Jose S. Loredo

Effect of Continuous Positive Airway Pressure on Blood Pressure: A Placebo Trial

This study examined the effect of continuous positive airway pressure (CPAP) treatment on blood pressure in patients with obstructive sleep apnea. Thirty-nine patients with sleep apnea were studied. Ambulatory blood pressure monitoring was obtained before and after patients were randomized to receive either 1 week of CPAP or placebo CPAP (CPAP administered at ineffective pressure). Blood pressure was examined over daytime hours (6 AM to 10 PM) and during nighttime hours (10 PM to 6 AM). Daytime mean arterial blood pressure decreased significantly but equally in both the active treatment group and the placebo treatment group (P=0.001). Nighttime mean arterial pressure levels decreased to a much greater extent over time in the patients who received active CPAP treatment (P=0. 032). CPAP does appear to decrease nighttime blood pressure. However, the decrease in daytime blood pressure may reflect a nonspecific response (ie, placebo), since both the active treatment group and the placebo treatment group developed comparable decreases in blood pressure.

Cognitive Effects of Treating Obstructive Sleep Apnea in Alzheimer's Disease: A Randomized Controlled Study

OBJECTIVES: To examine whether treatment of obstructive sleep apnea (OSA) with continuous positive airway pressure (CPAP) in patients with Alzheimers disease (AD) results in better cognitive function.

Effects of Continuous Positive Airway Pressure Versus Supplemental Oxygen on 24-Hour Ambulatory Blood Pressure

Obstructive sleep apnea (OSA) is associated with recurrent episodes of nocturnal hypoxia and increased risk for development of systemic hypertension. Prior studies have been limited, however, in their ability to show reduction in blood pressure after continuous positive airway pressure (CPAP) therapy, and the effect of supplemental oxygen alone on blood pressure in OSA has not been evaluated. We performed a randomized, double-blind, placebo-controlled study comparing the effects of 2 weeks of CPAP versus sham-CPAP versus supplemental nocturnal oxygen on 24-hour ambulatory blood pressure in 46 patients with moderate-severe OSA. We found that 2 weeks of CPAP therapy resulted in a significant reduction in daytime mean arterial and diastolic blood pressure and nighttime systolic, mean, and diastolic blood pressure (all Ps <0.05). Although nocturnal supplemental oxygen therapy improved oxyhemoglobin saturation, it did not affect blood pressure. We conclude that CPAP therapy reduces both daytime and nighttime blood pressure in patients with OSA, perhaps through mechanisms other than improvement of nocturnal oxyhemoglobin saturation.

Association Between Polysomnographic Measures of Disrupted Sleep and Prothrombotic Factors

BACKGROUND Subjective sleep disturbances have been associated with increased risk of coronary artery disease (CAD). We hypothesized that disrupted sleep as verified by polysomnography is associated with increased levels of prothrombotic hemostasis factors previously shown to predict CAD risk. METHODS Full-night polysomnography was performed in 135 unmedicated men and women (mean age +/- SD, 36.8 +/- 7.8 years) without a history of sleep disorders. Morning fasting plasma levels of von Willebrand Factor (VWF) antigen, soluble tissue factor (sTF) antigen, d-dimer, and plasminogen activator inhibitor (PAI)-1 antigen were determined. Statistical analyses were adjusted for age, gender, ethnicity, body mass index, BP, and smoking history. RESULTS Higher total arousal index (ArI) was associated with higher levels of VWF (beta = 0.25, p = 0.011, DeltaR(2) = 0.045), and longer wake after sleep onset was associated with higher levels of sTF (beta = 0.23, p = 0.023, DeltaR(2) = 0.038). More nighttime spent at mean oxygen saturation < 90% (beta = 0.20, p = 0.020, DeltaR(2) = 0.029) and higher apnea-hypopnea index (AHI) [beta = 0.19, p = 0.034, DeltaR(2) = 0.024] were associated with higher PAI-1. There was a trend for a relationship between mean oxygen desaturation < 90% and PAI-1 (p = 0.053), even after controlling for AHI. Total ArI (beta = 0.28, p = 0.005, DeltaR(2) = 0.056) and WASO (beta = 0.25, p = 0.017, DeltaR(2) = 0.042) continued to predict VWF and sTF, respectively, even after controlling for AHI. CONCLUSIONS Polysomnographically verified sleep disruptions were associated with prothrombotic changes. Measures of sleep fragmentation and sleep efficiency were related to VWF and sTF, respectively. Apnea-related measures were related to PAI-1. Our findings suggest that sleep disruptions, even in a relatively healthy population, are associated with potential markers of prothrombotic cardiovascular risk.

