The Relationship Between Obstructive Sleep Apnea and Ruptured Intracranial Aneurysms

Abstract

Study Objectives:

The role of obstructive sleep apnea (OSA) in the overall outcome of ruptured intracranial aneurysms (RIAs) is unknown. We have investigated the role of OSA in overall outcome of RIAs.

Methods:

Data from 159 consecutive patients were retrospectively reviewed. A chi-square test and regression analysis were performed to determine the significant difference. A value of P < .05 was considered significant.

Results:

The prevalence of OSA in RIAs was fivefold higher in the nonaneurysm patient group, P = .002. The number of patients with hypertension

(P < .0001), body mass index ≥ 30 (P < .0001), hyperlipidemia (P = .018), chronic heart disease (P = .002) or prior ischemic stroke (P = .001) was significantly higher in the OSA group. Similarly, the number of wide-neck aneurysms (P < .0001) and aneurysm > 7 mm (P = .004), poor Hunt and Hess grade IV-V (P = .005), vasospasms, (P = .03), and patients with poor Modified Rankin Scale scores (3–6) was significantly higher in the OSA group (P < .0001). Interestingly, for the first time in univariate (P = .01) and multivariate (P = .003) regression analysis, OSA was identified as an individual predictor of unfavorable outcome of RIAs. In addition, hypertension (P = .04), smoking (P = .049), chronic heart disease (P = .01), and Hunt and Hess grade IV-V (P = .04) were revealed as predictors of poor outcome of RIAs.

Conclusions:

This is a novel study to determine the association between OSA and ruptured cerebral aneurysm in terms of comorbidities, size of aneurysm, severity of symptoms, and outcomes after treatment. In addition, for the first time, OSA is identified as a positive predictor of unfavorable outcome of RIAs.

Citation:

Chernyshev OY, Bir SC, Maiti TK, Patra DP, Sun H, Guthikonda B, Kelley RE, Cuellar H, Minagar A, Nanda A. The relationship between obstructive sleep apnea and ruptured intracranial aneurysms. J Clin Sleep Med. 2019;15(12):1839–1848.

BRIEF SUMMARY

Current Knowledge/Study Rationale: It is well known that obstructive sleep apnea (OSA) plays an important role in the progression and rupture of abdominal aortic aneurysms. However, the role of OSA in cerebral aneurysm is not well known.

Study Impact: OSA is a predictor of unfavorable outcome in patients with ruptured intracranial aneurysms. This study will bridge the fields of sleep medicine and neurosurgery to treat these complex patients with OSA and ruptured intracranial aneurysms.

INTRODUCTION

Ruptured intracranial aneurysms (RIAs) can lead to lifethreatening conditions such as subarachnoid hemorrhage and stroke. Approximately 30,000 people in United States are affected by subarachnoid hemorrhage each year.^1,2 The clinical outcome of patients with subarachnoid hemorrhage remains very poor, with 45% mortality and significant morbidity.^3,4 Several factors such as hypertension, smoking, obesity, size of aneurysm, and hyperlipidemia are responsible for the progression and rupture of cerebral aneurysms.⁵ In addition, a previous study showed that obstructive sleep apnea (OSA) worsens the overall outcome of patients with vascular aneurysms.⁶ OSA provokes endothelial dysfunction by inducing oxidative stress, sympathetic activity, and vascular shear stress as well as rupture of the aneurysms.⁷ OSA-associated factors including hypertension, diabetes mellitus, obesity, and hyperlipidemia may also contribute to progression and rupture of the aneurysms.^8,9 Therefore, controlling the risk factors is important to prevent progression and rupture of aneurysms.¹⁰ In the existing literature, there are no established and detailed data on the effect of OSA on the outcome of RIAs. In a series of 159 cases, this issue was addressed retrospectively by determining the prevalence of OSA based on positive screening, the characteristics of aneurysms, and the outcomes in patients with RIAs and OSA. The predictors of unfavorable outcome were also identified in the patients with RIAs.

