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1 pite falling TP EMG and obstructive apnea or hypopnea.
2 esponsible for the development of apneas and hypopneas.
3 uctive, central, and mixed apnea, as well as hypopneas.
4 er, the hourly rate of episodes of apnea and hypopnea (36 +/- 10 versus 47 +/- 21), episodes of arous
5 he mean (+/- SD) hourly episodes of apnea or hypopnea (36 +/- 25 and 20 +/- 27; P = 0.015), the preva
6 re 40 patients without (hourly rate of apnea/hypopnea, 4 +/- 4; group 1) and 41 patients with (51% of
9 nd fragmentation; standard measures of apnea/hypopnea and periodic leg movement; and results of the m
10 reduced the number of episodes of apnea and hypopnea and the duration of arterial oxyhemoglobin desa
12 king systems, but the residual events (apnea/hypopnea) and leak data are not as easy to interpret as
13 isturbance index (RDI(Total), sum of apneas, hypopnea, and flow limitation events) of 18 events/h was
16 er design to determine whether apneas and/or hypopneas are temporally associated with episodes of par
17 In contrast, nocturnal rates of apneas and hypopneas, as well as minimal oxygen saturation, did not
18 h percentage of sleep time (>7%) in apnea or hypopnea (both measures of disordered breathing) were as
19 a (OSA) is characterized by repetitive apnea-hypopnea cycles during sleep associated with oxygen desa
20 TI (10 and 15 L/min), obstructive apneas and hypopneas decreased but periodic laryngeal obstructions
21 apnea defined as a cessation of airflow and hypopnea defined as a > or = 30% reduction in airflow or
25 t Anxiety Scale) and the number of apnea and hypopnea events per hour of sleep (AHI), but were associ
26 was indicated by the frequency of apnea and hypopnea events per hour of sleep, measured by in-labora
27 opause; odds ratios for 15 or more apnea and hypopnea events per hour were 1.1 (0.5, 2.2) with perime
28 confounding factors, for 5 or more apnea and hypopnea events per hour were 1.2 (0.7, 2.2) with perime
29 -hypopnea index (AHI; the number of apnea or hypopnea events per hour, with a score of >/=15 indicati
31 index, and the fraction of events that were hypopneas (Fhypopneas) were independent predictors of th
32 ived from combinations of conventional apnea/hypopnea, flow limitation events (transient elevated upp
35 t, for clinically defined sleep apnea (apnea/hypopnea index > or = 10 and daytime symptoms), men had
36 lity of life in 122 patients with SDB (apnea-hypopnea index > or = 5 events/hour), this study found t
37 polysomnography between 1992 and 2004 (apnea-hypopnea index > or =15) who subsequently underwent a PC
38 eight/obese matched patients with OSA (apnea-hypopnea index >/= 15 events per hour) and 11 normal-wei
41 -to-severe sleep-disordered breathing (apnea-hypopnea index >/=15%) was significantly higher in parti
42 with newly revascularized CAD and OSA (apnea-hypopnea index >/=15/h) without daytime sleepiness (Epwo
43 aroxysmal AF (43 with >/=moderate OSA [apnea-hypopnea index >/=15] and 43 without OSA [apnea-hypopnea
44 predicted by age >60 years (HR: 5.53), apnea-hypopnea index >20 (HR: 1.60), mean nocturnal O2sat <93%
45 erweight/obese subjects without apnea (apnea-hypopnea index < 15 events per hour) with 25 overweight/
46 normal subjects (n = 15) without SDB (apnea-hypopnea index < 5 events/hour) recruited from the gener
48 opnea index >/=15] and 43 without OSA [apnea-hypopnea index <5]), right atrial and left atrial voltag
49 ragmentation, all participants with an apnea-hypopnea index (AHI) > or = 1 were analyzed separately.
52 table monitors, or association between apnea-hypopnea index (AHI) and health outcomes among community
58 for all-cause mortality, with FEV1 and apnea-hypopnea index (AHI) as the primary exposure indicators
60 te to severe SDB, defined as having an Apnea-Hypopnea Index (AHI) greater than 15 as assessed by poly
61 n fully adjusted models, patients with apnea-hypopnea index (AHI) greater than 30 had a 30% higher ha
63 on a nondialysis day, subjects with an apnea-hypopnea index (AHI) greater than or equal to 20 had flu
64 nce of periodontal disease between the apnea-hypopnea index (AHI) groups, with a negligible Spearman
65 ation of head and facial form with the apnea hypopnea index (AHI) in 364 white individuals and 165 Af
70 r ejection fraction of 45% or less, an apnea-hypopnea index (AHI) of 15 or more events (occurrences o
71 A total of 14.7% of subjects with an apnea-hypopnea index (AHI) of 15 or more had a diagnosis of di
73 The prevalence varies based on the apnea-hypopnea index (AHI) threshold used for the evaluation (
74 olution of symptoms and a reduction in Apnea/Hypopnea Index (AHI) to < 5/h, and partial response (PR)
77 OSA, physiological data including the apnea-hypopnea index (AHI), and nocturnal oxygen saturation (O
78 have variable success at reducing the apnea-hypopnea index (AHI), and predicting responders is chall
79 ith hsCRP and MRP 8/14 levels and with apnea-hypopnea index (AHI), BMI z score, and apolipoprotein B
80 ur main exposures were the obstructive apnea-hypopnea index (AHI), central apnea index (CAI >/= 5), a
81 o four severity groups on the basis of apnea-hypopnea index (AHI), followed by comparisons of cogniti
83 associated with a 55% reduction in the apnea-hypopnea index (AHI), which decreased from a preflight v
84 rdered breathing was quantified by the apnea-hypopnea index (AHI)-the average number of apneas and hy
87 divided into 3 sub-groups based on the apnea/hypopnea index (AHI): mild, moderate, or severe OSA.
