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Biomedical subjects

David Sparrow

Publications and source records attributed to David Sparrow.

At least 19 recordsLinked to original sources
PubMed2007

Prospective study of posttraumatic stress disorder symptoms and coronary heart disease in the Normative Aging Study.

CONTEXT: Various correlates of posttraumatic stress disorder (PTSD), such as high levels of sympathetic activation and hypothalamic-pituitary-adrenal axis dysregulation, have been linked to arterial damage and coronary heart disease (CHD) risk. While psychological disturbance is frequently found among patients with cardiac disease, whether psychological problems precede or occur as a result of having a potentially fatal disease is not clear. To our knowledge, no prospective studies to date have evaluated whether PTSD is associated with increased risk of CHD. OBJECTIVE: To test the hypothesis that high levels of PTSD symptoms may increase CHD risk, using 2 different measures of PTSD. DESIGN: Prospective cohort study. SETTING: Community-dwelling men from the Greater Boston, Mass, area who served in the military. PARTICIPANTS: Data are from the Veterans Affairs Normative Aging Study. Men who completed either the Mississippi Scale for Combat-Related PTSD in 1990 (n = 1002) or the Keane PTSD scale in 1986 (n = 944) were included in the study. MAIN OUTCOME MEASURE: Incident CHD occurring during follow-up through May 2001. RESULTS: Levels of PTSD symptoms in this cohort were low to moderate. Men with preexisting CHD at baseline were excluded, and PTSD was measured with the Mississippi Scale for Combat-Related PTSD. For each SD increase in symptom level, men had age-adjusted relative risks of 1.26 (95% confidence interval, 1.05-1.51) for nonfatal myocardial infarction and fatal CHD combined and 1.21 (95% confidence interval, 1.05-1.41) for all of the CHD outcomes combined (nonfatal myocardial infarction, fatal CHD, and angina). Findings were replicated using the Keane PTSD scale and somewhat strengthened after controlling for levels of depressive symptoms. CONCLUSIONS: To our knowledge, this is the first study to demonstrate a prospective association between PTSD symptoms and CHD even after controlling for depressive symptoms. These results suggest that a higher level of PTSD symptoms may increase the risk of incident CHD in older men.

Adult↗
PubMed2007

Cumulative lead exposure and cognitive performance among elderly men.

BACKGROUND: Recent evidence suggests that cumulative lead exposure among adults in nonoccupational settings can adversely affect cognitive function. Which cognitive domains are affected has not been explored in detail. METHODS: We used nonlinear spline regressions and linear repeated-measures analysis to assess the association between scores on a battery of cognitive tests over time and both blood and bone lead concentrations in the Normative Aging Study, a cohort of community-dwelling elderly men. Bone lead was measured from 1991 through 1999 with K-shell x-ray fluorescence. A total of 1089 men with a mean (+/-standard deviation) age of 68.7 (+/-7.4) years with blood lead measurements, 761 of whom also had valid bone lead measurements, completed at least one of a battery of cognitive tests. Approximately 3.5 years later, 69% of the men had at least one repeat test. Cognitive testing was performed from 1993 through 2001. RESULTS: On a cross-sectional basis, there was little association between blood or bone lead and cognitive test scores. Change in performance over time on virtually all tests worsened as bone lead increased, with the most robust effects on performance and reaction time scores on visuospatial/visuomotor tests. CONCLUSIONS: Low-level cumulative exposure to lead in nonoccupational settings may adversely affect cognitive function, particularly in the visuospatial/visuomotor domain.

Age Factors↗
PubMed2006

HFE genotype, particulate air pollution, and heart rate variability: a gene-environment interaction.

BACKGROUND: Particulate air pollution has been associated with cardiovascular mortality and morbidity. Transition metals such as iron bound to the particles may be responsible for those associations. The protein product of the hemochromatosis (HFE) gene modulates uptake of iron and divalent cations from pulmonary sources and reduces their toxicity. Two HFE polymorphisms (C282Y and H63D) associated with increased iron uptake may modify the effect of metal-rich particles on the cardiovascular system. METHODS AND RESULTS: We investigated the association between particulate matter < or = 2.5 microm in aerodynamic diameter and heart rate variability in 518 older men from the Normative Aging Study who were examined between November 2000 and December 2004. Linear regression models were fit to evaluate interactions between HFE genotype and particulate matter < or = 2.5 microm in aerodynamic diameter in relation to heart rate variability, controlling for potential confounders. A 10-microg/m3 increase in particulate matter < or = 2.5 microm in aerodynamic diameter during the 48 hours before heart rate variability measurement was associated with a 31.7% (95% CI, 10.3% to 48.1%) decrease in the high-frequency component of heart rate variability in persons with the wild-type genotype, whereas no relationship in the high-frequency component was observed in persons with either HFE variant. The difference in effect of particulate matter < or = 2.5 microm in aerodynamic diameter on the high-frequency component between persons with and without HFE variants was significant (P for interaction=0.02). CONCLUSIONS: The effect of particles on cardiac autonomic function was shielded in subjects with at least 1 copy of an HFE variant compared with wild-type subjects. Transition metals, including iron, bound to ambient particles and the related oxidative stress may play an important role in cardiac toxicity of particles.