METHODS

The current study was accomplished after approval by the local Institutional Review Board. This study was performed retrospectively by reviewing the clinical records of patients with symptoms of RIAs who presented to the neurology and neurosurgery services in the Louisiana State University (LSU) Health Sciences Center. Documents related to clinical history, neuroimaging, treatment procedures, and outcomes of patients with RIAs between January 2010 and September 2016 were accumulated by reviewing the medical records and relevant imaging studies.

Diagnosis of Intracranial Aneurysm

RIAs were diagnosed according to the institutional policy. RIA was initially suspected in the patients with presenting clinical symptoms including neurological deficits, loss of consciousness, altered mental status, and what the patients describe as “the worst headache in my life.” RIAs were confirmed either by performing a computed tomography scan of the head followed by a four-vessel angiogram or by a magnetic resonance angiogram. A total of 159 patients with RIAs were included in the current study to investigate our hypothesis.

Diagnosis of OSA

Initially the STOP-BANG sleep questionnaire was used to screen the patients for OSA. Thereafter, positively screened patients with STOP-BANG score ≥ 3 underwent polysomnography to confirm OSA.¹¹ Polysomnography was performed in an American Academy of Sleep Medicine (AASM)-certified sleep laboratory in the LSU Health Sciences Center. In addition, polysomnography reports were documented from the subset of patients who choose to undergo testing in outside facilities and provide reports to the LSU Health Sciences Center medical record system. Portable polysomnography was not used in diagnosis of OSA. One hundred forty-one nonaneurysmal neurosurgical patients’ charts were retrospectively reviewed and screening was performed in a manner similar to that of the aneurysm group to determine the prevalence of OSA.

Parameters used in polysomnography were as follows: (1) electroencephalogram (EEG) derivations (standard recommended EEG montages including F4-M1, C4-M1, and O2-M1 were used), (2) electrooculogram (EOG) derivation, (3) chin electromyelogram (EMG), (4) leg electromyelogram, (5) airflow signals, (6) respiratory effort signal, (7) oxygen saturation, (8) body position, and (9) electrocardiogram. Diagnosis of OSA was determined based on International Classification of Sleep Disorder, Third Edition and The AASM Manual for the Scoring of Sleep and Associated Events Version 2.2 (AASM Scoring Manual Version 2.2). The cases diagnosed before 2015 were reviewed to clarify criteria for respiratory events, especially respiratory apnea. Studies with the following respiratory criteria were included in the analysis:

• 1. Scoring of all respiratory events including apnea, hypopnea, and respiratory effort-related arousals were performed by AASM Scoring Manual Version 2.2 criteria.

• 2. The following criteria were used to diagnose obstructive hypopnea:

  • A. The peak signal excursions drop by ≥ 30% of pre-event baseline using nasal pressure (diagnostic study), positive airway pressure device flow (titration study), or an alternative hypopnea sensor (diagnostic study).

  • B. The duration of the ≥ 30% drop in signal excursion is ≥ 10 seconds.

  • C. There is a 4% oxygen desaturation from pre-event baseline.

Polysomnography Measures

Polysomnography data was retrieved in 28% (n = 9) of patients with OSA and RIA. The average apnea-hypopnea index and respiratory disturbance index as assessed by polysomnography were 41 events/h and 45 events/h, respectively in these patients. The mean oxygen saturation was 77% (Table S1 in supplemental material).

Hunt and Hess Scale

Patients’ preoperative clinical symptoms were graded using the 5-point (1 to 5) Hunt and Hess (H and H) scale: 1 = asymptomatic or slight headache and neck stiffness, 2 = moderate to severe headache and neck stiffness, 3 = drowsy and minimal neurological deficits, 4 = stuporous and moderate to severe hemiparesis, 5 = coma.¹²

Modified Rankin Scale

Postoperative clinical outcome was evaluated using the 7-point (0 to 6) Modified Rankin Scale (mRS): 0 = no symptoms, 1 = no significant disability, 2 = slight disability, 3 = moderate disability (needs some help), 4 = moderately severe disability (cannot walk without help), 5 = bedridden and needing continuous nursing care, 6 = dead.¹³

Follow-Up

The patients were followed clinically and radiologically. Fourvessel angiography was performed after treatment procedures and annually thereafter. The average duration of clinical follow-up was 25 months (range 3–126 months).

