Publications by authors named "Michele Ostrowski"

Objectives: To determine if the large and highly reproducible interindividual differences in arousal intensity and heart rate response to arousal (ΔHR) during non-REM sleep are heritable.

Methods: Polysomnograms of 55 monozygotic (14 male and 41 female pairs) and 36 dizygotic (15 male and 21 female pairs) same-sex twin pairs were analyzed. Arousals were scored using the 2012 American Academy of Sleep Medicine criteria.

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Study Objectives: Arousal intensity and heart rate (HR) response to arousal during polysomnography (PSG) vary considerably between patients with sleep disorders. Our objective was to determine the range of these arousal characteristics in healthy young adults and whether they are consistent on repeated testing.

Design: Post hoc analysis of 56 preexisting PSG files recorded from 28 healthy adults on 2 consecutive nights.

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Study Objectives: To determine if activation of the genioglossus (GG) muscle during obstructive apnea events involves short-term potentiation (STP) and is followed by sustained activation beyond the obstructive phase (after-discharge).

Design: Physiological study.

Setting: Sleep laboratory in a tertiary hospital.

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Study Objectives: To develop and validate an algorithm that provides a continuous estimate of sleep depth from the electroencephalogram (EEG).

Design: Retrospective analysis of polysomnograms.

Setting: Research laboratory.

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Study Objectives: The visual appearance of cortical arousals varies considerably, from barely meeting scoring criteria to very intense arousals. Arousal from sleep is associated with an increase in heart rate (HR). Our objective was to quantify the intensity of arousals in an objective manner using the time and frequency characteristics of the electroencephalogram (EEG) and to determine whether HR response to arousal correlates with arousal intensity so determined.

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Study Objectives: Heart rate increases after obstructive events in patients with obstructive sleep apnea (OSA). This response is generally attributed to arousal from sleep. Opening of the obstructed airway, however, is associated with ventilatory and hemodynamic changes that could result in physiologic responses unrelated to arousal.

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It is generally believed that reflex recruitment of pharyngeal dilator muscles is insufficient to open the airway of obstructive apnea (OSA) patients once it is closed and, therefore, that arousal is required. Yet arousal promotes recurrence of obstruction. There is no information about how much dilator [genioglossus (GG)] activation is required to open the airway (GG Opening Threshold) or about the capacity of reflex mechanisms to increase dilator activity before/without arousal (Non-Arousal Activation).

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Study Objectives: Subjects with a collapsible upper airway must activate their pharyngeal dilators sufficiently in response to increasing chemical drive if they are to maintain airway patency without arousal from sleep. Little is known about the response of pharyngeal dilators to increasing chemical drive in these subjects. We wished to determine, in obstructive apnea patients, the response of the genioglossus to increasing chemical drive and the contribution of mechanoreceptor feedback to this response.

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Study Objectives: Certain respiratory control characteristics determine whether patients with collapsible upper airway develop stable or unstable breathing during sleep, thereby influencing the severity of obstructive apnea (OSA). These include arousal threshold (T(A)), response to transient hypoxia and hypercapnia (Dynamic Response) and the increase in respiratory drive required for arousal-free airway opening (T(ER)). We wished to determine whether these characteristics are inherent or are acquired during untreated OSA.

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The purpose of this study was to assess whether the cerebrovascular response to hypercapnia is blunted in OSA patients and if this could alter the ventilatory response to hypercapnia before and after CPAP therapy. We measured the cerebrovascular, cardiovascular and ventilatory responses to hypercapnia in 8 patients with OSA (apnoea-hypopnoea index=101+/-10) before and after 4-6 weeks of CPAP therapy and in 10 control subjects who did not undergo CPAP therapy. The cerebrovascular and ventilatory responses to hypercapnia were not different between OSA and controls at baseline or follow-up.

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The response to chemical stimuli (chemical responsiveness) and the increases in respiratory drive required for arousal (arousal threshold) and for opening the airway without arousal (effective recruitment threshold) are important determinants of ventilatory instability and, hence, severity of obstructive apnea. We measured these variables in 21 obstructive apnea patients (apnea-hypopnea index 91 +/- 24 h(-1)) while on continuous-positive-airway pressure. During sleep, pressure was intermittently reduced (dial down) to induce severe hypopneas.

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Rationale: The mechanism leading to increased risk of stroke in patients with obstructive sleep apnea (OSA) is unknown. It may occur through alteration in the regulation of cerebral blood flow, reflected in part by the response of the cerebral vasculature to hypoxia. We hypothesized that the cerebrovascular response to hypoxia is reduced in patients with OSA.

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