Adult↗
PubMed2006

Uric acid and the development of hypertension: the normative aging study.

Experimental evidence supports a causative role for uric acid in the pathogenesis of hypertension. Prospective studies have variably adjusted for relevant confounders and have been of relatively limited duration. We prospectively examined the relationship between uric acid level and the development of hypertension in the Normative Aging Study, a longitudinal cohort of healthy adult men. Of the 2280 initial men in the Normative Aging Study, 2062 had available information for inclusion in the analysis. Cox proportional hazards model was used to examine the relationship between baseline serum uric acid level and the development of hypertension adjusting for age, body mass index, abdominal circumference, smoking, alcohol, plasma triglycerides, total cholesterol, and plasma glucose. A total of 892 men developed hypertension over a mean of 21.5 years of follow-up. Serum uric acid level independently predicted the development of hypertension in age-adjusted (relative risk [RR]: 1.10; 95% CI: 1.06 to 1.15: P<0.001) and multivariable (RR: 1.05; 95% CI: 1.01 to 1.10; P=0.02) models. Among 1277 men at risk for the development of hypertension at the time of their first serum creatinine measurement, 508 (39.8%) developed hypertension over a mean of 10.3+/-5.5 years of follow-up. Additionally adjusting for calculated glomerular filtration rate in this subset, serum uric acid remained associated with the development of hypertension (RR: 1.06; 95% CI: 1.01 to 1.12; P=0.03). The baseline serum uric acid level is a durable marker of risk for the development of hypertension. The association is independent of elements of the metabolic syndrome, alcohol intake, and renal function.

Adult↗
PubMed2006

Inflammatory markers and particulate air pollution: characterizing the pathway to disease.

BACKGROUND: Increased concentrations of particles in air have been related to changes in inflammatory markers that in turn are hypothesized in mediating the particle effects on cardiovascular disease. The present work examined this association in an elderly cohort in the Greater Boston area and addresses the relative role of particles from different sources. METHODS: The study included 710 subjects, active members of the VA Normative Aging Study cohort with measurements of blood markers. Concentrations of particle number (PN), black carbon (BC), fine particulate matter (PM(2.5)), and sulphates were measured at a central site near the examination site. RESULTS: Positive associations were found between traffic-related particles (PN and BC) and inflammatory markers, but only suggestive associations were found with exposures to PM(2.5) and sulphates. The particle effect on the inflammatory markers was greater among subjects older than 78 years and among obese. A suggestion for a greater effect of particles on inflammatory markers among GSTM1-null subjects and non-users of statin drugs was also seen. CONCLUSIONS: The findings of the study support the hypothesis that particles can induce cardiovascular disease through inflammatory pathways, suggestive of a greater toxicity of traffic-related particles.

Adult↗
PubMed2006

Dietary calcium as a potential modifier of the relationship of lead burden to blood pressure.

BACKGROUND: Cumulative lead burden and low dietary calcium have been independently associated with increased risk of hypertension. There is evidence of an interaction between these factors. We tested the hypothesis that dietary calcium intake modifies the relationship between lead burden and hypertension. METHODS: A total of 471 men from the Normative Aging Study were evaluated. Bone lead was assessed using a K-x-ray fluorescence instrument, and information on dietary calcium intake was obtained with a self-administered semiquantitative food frequency questionnaire. RESULTS: We categorized 259 subjects (55%) as having low calcium intake (< or =800 mg/d) and 212 subjects (45%) as having higher calcium intake. In logistic regression models stratified by dietary calcium intake, tibia lead had a weak association with hypertension among subjects with low dietary calcium (odds ratio for 1-standard deviation increase in tibia lead = 1.30; 95% confidence interval = 0.97-1.74) but not in subjects with higher dietary calcium intake. Similarly, blood lead was associated with hypertension only in subjects with low calcium intake. We also found evidence of an interaction between dietary calcium intake and body mass index. CONCLUSIONS: High bone and blood lead increased the likelihood of hypertension, particularly among subjects with low dietary calcium intake. Dietary calcium may be helpful in prevention of hypertension induced by elevated lead burden.