Statistical Analysis

Statistical Package for Social Sciences (SPSS) software, version 24.0 (IBM Corp., Armonk, New York, United States) was utilized to conduct statistical analysis. A chi-square test was used to determine the significance between the groups (OSA versus non-OSA). A regression analysis was performed to identify independent risk factors of aneurysm progression and outcome after treatment. A value of P < .05 was considered significant.

RESULTS

Demography of the Patients

Among 159 patients with RIAs, 39 (24.5%) were males, and 120 (75.5%) were females. Eighty-three patients (52.2%) were Caucasian, and 76 (47.8%) were African American. The median age of patients was 52 years (range 17–84 years). Differences in age, sex, and race distribution between the patient groups with RIA (OSA versus non-OSA) was not observed (Table 1).

Table 1.

Patients’ demographics of those with and without RIAs stratified by OSA group.

OSA-Associated Risk Factors

Hypertension

In the OSA group, out of 32 cases, 28 (87.5%) had hypertension. In the non-OSA group (n = 127), 76 (60%) had hypertension. The difference in prevalence of hypertension achieved statistical significance between these groups (P < .0001), as shown in Figure 1A.

Figure 1.

Distribution of comorbidities in the OSA and non-OSA groups.

Obesity (Body Mass Index > 30)

The percentage of obesity was 84.4% and 25% in the OSA and non-OSA groups, respectively. The prevalence of obesity was fivefold higher in the OSA group and reached statistical significance (P < .0001), as shown in Figure 1B.

Hyperlipidemia

Ten cases (31.3%) in the OSA group and 14 cases (11%) in the non-OSA group had high lipid levels. There was a significant difference in the presence of high lipid levels between these groups (P = .008), as shown in Figure 1C.

Chronic Heart Disease

Eight patients (25%) patients in the OSA group and 10 (8%) in the non-OSA group experienced chronic heart disease (CHD). Likewise, there was a significant difference in prevalence of CHD between these groups (P = .001), as shown in Figure 1D.

Prior Ischemic Stroke

Eleven patients (34.4%) in the OSA group and 10 patients (8%) in the non-OSA group had suffered prior stroke. The difference in prevalence of prior stroke achieved statistical significance between these groups (P < .0001), as shown in Figure 1E.

STOP-BANG Score

The STOP-BANG scores in the OSA and non-OSA groups were 5 and 2, respectively. The difference in this score reached statistical significance between these groups (P < .0001), Table 1. There was no significant difference in the prevalence of diabetes mellitus and the history of smoking and drug abuse between these groups.

In the non-neurosurgical aneurysm cohort, 141 patients were investigated to determine the prevalence of OSA. The average STOP-BANG score was 5 and 2 in OSA and non-OSA group, respectively. Of 141 patients, only 6 (4.2%) received a diagnosis of OSA. In the aneurysm cohort, 32 patients (20%) had OSA. Therefore, prevalence of OSA in RIAs was fivefold higher than in the patients without RIAs, P = .002 (4.7, 1.70–13.23), see Figure S1 in the supplemental material. Similar to the patients with aneurysms and OSA, the group of patients without aneurysms with OSA had more hypertension (P < .0001), obesity (P < .0001), hyperlipidemia (P = .02), and prior ischemic stroke (P = .01) compared to the non-OSA group, as outlined in Table 1.

Characteristics of Aneurysms

Based on the location of aneurysms in brain circulation, most patients with RIAs had aneurysms in anterior circulation (86.8%). There was no significant difference in the distribution of the aneurysms’ primary locations. However, the OSA group had more aneurysms in anterior communicating arteries (43.8%, P = .04) (Table 2 and Figure 2A). The non-OSA group had more aneurysms in posterior communicating arteries (30%, P = .005). There was no significant difference in the number of aneurysms between the OSA and non-OSA groups (P = .06).

