability might be implicated in the subsequent development of overt cardiovascular disease in patients with OSA. We basically agree with the authors that patients with OSA in the absence of hypertension (HT) or heart failure have an altered cardiovascular variability. However, the role of altered cardiovascular variability in the development of cardiovascular disease has not been determined. Although an association of OSA with HT has been documented, this association may also be affected by confounding factors such as age and obesity, which commonly occur along with both OSA and HT.2– 4 Because OSA is associated with repetitive arousals, hypoxia, and a rise in catecholamine and sympathetic nervous system activity, all of which can lead to HT, there is no doubt that OSA is a risk factor for HT and other cardiovascular diseases.2 A recent experimental study also suggests that apnea, but not hypoxia or arousal, is responsible for the development of HT.3 However, similar conditions have also been observed in patients who snore in the absence of OSA, ie, upper-airway resistance syndrome (UARS). Thus, although there is a significant link between OSA and the altered cardiovascular variability, the association between OSA/UARS and HT/cardiovascular disease may depend on repetitive arousals, repetitive hypoxia, and increased sympathetic nervous system activity rather than the impaired cardiovascular variability.2– 4 Furthermore, it has been reported that treatment of OSA with prosthetic mandibular advancement does not yield changes in the frequencies of heart rate variability, such as high-, low-, and ultra-low-frequency component values.5 Because the treatment of OSA with nasal continuous positive airway pressure reverses HT in these patients, the fact that no obvious changes in heart rate variability occur before and during treatment of OSA suggests that a direct causal relationship between altered cardiovascular variability and cardiovascular disease may not exist. Considered together, OSA likely affects autonomic sympathetic and parasympathetic activities, leading to altered cardiovascular variability. The contributory role of diminished cardiovascular variability in the development of cardiovascular disease may be limited.