Cross-Sectional Relationship Between Atrial Conduction Delay and Arterial Stiffness in Patients with Obstructive Sleep Apnea.

Aim: Prolonged P-wave duration (PWD), which indicates atrial conduction delay, is a potent precursor of atrial fibrillation (AF) that may be induced by obstructive sleep apnea (OSA). The cardio-ankle vascular index (CAVI), which is an arterial stiffness parameter, is elevated in patients with OSA; moreover, an increased CAVI is associated with atrial conduction delay through left atrium enlargement in association with left ventricular diastolic dysfunction. We aimed to examine the relationship between the CAVI and PWD in patients with OSA. Methods: We included patients with a sinus rhythm who underwent overnight polysomnography. We measured the PWD and CAVI on standard 12-lead electrocardiograms; further, we analyzed the relationship between PWD and CAVI. Results: We analyzed data from 300 participants (men, 89.0%; mean age, 52.3 ± 13.1 years; and body mass index, 26.2 ± 3.9 kg/m2). The mean PWD was 104.4 ± 10.4 ms while the mean CAVI was 7.5 ± 1.5. PWD was significantly correlated with CAVI (r = 0.478, p < 0.001); additionally, PWD and CAVI were directly associated with OSA severity (p = 0.002 and p = 0.002, respectively). Multivariate regression analysis revealed an independent significant correlation of PWD and CAVI with OSA severity. Conclusion: In patients with OSA, an increase in arterial stiffness is associated with atrial conduction delay.

Change in cardio-ankle vascular index by long-term continuous positive airway pressure therapy for obstructive sleep apnea.

BACKGROUND: It has been reported that patients with obstructive sleep apnea (OSA) have an elevated arterial stiffness, and alleviation of OSA by continuous positive airway pressure (CPAP) might attenuate this. Recently, the cardio-ankle vascular index (CAVI) has been reported to be a highly reproducible arterial stiffness parameter in OSA patients. However, the change in CAVI that occurs following long-term CPAP treatment for OSA remains unclear. METHODS: Patients with moderate-to-severe OSA were enrolled. Changes in CAVI at 1 and 12 months after CPAP initiation (ΔCAVI(1) and ΔCAVI(12), respectively) were assessed. Factors associated with ΔCAVI(1) and ΔCAVI(12) were determined by multivariable regression analyses. RESULTS: Thirty subjects were assessed. CAVI was significantly reduced at 1 month compared with the baseline from 7.80 ± 1.19 to 7.56 ± 1.08 (p = 0.013). A non-significant reduction was observed at 12 months (7.72 ± 1.18, p = 0.365 versus baseline) and CAVI had actually increased compared with that measured at 1 month. In multivariable analyses, ΔCAVI(1) was inversely correlated with CPAP usage (coefficient: -0.500, p = 0.006) and was directly correlated with the change in the ratio of low frequency to high frequency in heart rate variability (coefficient: 0.607, p < 0.001), whereas ΔCAVI(12) was related to the use of angiotensin-converting enzyme inhibitors (ACE-I) or angiotensin-II-receptor blockers (ARB; coefficient: 0.464, p = 0.013), was directly correlated with the change in hemoglobin A1c levels (coefficient: 0.644, p < 0.001), and was inversely correlated with the change in CPAP usage (coefficient: -0.380, p = 0.046). CONCLUSIONS: CAVI was significantly reduced by short-term CPAP and then slightly increased from 1 to 12 months, which was probably due to natural progression associated with the aging process. However, long-term CPAP treatment had the beneficial effect of maintaining CAVI below baseline levels when associated with the use of ACE-I/ARB, the control of blood glucose and the CPAP compliance.

Plasma pentraxin3 and arterial stiffness in men with obstructive sleep apnea.

BACKGROUND: Obstructive sleep apnea (OSA) induces inflammation and vascular damage that might contribute to an increased risk of cardiovascular disease (CVD). However, the mechanisms linking OSA and CVD are not fully understood. Pentraxin3 may play a significant role in vascular inflammation and damage. Currently, there is lack of data on pentraxin3 and its role in vascular damage associated with OSA. METHODS: We enrolled 50 males with OSA and 25 controls matched for age and body mass index (BMI). Patients with OSA were further divided into mild and moderate to severe groups. We measured plasma pentraxin3 and evaluated vascular damage using an arterial stiffness parameter--the cardio-ankle vascular index (CAVI)--in all subjects. In the moderate to severe OSA group, pentraxin3 and CAVI were repeatedly measured following continuous positive airway pressure (CPAP) therapy for 1 month. RESULTS: Pentraxin3 levels in the moderate-to-severe OSA group were significantly higher than those in the mild OSA and control groups, with median levels (25th-75th percentile) of 2.36 (1.79-2.78), 1.63 (1.15-2.05), and 1.53 (1.14-2.04) ng/ml, respectively (P < 0.01). Pentraxin3 level was independently correlated with CAVI (coefficient, 0.34 P < 0.01). In the moderate-to-severe OSA group, pentraxin3 and CAVI levels were significantly reduced (P < 0.01 and P = 0.04, respectively) after 1 month of CPAP therapy. CONCLUSIONS: Plasma pentraxin3 and arterial stiffness levels in the moderate-to-severe OSA group were greater than the corresponding levels in patients without OSA. However, pentraxin3 level can be managed by CPAP therapy for OSA.

Establishment of the cardio-ankle vascular index in patients with obstructive sleep apnea.

BACKGROUND: An arterial stiffness parameter, the cardio-ankle vascular index (CAVI), has been developed. CAVI is adjusted for BP and can be used to measure arterial stiffness with little influence of BP. The purpose of this study was to evaluate the reproducibility, validity, and clinical usefulness of CAVI among patients with obstructive sleep apnea (OSA), who often have elevated BP during measurement. METHODS: Overall, 543 consecutive patients with OSA were studied. CAVI was automatically calculated from the pulse volume record, BP, and the vascular length from the heart to the ankle. First, CAVI was measured three times on different days in 25 patients to evaluate its reproducibility. Second, the correlation between CAVI and BP was assessed. Third, patients were classified into two groups (mild OSA or moderate-to-severe OSA), and the CAVIs of these groups were compared. Fourth, the correlation between CAVI and carotid intima-media thickness (IMT) was also assessed in 74 patients. RESULTS: The mean coefficient of variation was 2.8. CAVI demonstrated weak or no correlations with BP (with systolic BP, r = 0.184; with diastolic BP, r = 0.223). Patients with moderate-to-severe OSA (n = 469) had a significantly greater CAVI than patients with mild OSA (p = 0.034). CAVI was positively correlated with IMT (r = 0.487). CONCLUSIONS: The measurement of CAVI demonstrated good reproducibility and was not affected by the BP during measurement. Additionally, CAVI was positively correlated with another arteriosclerosis indicator. CAVI was higher in patients with more severe OSA and is regarded as a clinically useful index for the progression of vascular damage.