Table 2.

Characteristics of RIAs stratified by OSA group.

Figure 2.

Distribution of size and location of aneurysms and Hunt and Hess grade variables in the OSA and non-OSA groups.

Size of the Aneurysms

There was no significant difference in mean size of the aneurysms between the groups (7.25 mm versus 6.7 mm, P = .62). However, the number of aneurysms > 7 mm was significantly higher in the OSA group compared to the non-OSA group (59% versus 38%, P = .004), as shown in Figure 2B.

Similar to the size of the aneurysms, the number of wide neck aneurysms was significantly higher in the OSA group compared to the non-OSA group (56% versus 25%, P < .0001), as shown in Figure 2C.

Clinical Presentation

Depending on initial clinical presentation, the patients were divided into H and H grading. The number of severe (H and H grade 5) cases was significantly higher in the OSA group compared to the non-OSA group (12.5% versus 2.4%, P = .005), as shown in Figure 2D.

Outcome After Treatment

Modified Rankin Scale Score

In last follow-up, the median mRS score in the OSA group was 1, and in the non-OSA group, the median mRS was 0 (Table 3). The difference in median mRS score reached statistical significance, P = .016, as shown in Figure 3A. Likewise, the number of patients with poor mRS grade 3–6 was significantly higher in the OSA group (34.4%) compared to the non-OSA group (8.7%), P = .00002.

Table 3.

Follow-up results in the patients with RIAs.

Figure 3.

Outcome after treatment in the OSA and non-OSA groups.

Vasospasm

There was no significant difference in the number of residual aneurysms between the groups (10% versus 8%, in the OSA and non-OSA groups respectively, P = .080). However, the number of vasospasms was significantly higher in the OSA group compared to the non-OSA group (34.4% versus 18%), P = .01), as shown in Figure 3B.

There was no significant difference between the groups in the number of required ventriculoperitoneal shunts (P = .99), amount of blood loss (P = .89), length of stay in the hospital (P = .99), or complications (Figure 3C) including infection, new hydrocephalus, stroke, cranial nerve palsy, or mortality.

Procedural Outcome Based on Coexistence of OSA

Based on coexistence of OSA, endovascular coiling showed significantly better outcome compared to surgical clipping (coiling, 12 [75%] versus clipping, 9 [56.3%]), P = .015, hazard ratio: 2.0, confidence interval: 1.17–3.64, see Figure 4A.

Figure 4.

Outcome based on coiling or clipping treatment procedures.

Outcome of Continuous Positive Airway Pressure Therapy for Patients With OSA

In the group of patients who underwent continuous positive airway pressure (CPAP) therapy, the number of patients with good outcome (mRS 0–2) was significantly higher compared to patients without CPAP therapy (OSA with CPAP therapy, 83% versus OSA without CPAP therapy, 65%, P = .003, odds ratio = 2.6, confidence interval 1.35–5.10).

Approach of Treatment

Approach of treatment for RIAs has been changed significantly in past decade. In anterior circulation of this series, clipping (Figure 4B) was significantly higher, however, in posterior circulation, coiling (Figure 4C) was significantly higher for the treatment of RIAs. Similar tendency of higher rate of endovascular coiling was observed even in posterior circulation of the patients with OSA and aneurysms.

