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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It has been speculated that because of increased left ventricular (LV) afterload, decreased intrathoracic pressure (ITP) is responsible for decreased cardiac output (CO) in obstructive sleep apnea. If this were true, then obstructive apnea (OA) should have a greater effect on CO than would central apnea (CA). To assess the importance of decreased ITP during OA, we studied seven preinstrumented sedated pigs with OA and simulated CA that were matched for blood gases and apnea periodicities (with 15- or 30-s apnea duration). Compared with OA, CA with 30-s apnea duration produced comparable decreases in heart rate (from baseline to end apnea: OA, 106.6 +/- 4.8 to 93.4 +/- 4.4 beats/min, P < 0.01; and CA, 111.1 +/- 6.2 to 94.0 +/- 5.2 beats/min, P < 0.01) and comparable increases in LV end-diastolic pressure and LV end-diastolic myocardial segment length but greater increases in mean arterial pressure (97.1 +/- 3.7 to 107.7 +/- 4.3 Torr, P < 0.05; and 97.3 +/- 4.8 to 119.3 +/- 7.4 Torr, P < 0.01) and systemic vascular resistance (2,577 +/- 224 to 3,346 +/- 400 dyn . s . cm-5, P < 0.01; and 2,738 +/- 294 to 5,111 +/- 1,181 dyn . s . cm-5, P < 0.01) and greater decreases in CO (3.18 +/- 0.31 to 2.74 +/- 0.26 l/min, P < 0. 05; and 3.07 +/- 0.38 to 2.30 +/- 0.36 l/min, P < 0.01) and stroke volume (32.2 +/- 2.9 to 25.9 +/- 2.4 ml, P < 0.05; and 31.5 +/- 1.9 to 19.8 +/- 3.1 ml, P < 0.01). Only CA increased LV end-systolic myocardial segment length. Similar findings were observed with 15-s apnea duration. We conclude that CA produced greater depression of CO and greater changes of afterload-related LV dysfunction than did OA. Therefore, decreased ITP was not the dominant factor determining LV function with apneas.
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PMID:Comparative hemodynamic effects of periodic obstructive and simulated central apneas in sedated pigs. 926 44

Obstructive sleep apnoea (OSA) produces immediate effects on pulmonary haemodynamics during sleep in all subjects. In addition, in some subjects, OSA is accompanied by chronic abnormalities of the pulmonary circulation. During sleep, pressure in the main pulmonary artery oscillates within each apnoea, in synchrony with intrathoracic pressure changes; in addition, it may increase progressively as a consequence of prolonged severe hypoxaemia. Pulmonary capillary wedge pressure may increase during inspiratory efforts, possibly reflecting a mechanical limitation of left ventricular function. Cardiac output decreases at apnoea resolution as an effect of a decreased right ventricular stroke volume, despite increased cardiac frequency. During wakefulness, postcapillary pulmonary hypertension occurs on exercise in many OSA patients, whilst pulmonary hypertension at rest is precapillary and occurs in patients with an altered daytime respiratory function. Development of right ventricular hypertrophy and a decrease in right ventricular ejection fraction appear to be related to the severity of respiratory alterations during sleep, whilst an overt right heart failure requires an altered daytime respiratory function. Long-term treatment of the obstructive sleep apnoea syndrome is more effective in increasing right ventricular ejection fraction than in decreasing pulmonary artery pressure during wakefulness.
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PMID:Acute and chronic influences of obstructive sleep apnoea on the pulmonary circulation. 927 Feb 54

