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Sleep Apnea

General Information

NEWS:

Sleep apnea linked to silent strokes, small lesions in brain

Sleep disordered breathing is associated with an increased risk of cancer mortality

Study links sleep apnea and sudden deafness

ARTICLES:

A Visual Guide to Sleep Disorders

Obstructive Sleep Apnea “Using their model the researchers induced 30 apneas (10 seconds duration) per hour in animals for 8-hours during the sleep cycle for up to one month. After one month of apnea, cerebral vessel dilatory function was reduced by up to 22 percent. This finding correlates with studies that show similar cell dysfunction in arteries and an increased risk of stroke in OSA patients. Damage to the vascular wall in brain arteries could be a factor predisposing an individual with OSA to stroke.”

Obstructive Sleep Apnea

Polysomnography

Sleep Apnea Guide

Sleeping Positions Research Summary (24 Studies) “While most internet sources, including official medical websites, recommend sleeping on one's back (as a best sleep position), medical evidence (all 24 published studies) revealed worsening of the following health problems due to sleeping on one's back (supine sleep): … Snoring, hypopneas and apneas (Jan et al, 1994) Stroke patients with sleep apnea (Brown et al, 1998) Stroke (elderly patients) (Schubert & Héraud, 1994) …Even in normal subjects, variety of adverse effects is normal, and most people can testify that mornings are the time of their health misery. Blood gases (arterial CO2 and O2 saturation) depend on our automatic breathing patterns. In several above studies the researchers measured blood oxygen saturation. These studies are marked with "*" sign above. It was found in all of them that the supine sleeping position produced the worst blood oxygenation in comparison with any other body postures (Fast & Hertz, 1992; Hjalmarsen & Hykkerud, 2008; Szollosi et al, 2006; Trakada et al, 2003; Brander et al, 1993).

Snoring Versus Obstructive Sleep Apnea: A Case Report

Sleep apnea

The Best Sleep Positions

JOURNAL ARTICLES:

At 68 yrs, unrecognized sleep apnoea is associated with elevated ambulatory blood pressure. (Eur Respir J. 2012)

Cardiovascular and metabolic effects of CPAP in obese males with OSA (Eur Respir J. 2007) “These data suggest that, while a reduction in sympathetic activation is likely when obstructive sleep apnoea is treated 37 and helps explain the altered cardiovascular responses, this is not sufficient to modify the degree of insulin resistance in the patients over this time frame and other mechanisms predominate to drive insulin resistance in these circumstances. The present results emphasise the need to offer multiple modalities of treatment to obese obstructive sleep apnoea patients if their cardiovascular risk profile is to be successfully modified.”

Case-control study of 24 hour ambulatory blood pressure in patients with obstructive sleep apnoea and normal matched control subjects (Thorax 2000)

Central sleep apnea is associated with increased risk of ischemic stroke in the elderly (Acta Neurologica Scandinavica 2012)

Day–Night Pattern of Sudden Death in Obstructive Sleep Apnea (NEJM 2005) “This study shows that persons with obstructive sleep apnea have a significantly increased risk of sudden death from cardiac causes during the sleeping hours, which is in striking contrast to the nadir of sudden death from cardiac causes during this time in persons without obstructive sleep apnea and in the general population. In the analysis of sudden death from cardiac causes from midnight to 6 a.m. (which allows for the comparison of our results to results of large studies in the general population) and in the analysis of sudden death from cardiac causes from 10 p.m. to 6 a.m. (which is more relevant to sleep-related pathophysiology), a marked nocturnal peak in sudden death from cardiac causes was observed in persons with obstructive sleep apnea. In more than half of persons with obstructive sleep apnea, sudden death from cardiac causes occurred between 10 p.m. and 6 a.m. By contrast, the persons without obstructive sleep apnea in our study sample had a day–night pattern of sudden death from cardiac causes very similar to that in the general population, with a peak in sudden death from cardiac causes from 6 a.m. to noon. … Obstructive sleep apnea is characterized by repetitive collapse of the pharyngeal airway during sleep, resulting in complete or partial cessation of airflow, sometimes hundreds of times nightly. The resultant hypoxemia can lead to nocturnal cardiac ischemia21 and ventricular arrhythmias.22 Apneic episodes elicit increased sympathetic activity,10 blood-pressure elevations,10 and platelet aggregation.23 Obstructive sleep apnea is associated with abnormalities in cardiac autonomic and electrophysiological factors, including heart rate variability,24 the duration of the QT interval,25 baroreflex function, and chemoreceptor sensitivity.26 Serious and potentially fatal arrhythmias occur during sleep in patients with obstructive sleep apnea12-14,22,27-31 and are attenuated by effective treatment.14,29-32 Thus, multiple pathophysiological mechanisms occur during sleep in persons with obstructive sleep apnea and may explain an increased risk of nocturnal sudden death from cardiac causes.”