Adult↗
PubMed2006

Shared and unique contributions of anger, anxiety, and depression to coronary heart disease: a prospective study in the normative aging study.

BACKGROUND: Anger, anxiety, and depression have each been identified as risk factors for coronary heart disease (CHD). Whether the apparent risk is a function of unique aspects of each emotion or due to a shared underlying dimension of negative affectivity is unclear. PURPOSE: The goal of this study was to assess shared and unique contributions of anger, anxiety, and depression to incident CHD. METHODS: Data are from the Veterans Administration Normative Aging Study, an ongoing cohort of older men. Measures of anger, anxiety, and depression were obtained from 1,306 men completing the revised Minnesota Multiphasic Personality Inventory in 1986. From these measures we derived three near-orthogonal scales termed iso(lated)-anger, iso-anxiety, and iso-depression and a fourth scale measuring general distress. RESULTS: During an average of 10.9 years of follow-up, 161 cases of incident CHD occurred. When considered individually, iso-anxiety, iso-anger, and shared general distress were each associated with CHD risk. When all emotions were considered simultaneously, only iso-anxiety and shared general distress were associated with incident CHD. CONCLUSIONS: Considering shared versus unique aspects of negative emotions may clarify the nature of their apparent toxicity in relation to CHD risk. General distress shared across negative emotions is an important component in the emotion-CHD relation. Aspects of anxiety may also independently increase CHD risk.

Adult↗
PubMed2006

Low-level lead exposure, metabolic syndrome, and heart rate variability: the VA Normative Aging Study.

BACKGROUND: Altered heart rate variability (HRV), a marker of poor cardiac autonomic function, has been associated with sudden cardiac death and heart failure. OBJECTIVE: We examined the association of low-level lead exposure measured in bone by K-X-ray fluorescence with alterations in HRV, and whether metabolic syndrome (MetS) or its individual components modify those associations. METHODS: HRV measures [power in high-frequency (HFnorm) and low-frequency (LFnorm) in normalized units, and LF/HF] were taken among 413 elderly men from the Normative Aging Study. MetS was defined as subjects having three or more of the following criteria: abdominal obesity, hypertriglyceridemia, low high-density lipoprotein, high blood pressure, and high fasting glucose. RESULTS: Of the subjects, 32% were identified as having MetS. Inverse but nonstatistically significant associations of both tibia and patella lead levels with HFnorm and nonstatistically significant positive relations with LFnorm and LF/HF were found in the entire cohort. There was a graded, statistically significant reduction in HFnorm and increases in LFnorm and LF/HF in association with an increase in patella lead as the number of metabolic abnormalities increased. We also observed that higher patella lead was consistently associated with lower HFnorm and higher LFnorm and LF/HF among subjects with MetS or its individual components. No statistically significant interaction between MetS and tibia lead was observed. CONCLUSION: The results suggest that elderly men with MetS were more susceptible to autonomic dysfunction in association with chronic lead exposure as measured in patella. The modification by MetS is consistent with a role for oxidative stress in lead toxicity on the cardiovascular system.

Adult↗
PubMed2005

The SERPINE2 gene is associated with chronic obstructive pulmonary disease.

Chronic obstructive pulmonary disease (COPD) is a complex human disease likely influenced by multiple genes, cigarette smoking, and gene-by-smoking interactions, but only severe alpha 1-antitrypsin deficiency is a proven genetic risk factor for COPD. Prior linkage analyses in the Boston Early-Onset COPD Study have demonstrated significant linkage to a key intermediate phenotype of COPD on chromosome 2q. We integrated results from murine lung development and human COPD gene-expression microarray studies with human COPD linkage results on chromosome 2q to prioritize candidate-gene selection, thus identifying SERPINE2 as a positional candidate susceptibility gene for COPD. Immunohistochemistry demonstrated expression of serpine2 protein in mouse and human adult lung tissue. In family-based association testing of 127 severe, early-onset COPD pedigrees from the Boston Early-Onset COPD Study, we observed significant association with COPD phenotypes and 18 single-nucleotide polymorphisms (SNPs) in the SERPINE2 gene. Association of five of these SNPs with COPD was replicated in a case-control analysis, with cases from the National Emphysema Treatment Trial and controls from the Normative Aging Study. Family-based and case-control haplotype analyses supported similar regions of association within the SERPINE2 gene. When significantly associated SNPs in these haplotypic regions were included as covariates in linkage models, LOD score attenuation was observed most markedly in a smokers-only linkage model (LOD 4.41, attenuated to 1.74). After the integration of murine and human microarray data to inform candidate-gene selection, we observed significant family-based association and independent replication of association in a case-control study, suggesting that SERPINE2 is a COPD-susceptibility gene and is likely influenced by gene-by-smoking interaction.

