Obstructive sleep apnea (OSA) is associated with increased cardiovascular morbidity and mortality.1,2 Although several comorbidities of OSA, such as obesity, hypertension, and dysglycemia, play a significant indirect role in the relationship between OSA and the development of cardiovascular diseases,3,4 it was recently reported that several pathogenetic mechanisms linked to OSA, such as inflammation, increased the production of reactive oxygen species, and endothelial dysfunction, might directly contribute to the progression of vascular damage, which is strongly associated with future cardiovascular events.5 In fact, in several studies,6,7 advanced vascular damage, evaluated by using several noninvasive techniques, such as flow-mediated dilatation, pulse wave velocity (PWV), and carotid intima-media thickness (IMT), was observed in subjects with OSA. Although all of these parameters are established predictors of cardiovascular events, the flow-mediated dilatation and the carotid IMT indicate only the local status of the brachial and carotid arteries, respectively. On the other hand, an arterial stiffness parameter would more accurately reflect the systemic status. The PWV has been used as a noninvasive clinical index of such arterial stiffness.8 An elevated carotid-femoral PWV (cfPWV) has been reported9,10 to predict cardiovascular events and all-cause mortality in hypertensive patients and in the general population. Although conventional techniques for measuring cfPWV are noninvasive, a femoral artery transducer carefully adjusted to obtain an accurate pulse wave is required, but it is technically difficult and has low reproducibility.11 A simple, noninvasive, and automatic method of measuring the brachial-ankle PWV (baPWV) has been developed, and a close correlation between baPWV and cfPWV has been reported.12 baPWV has also been shown to be a predictor of the presence of coronary artery disease.13 Among patients with OSA, an association between severity of OSA and these two arterial stiffness parameters has been reported.14–17 However, along with age, BP is a major determinant of PWV,18 and, therefore, the fact that PWV is affected by changes in BP during measurement is a problem. In particular, the PWV values among patients with OSA must be interpreted with caution, because it has been reported3,19 that hypertension and the white coat phenomenon are frequently observed in patients with OSA; thus, patients with OSA tend to have high BP during PWV measurement. An arterial stiffness parameter, the cardio-ankle vascular index (CAVI), was developed by measuring PWV and BP.20,21 CAVI is adjusted for BP, and it is believed to be little affected by the BP at the time of the measurement.