Predictors of Poor Outcome

Univariate and multivariate logistic regression analysis was performed to identify the predictors of unfavorable outcome in the patients with RIAs (Table 4). The following covariates were included in the model: age (older than 50 years or younger than 50 years); sex (male or female); race (Caucasian or African American); number of aneurysms (single or multiple); location of aneurysm (posterior or anterior circulation); size of the aneurysms (> 7 mm or < 7 mm); neck size of aneurysm (> 4 mm or < 4 mm); the presence or absence of hyperlipidemia, obesity, hypertension, diabetes mellitus, CHD, OSA, or prior ischemic stroke; current smoker, drug abuse, or depression (yes or no); H and H grade (4–5 or 1–3); treatment type (clipping or coiling); and vasospasm (yes or no). In univariate analysis, hypertension (P = .024), smoking (P = .03), CHD (P = .01), prior stroke (P = .004), aneurysm size > 7 mm (P = .04), H and H grade 4–5 (P = .02) and OSA (P < .0001) were identified as positive predictors of unfavorable outcome in these patients. However, in multivariate analysis, presence of hypertension (P = .03), smoking (P = .02), H and H grade 4–5 (P = .03), and OSA (P = .007) were identified as positive predictors of unfavorable outcome. In this series, all other factors including age, sex, race, obesity, and treatment procedure did not show any significant relation to poor outcome.

Table 4.

Regression analysis to determine predictors of poor outcome in the patients with ruptured intracranial aneurysms.

DISCUSSION

Although OSA has been shown to be associated with hypertension and cardiovascular disease, there is no single study related to OSA and RIA. Therefore, our interest was to investigate the effect of OSA as well as type and timing of procedure in overall outcome of patients with RIA. The new findings of this study include the following: (1) there was a fivefold higher incidence of OSA in patients with RIAs compared to those without RIAs, (2) coexistence of OSA worsens the overall outcome of RIAs, (3) OSA is an individual predictor of unfavorable outcome in patients with RIAs, and (4) RIAs patients with OSA may benefit from coiling rather than clipping. The results of this study also revealed that the size of the aneurysms and incidence of wide-neck aneurysm and vasospasm were significantly higher in the patients with RIA and OSA. In addition, this current study confirms the well-established OSA-associated risk factors for poor outcome in the patient with intracranial aneurysm including obesity, hyperlipidemia, hypertension, CHD, and prior stroke.^14–19 Previous studies have shown that the incidence of ruptured aneurysm is higher in those with OSA compared to those without OSA.^6,20 Therefore, along with associated risk factors, OSA either directly or indirectly plays an important role in the poor outcomes of patients with RIA.

OSA-Associated Comorbidities

Obesity

Obesity is a potential risk factor for OSA. Mild to moderate obesity has been shown to be associated with markedly increased prevalence of OSA.²¹ In this series, a higher percentage of obesity was observed in the patients with OSA compared to non-OSA subjects. Obesity may cause OSA by increasing adipokines’ mediated distribution of body fat. Weight reduction is an important treatment option for OSA, and earlier studies showed that a 10% to 15% reduction in body weight can lead to approximately 50% reduction of OSA.^22,23

Hyperlipidemia

Intermittent hypoxia in a patient with OSA can cause hyperlipidemia either by delaying clearance of lipids (after hepatic secretion or intestinal absorption) or by increasing hepatic synthesis of lipids. In addition, intermittent hypoxia is a direct cause of dyslipidemia.²⁴ In this study, a higher percentage of patients with OSA had hyperlipidemia compared to those without OSA.

Hypertension

OSA is a well-established cause of secondary hypertension. In the current study, 87% of patients with OSA had hypertension. Primary mechanisms of hypertension in OSA include overactivity of the sympathetic nervous system and oxidative stress and inflammation-mediated alterations in vascular structure and function. In addition, CPAP therapy reduces blood pressure in patients with OSA.¹⁵

Chronic Heart Disease

A previous report suggested that the prevalence of CHD was significantly higher in patients with OSA, and our finding was in agreement with the results of the earlier study.²⁵

Stroke

Evidence-based literature suggested that the incidence of OSA in patients with recent stroke was significantly higher than in those without stroke.²⁶ Similarly, our data revealed that a higher percentage of patients experienced stroke in the OSA group compared to the non-OSA group.

