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OBJECTIVE: To evaluate whether obstructive sleep apnea (OSA) contributes directly to left ventricular (LV) diastolic dysfunction. METHODS: Seventy-four non-obese male OSA (apnea hypopnea index (AHI)⩾5/h) patients without cardiac disease, hypertension or diabetes were enrolled. Echocardiography, pulse wave velocity (PWV) measurements and laboratory testing were performed in all patients. LV diastolic function was assessed by the transmitral flow velocity (E/A ratio), and mitral annular velocity (Ea) was derived from tissue Doppler imaging (TDI). RESULTS: The E/A ratio and Ea in the severe OSA group (AHI⩾30/h) was significantly lower than those in the mild to moderate OSA group (5⩽AHI<30/h) (P<0.0001), whereas the S/D ratio, an indicator of pulmonary vein flow velocity, in the severe OSA group was significantly higher than that in the mild to moderate OSA group (P=0.04). AHI exhibited a statistically significant inverse correlation with the E/A ratio (r=-0.47, P=0.0001), but not with relative wall thickness (RWT), LV mass index (LVMI) or PWV. RWT, LVMI and PWV exhibited an inverse correlation with the E/A ratio. Multivariate linear regression analysis revealed that severe OSA was independently associated with the E/A ratio even after adjusting for age, insulin resistance, blood pressure, LV geometry, and PWV (ß=-0.23, P=0.001). CONCLUSIONS: These results indicate that severe OSA itself may contribute directly to LV diastolic dysfunction irrespective of LV geometry, arterial stiffness, obesity and its associated cardiovascular risk factors.

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The chronic obstructive pulmonary disease (COPD) and obstructive sleep apnea (OSA) have been recently much focused as independent risks for cardiovascular disease. Furthermore, the complication of both has a worse prognosis compared with patients with only one of these diseases. However, the details of the underlying mechanisms of this worsened prognosis have not been clear. The cross-sectional study was conducted to examine whether the overlap of COPD augment the increase in arterial stiffness in subjects with OSA. If so, we examined the exaggeration of nocturnal hypoxemia and its related inflammation are related to this augmentation of increased arterial stiffness. In 524 male subjects with OSA diagnosed by polysomnography (apnea-hypopnea index >5/h) (52 ± 14 years old), the forced expiratory volume at 1 s/the forced vital capacity (FEV(1)/FVC) ratio, brachial-ankle pulse wave velocity (baPWV), blood C-reactive protein (CRP) and B-natriuretic peptide (BNP) levels were measured. The prevalence rate of COPD was 12% in this study subjects. Plasma BNP levels and the crude (median value, 17.2 vs. 14.1 m/s, p < 0.01) and adjusted value of baPWV were significantly higher in subjects with overlap syndrome than in those with OSA alone. However, parameters of nocturnal hypoxemia and serum CRP levels were similar between both groups. Thus, the overlap of COPD in patients with OSA augments increase in arterial stiffness without the exaggeration of nocturnal hypoxemia and inflammation. Even so, this augmentation may partially contribute to the increased cardiovascular risk in the overlap syndrome.

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Obstructive sleep apnea (OSA) is not only a cause of hypertension; it also possibly affects the pathogenesis and progression of aortic disease because an inspiratory effort-induced increase in negative intrathoracic pressure generates mechanical stress on the aortic wall. The objective of the present study was to examine the incidence by location of OSA as a complication in patients with aortic aneurysm and patients with aortic dissection (AD). An overnight sleep study was conducted in the following study groups: the aortic disease group (n = 95) consisting of patients with thoracic aortic aneurysm (TAA, n = 32), patients with abdominal aortic aneurysm (AAA, n = 36), and patients with AD (n = 27); and a control group (n = 32), consisting of patients with coronary risk factors who were matched with the aortic disease group for age, gender, and body mass index (BMI). The 3% oxygen desaturation index (ODI) was significantly higher in all the TAA, AAA, and AD groups (P = 0.045, P = 0.003, and P = 0.005, respectively) than in the control group. The incidence of moderate to severe OSA [apnea hypopnea index (AHI) ≥15 events/h] was significantly higher in the first three groups (P = 0.026, P = 0.001, P = 0.003, respectively) than in the control group, while no significant difference was found between the TAA group and the AAA group with respect to these variables. Furthermore, no significant differences were found between the thoracic AD subgroup and the abdominal AD subgroup with respect to AHI and 3% ODI, as well as with respect to the incidences of moderate to severe OSA. Patients with TAA, patients with AAA, and patients with AD showed high incidences of moderate to severe OSA. Although this result suggests that OSA may be one of risks for aortic disease, unelucidated mechanism(s) other than negative intrathoracic pressure may be involved in the pathogenesis of aortic disease.