91 The primary outcome measures were the apnea-hypopnea index (AHI; the number of apnea or hypopnea eve
92 channel home polysomnography, were the apnea-hypopnea index (average number of apneas/hypopneas per h
93 ea (OR, 6.31; 95% CI, 1.94-20.51), and apnea-hypopnea index (OR, 1.22; 95% CI, 1.08-1.39 [per 5-unit
94 iated with significant improvements in apnea-hypopnea index (P < 0.001); microarousal index (P = 0.00
95 y with DeltaNC (r=-0.755, P<0.001) and apnea-hypopnea index (r=-0.765, P<0.001), it did not in women.
97 n diffusivity correlated with a higher apnea hypopnea index (Spearman's r = -0.50, p = 0.008) and a g
98 isordered breathing, as defined by the apnea-hypopnea index (the number of episodes of apnea and hypo
99 le) with Cheyne-Stokes breathing (mean apnea-hypopnea index 19.8 [SD 2.6] and stable symptomatic chro
100 leep laboratory and clinical criteria (apnea/hypopnea index [AHI] > or = 10 and the presence of dayti
102 he 24-h prevalence of predominant CAs (apnea/hypopnea index [AHI] >/=5 events/h, with CA of >50%) was
103 e new outpatients diagnosed with SAHS (apnea/hypopnea index [AHI] >or= 5/hour, and >or= 2 symptoms in
105 cal responses (>/=50% reduction in the apnea-hypopnea index [AHI] and <10 events/hour) in patients wi
106 ipants were identified as free of OSA (apnea-hypopnea index [AHI] of <5 events/h and not treated) by
107 1.00 to 1.21] per 10-unit increase in apnea-hypopnea index [AHI]) but not in older men or in women o
108 126 patients with moderate-severe OSA (apnea hypopnea index [AHI], 25.6 [SD 12.3]) were randomly assi
109 patients (55 males, 13 females; median apnea-hypopnea index [AHI], 35) not receiving hypotensive medi
110 We examined 55 sleep apnea probands (apnea-hypopnea index [AHI]: 43.2 +/- 26.3 events/h), 55 proban
111 tal of 25 adults with positional OSAS (apnea-hypopnea index [AHI]supine:AHInon-supine >/= 2) were pro
112 each interval, we assessed the median apnea-hypopnea index and the relative risk of sudden death fro
113 -year follow-up study according to the apnea-hypopnea index at base line were estimated after adjustm
115 relation of incident CVD to change in apnea-hypopnea index between the 2 polysomnograms was tested w
117 causes during other intervals, and the apnea-hypopnea index correlated directly with the relative ris
118 Mean number of events measured by the apnea-hypopnea index decreased from 35.7/h to 2.1/h at 6 month
119 pothesis, we correlated loop gain with apnea-hypopnea index during supine, nonrapid eye movement slee
120 ation of all children with obstructive apnea-hypopnea index greater than 5/hour total sleep time in a
121 non-REM sleep was quantified using the apnea-hypopnea index in REM (AHIREM) and non-REM sleep (AHINRE
122 lation was found between loop gain and apnea-hypopnea index in the atmospheric group only (r = 0.88,
125 lative to the reference category of an apnea-hypopnea index of 0 events per hour at base line, the od
126 idence interval, 1.13 to 1.78) with an apnea-hypopnea index of 0.1 to 4.9 events per hour at base lin
127 sted rate ratio [caffeine/placebo] for apnea-hypopnea index of 0.89 [95% CI = 0.55-1.43]; P = 0.63).
128 disordered breathing was defined as an apnea-hypopnea index of 15 or more events per hour of sleep.