Amyloid beta-Protein Precursor↗
PubMed2005

T-bet polymorphisms are associated with asthma and airway hyperresponsiveness.

RATIONALE: T-bet (TBX21 or T-box 21) is a critical regulator of T-helper 1 lineage commitment and IFN-gamma production. Knockout mice lacking T-bet develop airway hyperresponsiveness (AHR) to methacholine, peribronchial eosinophilic and lymphocytic inflammation, and increased type III collagen deposition below the bronchial epithelium basement membrane, reminiscent of both acute and chronic asthma histopathology. Little is known regarding the role of genetic variation surrounding T-bet in the development of human AHR. OBJECTIVES: To assess the relationship between T-bet polymorphisms and asthma-related phenotypes using family-based association. METHODS: Single nucleotide polymorphism discovery was performed by resequencing the T-bet genomic locus in 30 individuals (including 22 patients with asthma). Sixteen variants were genotyped in 580 nuclear families ascertained through offspring with asthma from the Childhood Asthma Management Program clinical trial. Haplotype patterns were determined from this genotype data. Family-based tests of association were performed with asthma, AHR, lung function, total serum immunoglobulin E, and blood eosinophil levels. MAIN RESULTS: We identified 24 variants. Evidence of association was observed between c.-7947 and asthma in white families using both additive (p = 0.02) or dominant models (p = 0.006). c.-7947 and three other variants were also associated with AHR (log-methacholine PC(20), p = 0.02-0.04). Haplotype analysis suggested that an AHR locus is in linkage disequilibrium with variants in the 3'UTR. Evidence of association of AHR with c.-7947, but not with other 3'UTR SNPs, was replicated in an independent cohort of adult males with AHR. CONCLUSIONS: These data suggest that T-bet variation contributes to airway responsiveness in asthma.

Adolescent↗
PubMed2005

Glutathione-S-transferase M1, obesity, statins, and autonomic effects of particles: gene-by-drug-by-environment interaction.

RATIONALE: Air pollution by particulate matter (PM) has been associated with cardiovascular deaths, although the mechanism of action is unclear. One proposed pathway is through disturbances of the autonomic control of the heart. OBJECTIVES: We tested the hypothesis that such disturbances are mediated by PM increasing oxidative stress by examining the association between PM and the high-frequency (HF) component of heart rate variability as modified by the presence or absence of the allele for glutathione-S-transferase M1 (GSTM1) and the use of statins, obesity, high neutrophil counts, higher blood pressure, and older age. METHODS: We examined the association between particles less than 2.5 microM in aerodiameter (PM2.5) and HF in 497 participants in the Normative Aging Study, using linear regression controlling for covariates. MAIN RESULTS: A 10-microg/m3 increase in PM2.5 during the 48 h before HF measurement was associated with a 34% decrease in HF, 95% confidence interval (-9%, -52%), in subjects without the allele, but had no effect in subjects with GSTM1 present. Among GSTM1-null subjects, the use of statins eliminated the effect of PM2.5. Obesity and high neutrophil counts also worsened the PM effects with or without GSTM1. CONCLUSION: The effects of PM2.5 on HF appear to be mediated by reactive oxygen species. This may be a key pathway for the adverse effects of combustion particles.

Age Factors↗
PubMed2005

Lung function in type 2 diabetes: the Normative Aging Study.