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BACKGROUND: Obstructive sleep apnea (OSA) increases the risk of cardiovascular disease (CVD) and has been reported to be associated with chronic kidney disease (CKD). Recent studies have demonstrated that cystatin C is a prognostic biomarker of the risk of death and CVD even in patients without established CKD. METHODS: In a cross-sectional study, we enrolled 267 consecutive OSA patients without CKD who had an apnea-hypopnea index (AHI) ≥ 5 events per hour in overnight polysomnography. CKD was defined as an estimated glomerular filtration rate (eGFR) < 60 mL/min/1.73 m(2) according to the modification of diet in renal disease (MDRD) equation (modified for Japanese). Serum cystatin C levels were measured in all patients. RESULTS: Cystatin C was significantly correlated with age (r = 0.37), body mass index (BMI) (r = 0.12), AHI (r = 0.17), C-reactive protein (CRP) (r = 0.12), and Brachial-ankle pulse wave velocity (r = 0.18). Logistic regression analysis demonstrated that severe OSA defined by an AHI ≥ 30 events per hour was an independent variable for the highest quartiles of serum cystatin C levels (≥0.88 mg/L) (OR: 2.04, 95% CI: 1.04-4.01, P = 0.04) even after adjustment for age, BMI ≥ 25, hypertension, and diabetes mellitus. CONCLUSIONS: This study indicates that severe OSA independently increases serum cystatin C levels in patients without CKD. Cystatin C is considered to be a biomarker that reflects both clinically latent renal dysfunction and cardiovascular risk that are influenced by OSA.

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OBJECTIVE: Increased arterial stiffness and sympathovagal imbalance are noted in patients with obstructive sleep apnea (OSA). It has been thought that continuous positive airway pressure (CPAP) therapy can have beneficial effects on the vascular function in such cases. However, it is not yet clear whether the improvement of sympathovagal balance by CPAP might be related to reduction of the arterial stiffness, independent of changes in the blood pressure. METHODS: In 50 consecutive eligible patients with OSA (apnea-hypopnea index>/=20/hour) receiving CPAP therapy, the brachial-ankle pulse wave velocity (baPWV), heart rate variability (LF, HF and LF/HF ratio), baroreceptor sensitivity (BRS), plasma levels of C-reactive protein (CRP), and endothelial function as assessed by changes in the forearm blood flow before and after reactive hyperemia (END) were measured before and after 3-months' CPAP therapy. RESULTS: Significant decrease of the LF/HF ratio, plasma levels of CRP, baPWV and heart rate were observed after 3 months' CPAP therapy. The change in the baPWV following 3-months' CPAP therapy was significantly correlated with the change in the LF/HF ratio and mean blood pressure (MBP), but not with that of the BRS, CRP or END after the therapy. Multivariate linear regression analysis demonstrated a significant correlation between the change in the LF/HF ratio and that in the baPWV (beta=0.305, p=0.041), independent of the changes in the MBP, plasma CRP levels and heart rate. CONCLUSIONS: Improvement of the sympathovagal balance by CPAP therapy may be significantly related to decreased stiffness of the central to middle-sized arteries, independent of the changes in the blood pressure and vascular endothelial status.

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An 82-year-old male patient, who had been diagnosed with chronic heart failure due to dilated cardiomyopathy and combined valvular disease and who had atrial fibrillation with complete atrioventricular block, was admitted to our hospital owing to the exacerbation of chronic heart failure. During admission, the patient became aware of drowsiness during daytime hours and had periodic apnea during sleep. Polysomnography (PSG) revealed Cheyne-Stokes respiration with severe central sleep apnea as evidenced by an apnea-hypopnea index (AHI) of 93.5/h. Nocturnal oxygen therapy failed to sufficiently suppress apnea, and arousal reactions occurred frequently. Therefore, we conducted titration by adaptive-servo ventilation (ASV; HEART PAP™). Consequently, subjective symptoms and respiratory sleep parameters improved. The patient showed excellent adherence to loading the device at home. PSG at 3 months after implementation of HEART PAP™ indicated improvement in the AHI to 13.5/h, and the patient exhibited marked improvements in breathlessness and awareness of drowsiness during daytime hours. HEART PAP™ was found to be a useful device for Cheyne-Stokes respiration with central sleep apnea that is associated with chronic heart failure even for very elderly patients.

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BACKGROUND: Although obstructive sleep apnea (OSA) severity is evaluated by the apnea-hypopnea index (AHI), the value of AHI in evaluating cardiovascular risks, especially in mild to moderate OSA, is unclear. OBJECTIVES: The purpose of this study is to evaluate the validity of a new index, the integrated area of desaturation (IAD), to detect the incidence of cardiovascular events (CVEs) in such patients. METHODS: We enrolled 230 consecutive patients with mild to moderate OSA and 354 with severe OSA diagnosed by polysomnography, of whom 53 and 112, respectively, had CVEs. The IAD was calculated by dividing the area of desaturation by total sleep time in polysomnography. C-reactive protein (CRP) was also measured for all patients. RESULTS: In the mild to moderate OSA patients, the mean IAD of the CVEs group was significantly higher than that of the non-CVE group (94.4 +/- 82.7 vs. 62.3 +/- 50.8, p = 0.001), whereas mean AHI and 3% oxygen desaturation index were similar in both groups. Multivariate analysis demonstrated that the IAD was an independent variable for CVEs (OR 1.006, 95% confidence interval 1.001-1.012, p = 0.031). Moreover, the IAD level of the high CRP group was significantly higher than that of the low CRP group (92.9 +/- 84.8 vs. 63.9 +/- 54.5, p = 0.009). There was no significant difference in AHI, IAD or other polysomnographic parameters in the severe OSA patients. CONCLUSIONS: IAD might be superior to AHI alone in the evaluation of the history of CVEs in mild to moderate OSA patients, and it deserves attention as a possible predictor of future CVEs.

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