Role Of Sleep Apnea Research Articles

Obesity and Male Fertility: An In-Depth Review of the Impact of Elevated BMI

This paper discusses the complex relationship between obesity and male infertility in a detailed manner. According to the introduction, obesity-related infertility is importantly discussed since it affects some 15% of couples in which half cases are attributed for obesity-related infertility is important to discuss since it affects some 15% of couples, and half of cases are attributed to male factors. The body of the analysis discusses various factors related to obesity-associated male reproduction implications, including endocrinopathies insulin sensitivity, sperm DNA fragmentation, erectile dysfunction OSAS asshened semen characteristics chronic epididymitis and epigenetic changes. The above discussion on endocrinopathies shows that excessive white adipose tissues derail the HPG axis, triggering hormonal imbalances which lead to infertility. This paper explains the interaction between insulin resistance and testosterone levels in type 2 diabetes affected men. The paper also focuses on sperm DNA fragmentation, showing the association between obesity and increased levels of sperm DNA damage, mitochondrial dysfunction and abnormality in morphology. Erectile dysfunction is focused on obesity-induced oxidative stress, inflammation and hormonal abnormalities that impair male reproductive function. Additionally, the role of sleep apnea in testosterone secretion and possible association between its severity to lower level of this hormone are presented. There is a further discussion of altered sperm traits, chronic epididymitis and epigenetic changes with regard to the obesity which gives us a broad perspective on male fertility. The paper then concludes its discussion regarding weight loss interventions restoring fertility, focusing on diet and exercise as means for reducing certain parameters associated with modifiable inflammatory markers linked to infertility. In summary, the general assessment highlights that obesity management is crucial in male infertility.

Role of Sleep Apnea and Long-Term CPAP Treatment in the Prognosis of Patients With Melanoma: A Prospective Multicenter Study of 443 Patients

OSA has been associated with increased incidence and aggressiveness of melanoma. However, the long-term impact of OSA and CPAP treatment on the prognosis of melanoma remains unexplored. Are OSA and CPAP treatment associated independently with a poor prognosis for cutaneous melanoma? Four hundred forty-three patients with a diagnosis of cutaneous melanoma (2012-2015) underwent a sleep study within 6months of diagnosis. The main 5-year outcome of the study was a composite of melanoma recurrence, metastasis, or mortality. Patients were divided into four groups: baseline apnea-hypopnea index (AHI) of fewer than 10 events/h (no OSA; control group), OSA treated with CPAP and good adherence, untreated or poor CPAP adherence in moderate (AHI, 10-29 events/h), and severe OSA (AHI,≥ 30 events/h). Survival analysis was used to determine the independent role of OSA and CPAP treatment on melanoma composite outcome. Three hundred ninety-one patients (88.2%) were available for analysis at 5-year follow-up (mean age, 65.1 ± 15.2 years; 49%male; Breslow index, 1.7 ± 2.5mm). One hundred thirty-nine patients had AHI of fewer than 10 events/h (control group); 78 patients with OSA were adherent to CPAP; and 124 and 50 patients had moderate and severe OSA, respectively, without CPAP treatment. Median follow-up was 60months (interquartile range, 51-74months). During follow-up, 32 relapses, 53 metastases, and 52 deaths occurred (116 patients showed at least one of the main composite outcomes). After adjusting for age, sex, sentinel lymph nodes affected at diagnosis, BMI, diabetes,nighttime with an oxygen saturation below 90%, Breslow index, Epworth sleepiness scale scores, and melanoma treatment, moderate (hazard ratio [HR], 2.45; 95%CI, 1.09-5.49) and severe OSA (HR, 2.96; 95%CI, 1.36-6.42) were associated with poorer prognosis of melanoma compared with the control group. However, good adherence to CPAP avoided this excess risk (HR, 1.66; 95%CI, 0.71-3.90). Moderate to severe untreated OSA is an independent risk factor for poor prognosis of melanoma. Treatment with CPAP is associated with improved melanoma outcomes compared with untreated moderate to severe OSA.

Causal Association between Whole-Body Water Mass and Sleep Apnea: A Mendelian Randomization Study.