We examined the hemodynamic responses to normal breathing and induced upper airway obstructions during sleep in a canine model of obstructive sleep apnea. During normal breathing, cardiac output decreased (12.9 +/- 3.5%, P < 0.025) from wakefulness to non-rapid-eye-movement sleep (NREM) but did not change from NREM to rapid-eye-movement (REM) sleep. There was a decrease (P < 0.05) in systemic (7.2 +/- 2.1 mmHg) and pulmonary (2.0 +/- 0.6 mmHg) arterial pressures from wakefulness to NREM sleep. In contrast, systemic (8.1 +/- 1.0 mmHg, P < 0.025), but not pulmonary, arterial pressures decreased from NREM to REM sleep. During repetitive airway obstructions (56.0 +/- 4.7 events/h) in NREM sleep, cardiac output (17.9 +/- 3.1%) and heart rate (16.2 +/- 2.5%) increased (P < 0.05), without a change in stroke volume, compared with normal breathing during NREM sleep. During single obstructive events, left (7.8 +/- 3.0%, P < 0.05) and right (7.1 +/- 0.7%, P < 0.01) ventricular outputs decreased during the apneic period. However, left (20.7 +/- 1.6%, P < 0.01) and right (24.0 +/- 4.2%, P < 0.05) ventricular outputs increased in the post-apneic period because of an increase in heart rate. Thus 1) the systemic, but not the pulmonary, circulation vasodilates during REM sleep with normal breathing; 2) heart rate, rather than stroke volume, is the dominant factor modulating ventricular output in response to apnea; and 3) left and right ventricular outputs oscillate markedly and in phase throughout the apnea cycle.
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PMID:Systemic and pulmonary hemodynamic responses to normal and obstructed breathing during sleep. 937 38

It is unarguable that obstructive sleep apnea (OSA) causes pulsatile hypertension during sleep, but whether there is significant carryover of hypertension into waking hours is far from clear. It is perhaps more useful to consider whether OSA is related to the consequences of hypertension (e.g. stroke), since both nocturnal and daytime hypertension could be responsible for these. Furthermore, the effects of nasal continuous positive airway pressure (CPAP) on hypertension (or its consequences) must be assessed by randomized controlled studies, in exactly the same way as trials on hypotensive drugs would be carried out, before treatment is prescribed for OSA in the absence of any daytime symptoms.
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PMID:Sleep apnea and hypertension--what a mess! 940 30

The Sleep Heart Health Study (SHHS) is a prospective cohort study designed to investigate obstructive sleep apnea (OSA) and other sleep-disordered breathing (SDB) as risk factors for the development of cardiovascular disease. The study is designed to enroll 6,600 adult participants aged 40 years and older who will undergo a home polysomnogram to assess the presence of OSA and other SDB. Participants in SHHS have been recruited from cohort studies in progress. Therefore, SHHS adds the assessment of OSA to the protocols of these studies and will use already collected data on the principal risk factors for cardiovascular disease as well as follow-up and outcome information pertaining to cardiovascular disease. Parent cohort studies and recruitment targets for these cohorts are the following: Atherosclerosis Risk in Communities Study (1,750 participants), Cardiovascular Health Study (1,350 participants), Framingham Heart Study (1,000 participants), Strong Heart Study (600 participants), New York Hypertension Cohorts (1,000 participants), and Tucson Epidemiologic Study of Airways Obstructive Diseases and the Health and Environment Study (900 participants). As part of the parent study follow-up procedures, participants will be surveyed at periodic intervals for the incidence and recurrence of cardiovascular disease events. The study provides sufficient statistical power for assessing OSA and other SDB as risk factors for major cardiovascular events, including myocardial infarction and stroke.
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PMID:The Sleep Heart Health Study: design, rationale, and methods. 949 15

Obstructive sleep apnea (OSA) is a common condition characterized by snoring, recurrent episodes of cessation of breathing (obstructive apneas), disrupted sleep, and excessive daytime somnolence. Associated serious complications are hypertension, increased risk of heart disease, stroke, and increased susceptibility to industrial and motor vehicle accidents. OSA is considerably more common in men than in women. In postmenopausal women, the incidence of OSA increases. These factors suggest that reproductive hormones have a role in the cause of OSA. Treatment with testosterone has been reported to cause OSA in men, and exogenous androgen administration has been reported to cause OSA in one woman. In a review of the English literature, we found no previous reports of OSA that was induced by endogenous testosterone in women. Herein we describe a nonobese 70-year old woman with clinically significant OSA and a benign testosterone-producing ovarian tumor. After successful removal of the tumor, her OSA resolved, and her testosterone level normalized. This unique case supports the theory of male hormonal (testosterone) influence in the OSA syndrome.
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PMID:Obstructive sleep apnea due to endogenous testosterone production in a woman. 951 83