BACKGROUND: Cross-sectional studies have noted that subjects with diabetes have lower lung function than non-diabetic subjects. We conducted this analysis to determine whether diabetic subjects have different rates of lung function change compared with non-diabetic subjects. METHODS: We conducted a nested case-control analysis in 352 men who developed diabetes and 352 non-diabetic subjects in a longitudinal observational study of aging in men. We assessed lung function among cases and controls at three time points: Time0, prior to meeting the definition of diabetes; Time1, the point when the definition of diabetes was met; and Time2, the most recent follow-up exam. RESULTS: Cases had lower forced expiratory volume in 1s (FEV1) and forced vital capacity (FVC) at all time points, even with adjustment for age, height, weight, and smoking. In multiple linear regression models adjusting for relevant covariates, there were no differences in rates of FEV1 or FVC change over time between cases and controls. CONCLUSIONS: Men who are predisposed to develop diabetes have decreased lung function many years prior to the diagnosis, compared with men who do not develop diabetes. This decrement in lung function remains after the development of diabetes. We postulate that mechanisms involved in the insulin resistant state contribute to the diminished lung function observed in our subjects.

Adult↗
PubMed2005

Attempted replication of reported chronic obstructive pulmonary disease candidate gene associations.

Case-control studies have successfully identified many significant genetic associations for complex diseases, but lack of replication has been a criticism of case-control genetic association studies in general. We selected 12 candidate genes with reported associations to chronic obstructive pulmonary disease (COPD) and genotyped 29 polymorphisms in a family-based study and in a case-control study. In the Boston Early-Onset COPD Study families, significant associations with quantitative and/or qualitative COPD-related phenotypes were found for the tumor necrosis factor (TNF)-alpha -308G>A promoter polymorphism (P < 0.02), a coding variant in surfactant protein B (SFTPB Thr131Ile) (P = 0.03), and the (GT)(31) allele of the heme oxygenase (HMOX1) promoter short tandem repeat (P = 0.02). In the case-control study, the SFTPB Thr131Ile polymorphism was associated with COPD, but only in the presence of a gene-by-environment interaction term (P = 0.01 for both main effect and interaction). The 30-repeat, but not the 31-repeat, allele of HMOX1 was associated (P = 0.04). The TNF -308G>A polymorphism was not significant. In addition, the microsomal epoxide hydrolase "fast" allele (EPHX1 His139Arg) was significantly associated in the case-control study (P = 0.03). Although some evidence for replication was found for SFTPB and HMOX1, none of the previously published COPD genetic associations was convincingly replicated across both study designs.

Adult↗
PubMed2005

Effects of air pollution on heart rate variability: the VA normative aging study.

Reduced heart rate variability (HRV), a marker of poor cardiac autonomic function, has been associated with air pollution, especially fine particulate matter [< 2.5 microm in aerodynamic diameter (PM2.5)]. We examined the relationship between HRV [standard deviation of normal-to-normal intervals (SDNN), power in high frequency (HF) and low frequency (LF), and LF:HF ratio] and ambient air pollutants in 497 men from the Normative Aging Study in greater Boston, Massachusetts, seen between November 2000 and October 2003. We examined 4-hr, 24-hr, and 48-hr moving averages of air pollution (PM2.5, particle number concentration, black carbon, ozone, nitrogen dioxide, sulfur dioxide, carbon monoxide). Controlling for potential confounders, HF decreased 20.8% [95% confidence interval (CI), 4.6-34.2%] and LF:HF ratio increased 18.6% (95% CI, 4.1-35.2%) per SD (8 microg/m3) increase in 48-hr PM2.5. LF was reduced by 11.5% (95% CI, 0.4-21.3%) per SD (13 ppb) increment in 4-hr O3. The associations between HRV and PM2.5 and O3 were stronger in people with ischemic heart disease (IHD) and hypertension. The associations observed between SDNN and LF and PM2.5 were stronger in people with diabetes. People using calcium-channel blockers and beta-blockers had lower associations between O3 and PM2.5 with LF. No effect modification by other cardiac medications was found. Exposures to PM2.5 and O3 are associated with decreased HRV, and history of IHD, hypertension, and diabetes may confer susceptibility to autonomic dysfunction by air pollution.

Adrenergic beta-Antagonists↗
PubMed2004

Cumulative lead exposure and prospective change in cognition among elderly men: the VA Normative Aging Study.

Lead exposure has been found to affect cognitive function in several different populations. Whether chronic low-level environmental exposure to lead results in cognitive decline among adults has not been examined. The authors assessed the relation between biomarkers of lead exposure and change in Mini-Mental State Examination (MMSE) scores in the Normative Aging Study, a cohort of elderly US men. Bone lead was measured with K-shell x-ray fluorescence. A total of 466 men aged 67.4 (standard deviation, 6.6) years took the MMSE on two occasions that were an average of 3.5 (standard deviation, 1.1) years apart during the period 1993-2001 and had bone lead concentrations measured during the period 1991-2002. A one-interquartile range (20 microg/g of bone mineral) higher patella bone lead concentration was associated with a change in MMSE score of -0.24 (95% confidence interval: -0.44, -0.05) after adjustment for age, education, smoking, alcohol intake, and time between MMSE tests. This effect is approximately equivalent to that of aging 5 years in relation to the baseline MMSE score in study data. The association with tibia lead was weaker and that with blood lead was absent. The data suggest that higher patella bone lead levels, a marker of mobilizable accumulated lead burden, are associated with a steeper decline over time in performance on the MMSE test among nonoccupationally exposed elderly men.