Smoking

Smoking may act as a potential risk factor for OSA, and cumulatively both OSA and smoking can cause cardiovascular dysfunction. Smoking can also increase the severity of OSA by increasing the duration of hypoxia.²⁷ However, OSA, in turn, may be a predisposing factor for smoking.²⁸ Our results did not reveal any difference in prevalence of smokers in the OSA group versus the non-OSA group.

OSA Potentiates the Expansion of Intracranial Aneurysms

A previous study suggested that OSA significantly affects the progression or expansion of abdominal aortic aneurysms.⁶ This enlargement of an aneurysm finally leads to rupture and subsequently results in a poor outcome in these patients. In agreement with the earlier report, this study showed that a higher percentage of patients with OSA had aneurysms larger than 7 mm and poor outcome compared to those without OSA, indicating that OSA may have contributed directly or indirectly to enlarging the aneurysmal diameter. Likewise, large diameter of the aneurysmal neck also has been associated with increased chance of rupture.^29,30 In this series, the number of wide aneurysms was significantly higher in the OSA group with higher unfavorable outcome. Although there are no data at this point, it would not be surprising to find that these factors (an increased number of aneurysms with comparatively large size and wide neck) may have contributed to the early rupture of aneurysms in the OSA group.

OSA Heightens the Severity of Clinical Symptoms

The effect of OSA on the severity of clinical symptoms of RIA is lacking in the existing literature. However, previous studies revealed that the severity of aneurysms is directly related to the severity of the OSA.^6,31 In the current study, severity of clinical symptoms of RIA (eg, H and H grade 5) was significantly higher in the OSA group, indicating the direct or indirect role of OSA on deterioration of these patients. The rationale for this deterioration could be explained by early expansion and rupture of aneurysms, and also by the higher prevalence of obesity, hyperlipidemia, hypertension, CHD, and ischemic stroke in these patients with OSA.

OSA and Vasospasms

Cerebral vasospasm is a fatal complication in patients with RIAs. The mechanism of vasospasm after ruptured aneurysm is not yet well understood. Calcium-dependent and independent pathways, imbalance between the vasoconstrictor and vasodilator, inflammatory process, disrupted neuronal mechanism, and endothelial cell proliferation are involved in vasospasm after ruptured aneurysms.³² An earlier study suggested that there is an obvious association between OSA and reduced cerebrovascular diameter.³³ OSA is associated with impaired endothelial function and reduced endothelial regeneration. Levels of vasodilator, such as nitric oxide, and number of endothelial progenitor cells are lower in patients with OSA.^34–36 There is also an OSA-mediated increase of reactive oxygen species including peroxynitrite and inflammatory markers such as nuclear factor-kβ.³⁵ These factors cause vasoconstriction by decreasing the expression of endothelial nitric oxide synthase as well as production of nitric oxide.^7,35,37 However, CPAP therapy for OSA shows increases in serum levels of nitrite and nitrate as well as the number of endothelial progenitor cells. Endothelin-1 is a strong vasoconstrictor and is increased in patients with OSA.³⁶ Previous reports showed that vasospasm was significantly higher in those with OSA^20,33 and in this series, consistent with findings of previous studies, the percentages of vasospasm were higher in the OSA group.

Outcome Based on Coexistence of OSA

Previous studies have shown that patients with OSA and cerebrovascular disease had poor clinical outcomes including low survival,³⁸ but CPAP treatment reduced the risk of mortality.³⁹ Cerebral aneurysmal rupture causes subarachnoid hemorrhage, which results in a poor outcome in these patients and may require surgical intervention. These patients may need a longer hospital stay, which will increase the health cost. In addition, vasospasm after ruptured cerebral aneurysm can cause ischemic stroke. Results of this study concur with the findings of previous studies showing poor outcome in patients with OSA,^38,39 possibly due to the higher number of comorbidities and vasospasms in this group.

