Investigating the relationship between stroke and obstructive sleep apnea.
Large cross-sectional studies have shown associations between OSA and prevalent stroke with a dose response relationship according to severity of AHI [9, 10]. ORIGINAL INVESTIGATION. Obstructive Background: Sleep apnea occurs frequently among pa- tients with Conclusions: Patients with stroke and obstructive sleep apnea have an .. Three previous studies have investigated the relation-. Patients with OSA not only have an increased risk of stroke, but also a higher .. Investigating the relationship between stroke and obstructive sleep apnea.
Snoring was considered habitual if it was reported to occur often or always. An overnight polysomnography was performed in all patients. Sleep study Overnight polysomnography PSG was performed in all patients by a computerized system Somnostar alpha; Sensormedics, USA that included the following variables: Chest and abdominal efforts 2 channels were recorded using inductive plethysmography, and arterial oxyhemoglobin saturation SaO2: The diagnosis criteria for central sleep apnea syndrome is five or more central apneas per hour of sleep.
Investigating the relationship between stroke and obstructive sleep apnea. - Semantic Scholar
Patients with sleep disorders other than OSA, such as upper airway resistance syndrome, periodic leg movement syndrome, or narcolepsy, were excluded. The therapy and possible side effects were explained to the patients, and in patients who agreed to use CPAP treatment, the appropriate level of CPAP for each patient was determined during an all-night CPAP pressure determination study.
A polysomnographic study was performed with the same setup as the diagnostic study, except that nasal CPAP was applied during sleep. We measured compliance by the mean rate of CPAP use hours per day.
The differences between groups were assessed using the Fisher exact test for categorical variables and Mann-Whitney U test for the ordinal variables. The mean total counts of apneas-hypopneas were There were also no statistically significant differences in the percent of total sleep time in stage 2, stage 3, stage 4 non-rapid eye movement NREMand stage rapid eye movement REM sleep.
The OSA frequency of This frequency was also above the range of The discrepancy between the reported frequencies may have resulted from differences in the intervals between the onset of stroke and sleep recordings, stroke subtypes, sleep study methods, and sleep apnea definitions between these studies. Additionally, not all of these studies used in-laboratory comprehensive PSG recordings, which is the accepted test for diagnosing and determining the severity and treatment of OSA.
Another possible explanation for why our result is closer to the upper limit of reported frequencies though all our patients were in subaute or chronic stages of ischemic stroke, the sensitive detection methods and lower diagnostic criteria may have identified more mild cases of OSA. Central apneas are also observed in patients with stroke.
Central periodic breathing CPB most frequently results from congestive heart failure and is characterized by cyclic fluctuations in breathing drive, such as hyperpneas alternating with apneas or hypopneas in a gradual waxing and waning fashion.
Investigating the relationship between stroke and obstructive sleep apnea.
CPB may also develop in stroke patients without cardiopulmonary disease and disturbed consciousness. During recovery after stroke, the incidence of central apneas diminishes, whereas obstructive apneas remain at a similar level. Obstructive apneas were the most frequent apnea-related episodes in both stroke and TIA patients Central apneas amounted to In our study, all patients were ischemic stroke patients, and the mean time elapsed from the stroke onset was 11 months minimum 6 weeksrepresenting the stable phase of stroke.
Moreover, the study presumed that hemorrhagic strokes lead more often to central apneas. In contrast, OSA itself is a probable risk factor for ischemic stroke.
Apnea-related episodes lower the SaO2 during sleep, and OSA patients spent more time in the wake and transition stages between awake and sleep during the night due to apneas and arousals.
Sleep efficiency was also decreased in OSA patients, though we did not demonstrate a statistically significant difference. Although not statistically significant, the presence of habitual snoring and other clinical signs of OSA were also higher in OSA patients in accordance with the literature.
However, since the in-laboratory comprehensive PSG recordings technique used in this study was detailed, not readily available, and expensive, we had to conduct our study with a limited number of patients. These factors also contributed to the absence of an appropriate control group from the population, which was a limitation of our study. Since the history of habitual snoring and other clinical signs of OSA were present before stroke, we can presume that OSA might be a preceding risk factor for stroke, in accordance with the opinion that OSA constitutes a significant risk for cardiovascular diseases including stroke.