Adult↗
PubMed2004

Accumulated lead exposure and risk of age-related cataract in men.

CONTEXT: Low-level lead exposure may increase the risk for a number of chronic age-related diseases. Several studies have documented the presence of lead in lenses with cataract. The intrusion of lead into the lens may alter lens redox status and cause protein conformational changes that decrease lens transparency. OBJECTIVE: To determine the relationship of cumulative lead exposure with the development of cataract. DESIGN, SETTING, AND PARTICIPANTS: Tibial (cortical) and patellar (trabecular) bone lead levels were measured by K x-ray fluorescence between 1991 and 1999 in a subset of participants in the Normative Aging Study (NAS), a Boston-based longitudinal study of aging in men. Among the first 795 NAS participants to have bone lead levels measured, we reviewed eye examination data (collected routinely every 3-5 years) for the period after the bone lead measurements were taken. We limited the population to men aged 60 years and older who had sufficient eye examination information available (n = 642). Blood lead levels were also measured. MAIN OUTCOME MEASURES: Cataract assessment was done while masked to the lead level results. A participant was considered to have cataract if there was documentation for either eye of cataract surgery or a cataract graded clinically as 3+ or higher on a 4-point scale. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated as estimates of the magnitude and significance of the relationship of lead exposure with cataract, in logistic regression models. RESULTS: The mean age of the study participants was 69 years and cataract was identified in 122 men. The age-adjusted OR (95% CI) for cataract for men in the highest vs lowest quintile of tibia lead level was 2.68 (1.31-5.50). Further adjustment for pack-years of cigarette smoking, diabetes, blood lead levels, and intake of vitamin C, vitamin E, and carotenoids resulted in an OR of 3.19 (95% CI, 1.48-6.90). For patella lead level, there was an increased risk of cataract in the highest vs lowest quintile (OR, 1.88; 95% CI, 0.88-4.02), but the trend was not significant (P = .16). Blood lead levels, more indicative of short-term exposure levels, were not significantly associated with cataract (OR, 0.89; 95% CI, 0.46-1.72; P = .73). CONCLUSIONS: These epidemiological data suggest that accumulated lead exposure, such as that commonly experienced by adults in the United States, may be an important unrecognized risk factor for cataract. This research suggests that reduction of lead exposure could help decrease the global burden of cataract.

Aged↗
PubMed2004

A pilot trial of a telecommunications system in sleep apnea management.

BACKGROUND: Continuous positive airway pressure (CPAP) is an effective therapy for obstructive sleep apnea syndrome (OSAS), although many patients have difficulty adhering to this therapy. The purpose of this study was to investigate the effectiveness of totally automated telephone technology in improving adherence to prescribed CPAP therapy. RESEARCH DESIGN: This pilot study was a randomized clinical trial in 30 patients being started on CPAP therapy for OSAS. Patients were randomly assigned to use of a computer telephone system designed to improve CPAP adherence (telephone-linked communications for CPAP [TLC-CPAP]) in addition to usual care (n = 15) or to usual care alone (n = 15) for a period of 2 months. TLC-CPAP is a computer-based system that monitors patients' self-reported behavior and provides education and reinforcement through a structured dialogue. MEASURES: A sleep symptoms checklist and the Functional Outcomes of Sleep Questionnaire were administered at study entry and at 2-month follow up. Hours of CPAP use at effective mask pressure were measured by the CPAP device, stored in its memory, and retrieved at the 2-month visit. RESULTS: At 2 months, patients randomized to TLC-CPAP had fewer reported sleep-related symptoms (9.4 vs. 13.4, P = 0.047) than those receiving usual care. The average nightly CPAP use in the TLC-CPAP group was 4.4 hours compared with 2.9 hours (P = 0.076) in the usual-care group. CONCLUSIONS: This pilot study suggests that patients with OSAS started on CPAP and a concurrently administered automated education and counseling system had better CPAP adherence and better control of OSAS symptoms.

Adult↗