Predictors of Poor Outcome

Several factors (age, sex, hypertension, smoking, aneurysmal size and location) have been identified as positive predictors for unfavorable outcome of RIA.^5,40–42 Both in univariate and multivariate analysis, for the first time, presence of OSA was identified as a predictor of unfavorable outcome in RIAs. In earlier studies, elderly age has been established as an individual risk factor for an unfavorable outcome of RIAs.^5,42 In this study, age had no effect on overall outcome. Similarly, sex also did not show any significant difference in outcome in these patients.⁴² Most importantly, hypertension and smoking are identified as major risk factors for unfavorable outcome in ruptured aneurysms.^40–42 Similar to previous studies, the results of this study also confirmed these factors as predictors of poor outcome in RIAs. Previous studies suggested that severity of disease (H and H grade 4–5) has significant influence on overall outcome of RIAs.⁴³ In agreement with the earlier studies, the findings of this study also identified H and H grade 4–5 as a positive predictor of unfavorable outcome in these patients. Evidencebased research also suggested that coexistence of CHD, prior stroke, and size of the aneurysm affect the outcome of RIAs.⁴⁴ In univariate regression analysis of this series, CHD, prior stroke and aneurysm larger than 7 mm were revealed as risk factors for poor outcome; however, in multivariate analysis, there was no significant difference.

Mechanism of OSA-Mediated Rupture of Aneurysm

It has been shown that patients with abdominal aortic aneurysms had significantly higher levels of circulating endothelial progenitor cells. In addition, Choke et al suggested that the ruptured edge of an aneurysm contains not only a higher amount of vascular endothelial growth factor, vascular endothelial-cadherin, and monocyte chemo-attractive protein but also a higher number of fragile microvessels, indicating ongoing pathological angiogenesis.⁴⁵ This group also found that pathological angiogenesis is involved in the rupture of abdominal aortic aneurysms by elevating levels of matrix metalloproteinase, which degrade the membrane protein and facilitate the endothelial cell proliferation and migration.⁴⁶ Evidence-based research also suggested that patients with OSA have a high serum level of vascular endothelial growth factor, which is a strong cytokine to develop new fragile capillaries.⁴⁷ However, hypertension is an established potential risk for rupture of cerebral aneurysm.⁴⁸ Therefore, it is highly possible that along with hypertension, OSA can potentiate the rupture of an aneurysm either by pathological angiogenesis or by triggering hypertension.

Limitations

The current study has several limitations. First, it has an inherent limitation due to its retrospective nature. Second, this study is a single-institute study with a relatively small volume of cases in the OSA group. Third, confounders such as hyperlipidemia, hypertension, smoking, and cardiac and cerebral disorders may have directly or, associated with OSA, partially contributed to the overall outcome of this series. Fourth, use of OSA screening tools to suspect and identify the prevalence of OSA, and lack of polysomnography data from the respected sources might have affected the outcomes based on severity of OSA. Fifth, in this series, objective compliance of CPAP therapy was not available.

CONCLUSIONS

The prevalence of OSA is fivefold higher in patients with RIAs. OSA can be associated with a higher percentage of hypertension, obesity, hyperlipidemia, CHD, and ischemic stroke in these patients. In the presence of OSA, the complications of RIAs such as vasospasms are also influenced. Overall outcome (mRS) of RIAs is also affected by the coexistence of OSA. In addition, coiling would be good for patients with OSA. Therefore, concurrence of OSA in patients with RIAs serves as a risk factors for unfavorable outcome. Screening of patients with RIAs for initial diagnosis of OSA using the STOP-BANG questionnaire would be beneficial for this particular population. However, a randomized controlled trial in a large volume of patients is warranted to further evaluate the effect of OSA in this specific population.

DISCLOSURE STATEMENT

All authors have seen and approved the manuscript. The authors report no conflicts of interest.

ABBREVIATIONS

AASM

American Academy of Sleep Medicine

CHD

chronic heart disease

CPAP

continuous positive airway pressure

EEG

electroencephalogram

H and H

Hunt and Hess

mRS

Modified Rankin Scale

OR

odds ratio

OSA

obstructive sleep apnea

RIAs

ruptured intracranial aneurysms