Evening-to-morning blood pressure variations in snoring patients with and without obstructive sleep apnea. (Chest 1992)

Markers of Sleep-Disordered Breathing and Metabolic Syndrome in a Multiethnic Sample of US Adults: Results from the National Health and Nutrition Examination Survey 2005–2008 (Cardiology Research and Practice 2012) “Metabolic syndrome was defined as the presence of =3 of the following components: (1) abdominal obesity, (2) elevated blood triglycerides, (3) low HDL cholesterol, (4) high BP, and (5) hyperglycemia. SDB severity was defined based on an additive summary score including sleep duration, snoring, snorting, and daytime sleepiness. We found that short sleep duration, snoring, snorting, daytime sleepiness and the summary SDB score were significantly associated with metabolic syndrome independent of potential confounders.”

Non drowsy obstructive sleep apnea as a potential cause of resistant hypertension: a case report (BMC Pulmonary Medicine 2012)

Obstructive sleep apnea. (Neurol Int. 2011) “An epidemiological review by Young et al. estimates that 1 in 5 adults has at least mild OSA and 1 in 15 adults has at least moderate OSA.6 Sleep apnea can affect anyone at any age, even children.7,8 OSA is becoming increasingly prevalent. However, because of the lack of awareness by the public and health-care professionals, the vast majority remain undiagnosed and untreated. Data from the Wisconsin sleep cohort study of patients estimate that 93% of women and 82% of men with moderate-to-severe sleep apnea were undiagnosed.9 A follow-up publication from the Wisconsin Cohort Study five years later indicated that the prevalence of OSA in people aged 30–60 years was 9–24% for men and 4–9% for women.10,11 Primary risk factors for OSA include the male gender, those over age 40, overweight persons or recent weight gain, and persons with a large neck size or small chin/jaw (Table 1).12 … The American Academy of Sleep Medicine (AASM) defines an apnea as a cessation in airflow lasting at least 10 sec; apneic episodes can last anywhere from 10 sec to min, and may occur multiple times per hour.46 Hypopnea is defined as a recognizable transient reduction (but not complete cessation) of breathing for at least10 sec. This differs from apnea in that there remains some flow of air. In the context of sleep disorders, a hypopnea event is only considered to be clinically significant if there is a 30% or more reduction in flow with an associated 4% or greater desaturation in O2 level, lasting for 10 seconds or longer, or if it is associated with an arousal or fragmentation of sleep. Apneas and hypopneas are both considered in assessing the severity of a person's sleep disorder.47 … Hypertension that is primarily caused by OSA (in contrast to essential hypertension) is distinctive in that the blood pressure does not drop significantly when the individual is sleeping.59 OSA that remains untreated can also have a negative effect on memory. Research has recently shown that individuals with OSA have mammillary bodies that were nearly 20 percent smaller on MRI.60 This decreased tissue mass may be related to the memory problems seen in chronic OSA.”

Obstructive Sleep Apnea and Atrial Fibrillation: A Call for Increased Awareness and Effective Management (American Journal of Therapeutics 2012)

Obstructive Sleep Apnea and Morning Blood Pressure Surge in Never Treated Hypertensive Patients: Pp.14.01 (Journal of Hypertension 2010)

Obstructive sleep apnea and the risk of autoimmune diseases: A longitudinal population-based study. (Sleep Med. 2012)

Obstructive sleep apnea linked to wake-up strokes. (J Neurol. 2012)

Obstructive Sleep Apnea Severity Correlates with Cellular and Plasma Oxidative Stress Parameters and Affective Symptoms. (J Mol Neurosci. 2012)

Sleep apnea and glucose metabolism - a long-term follow-up in a community-based sample. (Chest. 2012) “SDB is independently related to the development of insulin resistance and thereby the risk of manifest diabetes mellitus.”

Sleep apnea is related to the atherogenic phenotype, lipoprotein subclass B. (J Clin Sleep Med. 2012)

Sleep apnoea attenuates the effects of a lifestyle intervention programme in men with visceral obesity. ( Thorax. 2012)

Sleep Disordered Breathing and Depression among U.S. Adults: National Health and Nutrition Examination Survey, 2005-2008. (Sleep. 2012)

Sleep-Disordered Breathing in a Population-Based Cohort: Behavioral Outcomes at 4 and 7 Years (Pediatrics 2012)

The relation of serum 25-hydroxyvitamin-D levels with severity of obstructive sleep apnea and glucose metabolism abnormalities. (Endocrine. 2012) “Vitamin D deficiency may play a role and/or worsen OSA's adverse outcomes on glucose metabolism. OSA patients may be considered for supplementation treatment which was shown to ameliorate abnormal glucose metabolism and inflammation.”

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