@article {993, title = {Power spectral analysis of EEG activity during sleep in cigarette smokers.}, journal = {Chest}, volume = {133}, year = {2008}, month = {2008 Feb}, pages = {427-32}, abstract = {

BACKGROUND: Research on the effects of cigarette smoking on sleep architecture is limited. The objective of this investigation was to examine differences in sleep EEG between smokers and nonsmokers.

METHODS: Smokers and nonsmokers who were free of all medical comorbidities were matched on different factors, including age, gender, race, body mass index, and anthropometric measures. Home polysomnography was conducted using a standard recording montage. Sleep architecture was assessed using visual sleep-stage scoring. The discrete fast Fourier transform was used to calculate the EEG power spectrum for the entire night within contiguous 30-s epochs of sleep for the following frequency bandwidths: delta (0.8 to 4.0 Hz); theta (4.1 to 8.0 Hz); alpha (8.1 to 13.0 Hz); and beta (13.1 to 20.0 Hz).

RESULTS: Conventional sleep stages were similar between the two groups. However, spectral analysis of the sleep EEG showed that, compared to nonsmokers, smokers had a lower percentage of EEG power in the delta-bandwidth (59.7\% vs 62.6\%, respectively; p < 0.04) and higher percentage of EEG power in alpha-bandwidth (15.6\% vs 12.5\%, respectively; p < 0.001). Differences in the EEG power spectrum between smokers and nonsmokers were greatest in the early part of the sleep period and decreased toward the end. Subjective complaints of lack of restful sleep were also more prevalent in smokers than in nonsmokers (22.5\% vs 5.0\%, respectively; p < 0.02) and were explained, in part, by the differences in EEG spectral power.

CONCLUSIONS: Cigarette smokers manifest disturbances in the sleep EEG that are not evident in conventional measures of sleep architecture. Nicotine in cigarette smoke and withdrawal from it during sleep may contribute to these changes and the subjective experience of nonrestorative sleep.

}, keywords = {Electroencephalography, Female, Humans, Logistic Models, Male, Middle Aged, Polysomnography, Sleep, Smoking, Spectroscopy, Fourier Transform Infrared}, issn = {0012-3692}, doi = {10.1378/chest.07-1190}, author = {Zhang, Lin and Samet, Jonathan and Caffo, Brian and Bankman, Isaac and Punjabi, Naresh M} } @article {1083, title = {Prospective study of sleep-disordered breathing and hypertension: the Sleep Heart Health Study.}, journal = {Am J Respir Crit Care Med}, volume = {179}, year = {2009}, month = {2009 Jun 15}, pages = {1159-64}, abstract = {

RATIONALE: Cross-sectional epidemiologic studies show an association between sleep-disordered breathing and hypertension, but only one cohort study has examined sleep-disordered breathing as a risk factor for incident hypertension.

OBJECTIVES: To examine whether sleep-disordered breathing increases the risk of incident hypertension among persons 40 years of age and older.

METHODS: In a prospective cohort study, we analyzed data from 2,470 participants who at baseline did not have hypertension, defined as blood pressure of at least 140/90 mm Hg or taking antihypertensive medication. The apnea-hypopnea index (AHI), the number of apneas plus hypopneas per hour of sleep, was measured by overnight in-home polysomnography. We estimated odds ratios for developing hypertension during 5 years of follow-up according to baseline AHI.

MEASUREMENTS AND MAIN RESULTS: The odds ratios for incident hypertension increased with increasing baseline AHI; however, this relationship was attenuated and not statistically significant after adjustment for baseline body-mass index. Although not statistically significant, the observed association between a baseline AHI greater than 30 and future hypertension (odds ratio, 1.51; 95\% confidence interval, 0.93-2.47) does not exclude the possibility of a modest association.

CONCLUSIONS: Among middle-aged and older persons without hypertension, much of the relationship between AHI and risk of incident hypertension was accounted for by obesity. After adjustment for body mass index, the AHI was not a significant predictor of future hypertension, although a modest influence of an AHI greater than 30 on hypertension could not be excluded.

}, keywords = {Adult, Blood Pressure, Confidence Intervals, Cross-Sectional Studies, Female, Follow-Up Studies, Humans, Hypertension, Incidence, Male, Middle Aged, Odds Ratio, Polysomnography, Prognosis, Prospective Studies, Risk Factors, Sleep Apnea Syndromes, Time Factors, United States}, issn = {1535-4970}, doi = {10.1164/rccm.200712-1809OC}, author = {O{\textquoteright}Connor, George T and Caffo, Brian and Newman, Anne B and Quan, Stuart F and Rapoport, David M and Redline, Susan and Resnick, Helaine E and Samet, Jonathan and Shahar, Eyal} }