The aim of this article is to present scientific and clinical evidence to support the role of proper head and neck posture in the management of snoring and obstructive sleep apnea. Obstruction of the upper-airway during sleep is a serious medical condition often associated with severe daytime somnolence, morning headache, and a host of cardiopulmonary complications, including but not limited to systemic and pulmonary hypertension, nocturnal cardiac dysrhythmias, myocardial infarction, and stroke. Though anti-snoring pillows are occasionally mentioned in the literature, the role of proper head-neck support during sleep has been largely neglected. In this article the effect of head-neck position on upper-airway obstruction during sleep is discussed from the perspective of both causation and treatment. Based on the evidence presented by the author, it is recommended that the use of cervical-support pillows be considered as an adjunctive treatment modality in patients suffering from snoring and obstructive sleep apnea.
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PMID:Snoring and obstructive sleep apnea: does head posture play a role? 958 90

In sleep-disordered breathing (SDB), the greatest clinical relevance attaches to obstructive sleep apnea on account of its high prevalence and its concomitance with diseases of the cardiovascular system. The high mortality rate of untreated patients is believed to be due to the consequences of these latter diseases. Thus, for example, in addition to systemic arterial hypertension, elevated rates of such disorders as pulmonary hypertension, right heart insufficiency, coronary heart disease, myocardial infarction and stroke are also found. Up until quite recently bradycardic and tachycardic arrhythmias occurring during sleep have been held responsible of the increased mortality rate of these patients. Till the mid-eighties the prevalence of bradycardic arrhythmias was reported to be more than 30%. However, the importance of cardiac arrhythmias has been overestimated, as is supported in particular by current studies on large non-selected samples showing a much lower prevalence of apnea-related arrhythmias. In the differential diagnosis, however, consideration must be given to SDB in patients with nocturnal arrhythmias and heart rate variations.
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PMID:[Cardiac arrhythmias in sleep apnea. Increased cardiovascular risk caused by nocturnal arrhythmia?]. 967 33

Many clinicians are familiar with the clinical symptoms and signs of obstructive sleep apnea (OSA). In its most blatant form, OSA is complete airway obstruction with repetitive, prolonged pauses in breathing, arterial oxyhemoglobin desaturation; followed by arousal with resumption of breathing. Daytime symptoms of this disorder include excessive daytime somnolence, intellectual dysfunction, and cardiovascular effects such as systemic hypertension, angina, myocardial infarction, and stroke. It has been recently recognized that increased pharyngeal resistance with incomplete obstruction can lead to a constellation of symptoms identical to OSA called "upper airway resistance syndrome" (UARS). The typical findings of UARS on sleep study are: (1) repetitive arousals from EEG sleep coinciding with a (2) waxing and waning of the respiratory airflow pattern and (3) increased respiratory effort as measured by esophageal pressure monitoring. There may be few, if any, obvious apneas or hypopneas with desaturation, but snoring may be a very prominent finding. Treatment with nasal positive airway pressure (NCPAP) eliminates the symptoms and confirms the diagnosis. Herein we describe two typical cases of UARS.
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PMID:Upper airway resistance syndrome. 967 67

Most disorders that cause daytime sleepiness can and should be identified and treated. Physicians should recognize that excessive daytime sleepiness is a symptom with serious consequences, including higher risk of accidents and, in the case of obstructive sleep apnea, hypertension, stroke, myocardial infarction, and death. An algorithm for office-based evaluation, indications for further testing, and sleep lab testing methods are described.
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PMID:Daytime sleepiness: when is it normal? When to refer? 983 Jul 88


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