Sleep quality and blood pressure dipping in obstructive sleep apnea

BACKGROUND Obstructive sleep apnea (OSA) is associated with poor sleep quality and a high incidence of nondipping. The aim of this study was to determine the association of sleep quality and nocturnal blood pressure (BP) dipping in an OSA population. METHODS A total of 44 untreated subjects with mild to severe OSA underwent overnight-attended polysomnography and 24-h ambulatory BP monitoring. Subjects were off antihypertensive medication. The percentage of slow wave sleep, percentage of time awake after sleep onset during the sleep period, sleep efficiency, and arousal index were chosen as measurements of sleep quality. Dipping was evaluated using the change in systolic BP, diastolic BP, and mean arterial pressure. Patients were classified as dippers and nondippers based on a nocturnal drop in mean arterial pressure > 10%. Differences between groups were evaluated by independent sample t tests. Pearson correlation and linear regression were used to evaluate the association of sleep quality and dipping. RESULTS There were no differences between dippers and nondippers with regard to body mass index, age, or respiratory disturbance index. A total of 84% were nondippers. No difference was found between dippers and nondippers in sleep quality. None of the sleep quality measures correlated with the measurements of dipping. In multiple regression analyses, the percentage of slow wave sleep and arousal index each independently predicted only a small percentage of the variance (approximately 10%) of nocturnal DBP dipping. CONCLUSIONS The prevalence of nondipping was very high in a population of untreated patients with mild to severe OSA. Nonetheless, sleep quality did not appear to be related to BP dipping.

Continuous positive airway pressure reduces subjective daytime sleepiness in patients with mild to moderate alzheimer's disease with sleep disordered breathing

OBJECTIVES: Studies have reported that 33% to 70% of patients with Alzheimers disease (AD) have sleep‐disordered breathing (SDB). Continuous positive airway pressure (CPAP) treatment has been shown to reduce daytime sleepiness and improve health‐related quality of life in nondemented older people with SDB. The effect of therapeutic CPAP treatment on daytime sleepiness in patients with mild‐moderate AD with SDB was assessed.

Sleep-disordered Breathing in Hispanic/Latino Individuals of Diverse Backgrounds. The Hispanic Community Health Study/Study of Latinos

RATIONALE Hispanic/Latino populations have a high prevalence of cardiovascular risk factors and may be at risk for sleep-disordered breathing (SDB). An understanding of SDB among these populations is needed given evidence that SDB increases cardiovascular risk. OBJECTIVES To quantify SDB prevalence in the U.S. Hispanic/Latino population and its association with symptoms, risk factors, diabetes, and hypertension; and to explore variation by sex and Hispanic/Latino background. METHODS Cross-sectional analysis from the baseline examination of the Hispanic Community Health Study/Study of Latinos. MEASUREMENTS AND MAIN RESULTS The apnea-hypopnea index (AHI) was derived from standardized sleep tests; diabetes and hypertension were based on measurement and history. The sample of 14,440 individuals had an age-adjusted prevalence of minimal SDB (AHI ≥ 5), moderate SDB (AHI ≥ 15), and severe SDB (AHI ≥ 30) of 25.8, 9.8, and 3.9%, respectively. Only 1.3% of participants reported a sleep apnea diagnosis. Moderate SDB was associated with being male (adjusted odds ratio, 2.7; 95% confidence interval, 2.3-3.1), obese (16.8; 11.6-24.4), and older. SDB was associated with an increased adjusted odds of impaired glucose tolerance (1.7; 1.3-2.1), diabetes (2.3; 1.8-2.9), and hypertension. The association with hypertension varied across background groups with the strongest associations among individuals of Puerto Rican and Central American background. CONCLUSIONS SDB is prevalent in U.S. Latinos but rarely associated with a clinical diagnosis. Associations with diabetes and hypertension suggest a large burden of disease may be attributed to untreated SDB, supporting the development and evaluation of culturally relevant detection and treatment approaches.