129 valence of sleep-disordered breathing (apnea-hypopnea index of 15 or more) among hormone users (61 of
133 tive patients were enrolled who had an apnea-hypopnea index of 20 h(-1) or greater and an Epworth Sle
134 e sleep apnea syndrome was based on an apnea-hypopnea index of 5 or higher (five or more events per h
135 idence interval, 1.29 to 3.17) with an apnea-hypopnea index of 5.0 to 14.9 events per hour, and 2.89
136 ore events per hour); patients with an apnea-hypopnea index of less than 5 served as the comparison g
140 t to 6 a.m. had a significantly higher apnea-hypopnea index than those with sudden death from cardiac
142 90 m than placebo and autoCPAP: median apnea/hypopnea index was 5.8 events per hour (5.8/h) (IQR, 3.0
146 (1,839 in fully adjusted models), the apnea-hypopnea index was used to classify OSA as none (0-4.9/h
147 rth Sleepiness Scale score >10) and an apnea-hypopnea index with 3% desaturation and from 5 to 30 eve
148 pneas and hypopneas per hour of sleep (apnea-hypopnea index) was determined by unattended, single-nig
149 ath, sleep study measures (such as the Apnea-Hypopnea Index), measures of cardiovascular status (such
151 ss: severe sleep-disordered breathing (apnea-hypopnea index, >30 episodes/hr), self-report of poor sl
152 to each criterion that was satisfied: (apnea-hypopnea index, <30 events per hour) + (nadir oxygen sat
153 Seventy-one subjects (ages, 55-76 yr; apnea-hypopnea index, 0.2-96.6 events/h) were evaluated by mag
154 sue structures in 48 control subjects (apnea-hypopnea index, 2.0 +/- 1.6 events/hour) and 48 patients
155 e recruited 30 obese control subjects (apnea-hypopnea index, 4.7 +/- 3.1 events per hour) and 72 obes
156 [10] yr; median [interquartile range] apnea-hypopnea index, 41 [35-53]; mean [SD] Epworth sleepiness
164 Cheyne-Stokes respiration, obstructive apnea-hypopnea index, and percentage of sleep time with less t
165 1765, GPR83, P = 1.90 x 10(-8) for the apnea-hypopnea index, and rs35424364; C6ORF183/CCDC162P, P = 4
166 uration as measured by pulse oximetry, apnea-hypopnea index, and the fraction of events that were hyp
168 metaanalyzed for association with the apnea-hypopnea index, average oxygen saturation during sleep,
169 s assessed for baseline sleep indices: apnea-hypopnea index, central sleep apnea (central apnea index
171 to severe sleep-disordered breathing (apnea-hypopnea index, measured as events/hour, >/=15) are 10%
172 es focused on traits defined using the apnea-hypopnea index, which contains limited information on po
181 tion (SaO2); right putamen tCho/Cr and apnea hypopnea index; right putamen GABA/Cr and baseline SaO2;
182 re nocturnal oxygen saturation and the apnea/hypopnea index; secondary outcomes were sleep structure,
183 sleep apnea characterized by high apnea and hypopnea indices during rapid eye movement (REM) sleep.
194 eases in the number of episodes of apnea and hypopnea per hour (18 +/- 17, vs. 37 +/- 23 with placebo
199 our (25.1 versus 17.1; P < 0.0001) and apnea-hypopneas per hour (27.2 versus 15.2; P < 0.0001) and gr
201 graphy to assess the frequency of apneas and hypopneas per hour of sleep (apnea-hypopnea index, AHI).
202 ratory disturbance indices (number of apneas/hypopneas per hour of sleep) corrected for normal increa
203 ea index (AHI; average number of apneas plus hypopneas per hour of sleep), systolic/diastolic hyperte
205 (RDI), defined as the number of apneas plus hypopneas per hour of sleep, measured during in-home pol
206 (RDI), defined as the number of apneas plus hypopneas per hour of sleep, was measured during in-home
207 ndex (AHI, the average number of apneas plus hypopneas per hour of sleep, with apnea defined as a ces
210 nea-hypopnea index (average number of apneas/hypopneas per hour) and the hypoxemia index (percentage
211 f 15 or more events (occurrences of apnea or hypopnea) per hour, and a predominance of central events
212 uctive airways disease (OAD) and sleep apnea-hypopnea (SAH) nor the sleep consequences of each disord
214 ice in patients with obstructive sleep apnea-hypopnea syndrome (OSAHS) who require higher CPAP (10 cm
216 Around 50% of patients with the sleep apnea/hypopnea syndrome (SAHS) are not obese: body mass index
217 is increasing evidence that the sleep apnea-hypopnea syndrome (SAHS) is associated with daytime hype
218 as performed with 46 adults with sleep apnea-hypopnea syndrome (SAHS) to determine the effect of ther
219 ted for treatment of snoring and sleep apnea/hypopnea syndrome (SAHS), but often it does not effect a
222 ess in patients with obstructive sleep apnea/hypopnea syndrome who are regular users of nasal continu
224 O2)) during spontaneous breathing, the apnea-hypopnea threshold for CO2, and then calculated the diff
226 ons were among RDIs that required apneas and hypopneas to be associated with some level of desaturati
227 starting bronchoscopy when hypoventilation (hypopnea, two successive breaths of at least 50% reducti
228 defined by various definitions of apneas and hypopneas were assessed in 5,046 participants in the Sle
229 ET(CO2) thereby protecting against apnea and hypopnea, whereas reduced ventilatory drive and hypovent
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