Although it is impossible to draw a conclusion about the effectiveness of CPAP with two patients, we wished to share the results of these patients. In one of the patients, sleep efficiency was obviously increased, and the percentage of total sleep time in the wake stage and stage 1 NREM sleep were decreased with the CPAP treatment. However, in the other patient, the percent of total sleep time in stage 1, stage 2, and deep sleep decreased, while the percent of total sleep time in the wake stage and REM sleep increased.
This second patient also experienced decreased sleep efficiency and did not continue the CPAP treatment at home due to the discomfort caused by the device. The obvious improvement in one of the patients confirms the effectiveness and usefulness of CPAP therapy13,14 in stroke patients with OSA.
To conclude, the OSA prevalence was fairly high in our small sample of ischemic stroke patients.
As the diagnosis and treatment of OSA is of particular importance in secondary stroke prevention, we suggest that the clinical assessment of OSA be a part of the evaluation of stroke patients in rehabilitation units. Since CPAP is an effective treatment of OSA and provides clinical improvements in compliant stroke patients, early treatment should be started. Rehabilitation in stroke syndromes. Malhotra A, White DP.
Bassiri AG, Guilleminault C. Clinical features and evaluation of obstructive sleep apnea-hypopnea syndrome. Obstructive sleep apnea syndrome as an uncommon cause of fibromyalgia: The occurrence of sleep-disordered breathing among middle-aged adults. N Engl J Med. Elevation of plasma cytokines in disorders of excessive daytime sleepiness: Role of sleep disturbance and obesity.
J Clin Endocrinol Metab. Fibrinogen levels and obstructive sleep apnea in ischemic stroke. In vivo platelet activation is increased during sleep in patients with obstructive sleep apnea syndrome. Platelet function in patients with obstructive sleep apnoea syndrome.
- Obstructive Sleep Apnea and its Association with Stroke: A Brief Review
Moderate to severe OSA was found to have a hazard ratio of 3. There have been two recent meta-analysis conducted on prospective studies looking at OSA as risk factor for stroke. Until recently, the effects of OSA and its treatment on cardiovascular outcomes in women was unknown. They showed a positive association of OSA and incident stroke in men with a linear trend p In women, however, incident stroke was not associated with obstructive AHI quartiles.
A recent publication followed women specifically for a median of 6. Does the presence of OSA affect stroke outcome? In addition to the growing support for OSA as a causal factor for stroke, there is growing evidence that co-morbid OSA may affect stroke outcomes. The literature suggests that those who have stroke and untreated OSA have higher morbidity and mortality compared to those without OSA. Higher desaturation indices post stroke have been associated with lower functional scores on the Barthal index and higher mortality at one year [ 19 ].
This suggests that OSA may play a role with those outcomes. Other studies have found increased mortality at one and 6 months in those with acute stroke and OSA [ 2021 ]. Similarly, Dyken et al. OSA was found to be an independent risk factor for death after adjusting for other confounding factors such as age, sex, BMI, smoking, hypertensiondiabetes, and atrial fibrillation as well as Barthal index of daily living.
Obstructive Sleep Apnea and its Association with Stroke: A Brief Review | OMICS International
OSA has also been associated with other post stroke outcomes such as length of stay, worse functional outcomes, and recurrent cerebrovascular events. It was found that presence of SBD was associated with higher risk of recurrent cerebrovascular events but interestingly, not mortality or functional outcome at 2 years [ 26 ]. The SDB group was mostly obstructive but those with central sleep apneas were included as well.
Perhaps including patients with CSA and very mild OSA contributed to the lack of significant difference for mortality and functional outcome. Does treatment of OSA affect stroke outcomes? The literature suggests that presence of OSA is associated with increased morbidity and mortality in those with stroke.
One should then ask, "Does treating OSA improve these outcomes? Observational trials suggest that CPAP treatment does improve mortality and decreases rate of recurrent vascular events in those with stroke and OSA compared to those stroke patients with untreated or sub optimally treated OSA.
The same group also looked at risk of recurrent vascular events. They found that at 18 months, those intolerant of CPAP had 5 fold increase risk of new vascular events odd ratio 5. Similarly, at 7 years, they found that those who did not tolerate CPAP had increased risk of new vascular events, particularly ischemic stroke, compared to those who tolerated CPAP [ 29 ].
Randomized controlled trials have suggested benefits of CPAP use in those with ischemic stroke and OSA in terms of functional recovery in the short term but not as robust for long term function. The same holds true for mortality and recurrent vascular events.
It is important to note, though, that the randomized trials have smaller number of subjects with shorter follow up compared to observational trials mentioned above.