Does obstructive sleep apnea increase hematocrit

This study assessed the relationship between hematocrit levels and severity of obstructive sleep apnea (OSA) and examined how this relationship was affected by the degree of hypoxia as well as by possible confounding factors. Two-hundred sixty three subjects (189 men and 74 women) underwent nocturnal polysomnography with oximetry and had measurements of hematocrit, hemoglobin, white blood cell count, body mass index (BMI), blood pressure (BP), and 24-h urine norepinephrine (NE). Patients with severe OSA [respiratory disturbance index (RDI) >30] had significantly higher hematocrit values than patients with mild to moderate OSA or nonapneic controls (p<0.01). However, only one patient had a hematocrit in the range of clinical polycythemia. Hematocrit levels were significantly correlated with BMI, BP, urinary NE, RDI, percent of time spent at oxygen saturation <90%, and with mean oxygen saturation. Multiple linear regression analysis revealed that mean oxygen saturation, RDI, and percent of time spent at oxygen saturation <90% were significant predictors of hematocrit level, even after controlling for gender, ethnicity, 24-h urine NE, BMI, and BP (p<0.05). The severity of OSA is significantly associated with increased hematocrit, even after controlling for possible confounding variables. However, nocturnal hypoxemia in OSA does not usually lead to clinical polycythemia.

The association between interleukin-6, sleep, and demographic characteristics.

We examined the relationship between the pro-inflammatory cytokine IL-6 and sleep architecture in 70 healthy men and women. Blood was drawn in the early morning for assessment of IL-6 followed by nocturnal sleep monitoring with polysomnography. Sleep records were scored for sleep stages using standard criteria. Morning IL-6 levels were positively correlated with REM latency after sleep onset [rho = .31, p = .01], percent (%) stage 1 sleep [rho = .23, p = .053], % wake after sleep onset (WASO) [rho = .29, p<.05]. IL-6 levels were negatively correlated with sleep efficiency [rho = -.36, p<.01] and slow wave sleep (SWS) [rho = -.26, p<.05]. After controlling for demographic variables including race, gender, age, and BMI, multiple hierarchical regression analyses revealed that morning IL-6 levels accounted for a significant portion of the variance of REM latency (p<.01), sleep efficiency (p<.01), and % WASO (p = .01). IL-6 was no longer associated with % stage 1 sleep, SWS, and total sleep time after controlling for the demographic characteristics. These findings suggest that the inflammatory marker IL-6 is associated with sleep quality and that certain individual characteristics such as race, gender, and age modify that relationship. Higher IL-6 levels were associated with lower quality of sleep among healthy asymptomatic men and women.

Continuous positive airway pressure deepens sleep in patients with Alzheimer's disease and obstructive sleep apnea.

OBJECTIVE Patients with Alzheimers disease (AD) and obstructive sleep apnea (OSA) experience disrupted sleep. This study examined the effect of continuous positive airway pressure (CPAP) on sleep parameters in AD patients with OSA. METHODS A randomized placebo-controlled trial of 3 weeks of therapeutic CPAP (tCPAP) vs. 3 weeks placebo CPAP (pCPAP) followed by 3 weeks tCPAP in patients with AD and OSA. Polysomnography data from screening after one night and after 3 weeks of treatment were analyzed. Records were scored for percent of each sleep stage, total sleep time (TST), sleep efficiency (SE), sleep period (SP), time in bed (TIB), sleep onset (SO), wake time after sleep onset (WASO), and arousals. A randomized design comparing one night of pCPAP to tCPAP and a paired analysis combining 3 weeks of tCPAP were performed. RESULTS Fifty-two participants (mean age=77.8 years, SD=7.3) with AD and OSA were included. After one treatment night, the tCPAP group had significantly less % Stage 1 (p=0.04) and more % Stage 2 sleep (p=0.02) when compared to the pCPAP group. In the paired analysis, 3 weeks of tCPAP resulted in significant decreases in WASO (p=0.005), % Stage 1 (p=0.001), arousals (p=0.005), and an increase in % Stage 3 (p=0.006). CONCLUSION In mild to moderate AD patients with OSA, the use of tCPAP resulted in deeper sleep after just one night, with improvements maintained for 3 weeks.