Rationale: Growing evidence has suggested that body water content plays a critical role in sleep apnea. However, the causal relationship has not been established. Objectives: This study aimed to investigate whether increased whole-body water mass is causally associated with a higher risk of sleep apnea using two-sample Mendelian randomization (MR) analysis. Methods: Body water mass (BWM)-associated genetic instruments were extracted from a genome-wide association study conducted by Neale Lab, which incorporates 331,315 individuals of European ancestry. Genetic variants for sleep apnea were derived from the FinnGen dataset. MR analysis was performed using inverse variance-weighted and weight median methods, respectively. MR-Egger regression and MR-Pleiotropy Residual Sum and Outlier tests were applied to evaluate the directional pleiotropy. In addition, we performed a multivariable MR analysis that includes body mass index, snoring, and waist-to-hip ratio as covariate exposures to address their confounding effects. To elucidate mechanisms of the association between BWM and sleep apnea, we further conducted MR analysis on common edematous diseases. Results: MR estimates showed that per standard deviation increase in BWM led to an increase in the risk of sleep apnea by 49% (odds ratio [OR], 1.490; 95% confidence interval [CI], 1.308-1.696; P = 1.75 × 10-9). The result after MR-Pleiotropy Residual Sum and Outlier correction further supports their causal association (OR, 1.414; 95% CI, 1.253-1.595; P = 1.76 × 10-8). In addition, the multivariable MR analysis indicates a significant causal association between a higher BWM and increased risk of sleep apnea (OR, 1.204; 95% CI, 1.031-1.377; P = 0.036). Genetic predisposition to a higher BWM was also causally related to increased risk of edematous diseases. Conclusions: Our results suggested that increased BWM is a potential risk factor for sleep apnea. Pathologic edema is a possible intermediate factor mediating this causal association.

Sleep Dysfunction in COVID-19 Patients: Prevalence, Risk Factors, Mechanisms, and Management.

During the COVID-19 pandemic, the need to establish the prevalence of sleep dysfunction and psychological distress, identify predisposing and protective factors, and explore effective management strategies remains an important priority. Evidence to date suggests that a considerable proportion of COVID-19 patients experience significant sleep disturbances (estimated to afflict up to 50–75%) as well as psychological distress such as depression, anxiety, and traumatic stress. Duration of hospitalization, pre-existing mental health concerns, lower absolute lymphocyte count, and increased neutrophil-to-lymphocyte ratio have been all associated with a greater risk of sleep dysfunction in infected and hospitalized patients. Furthermore, in this review, we discuss the link between sleep deprivation, susceptibility to viral infections, and psychosocial wellbeing in relevance to COVID-19 and summarize the existing evidence regarding the presence and role of sleep apnea in infected individuals. Finally, we highlight the importance of suitable interventions in order to prevent and manage sleep dysfunction and avoid long-term physical and psychological implications. Future research should aim to provide high-quality information including in high risk, underserved, or difficult to reach populations and on the long-term consequences and effectiveness of applied interventions.

The role of sleep apnea in APOE‐Alzheimer's disease pathway

AbstractBackgroundPrevious studies have shown contradictory findings on if the APOE gene is associated with sleep apnea. Thus, the goal of this study is to examine the relationship between the APOE gene and sleep apnea and investigate whether levels of amyloid beta in cerebrospinal fluid (CSF) depend on sleep apnea and/or APOE gene.MethodData was obtained from the National Alzheimer’s Coordinating Center (NACC). We restricted participants to those who were enrolled at or after 2015 due to availabilities of sleep apnea measurements and with normal cognition status at enrollment. CSF sample data for a subset of these participants were merged to initial visit data by subject ID and year of visit. Logistic regression was used to investigate the association between sleep apnea and APOE and backward elimination was used to identify a final model. T‐tests were used to compare the mean levels of CSF amyloid beta between APOE gene groups and between sleep apnea groups, respectively.ResultOf a total of 1630 subjects identified to meet criteria, 3.83% participants had sleep apnea and are APOE ε4 carriers, 26.87% did not have sleep apnea and are APOE ε4 carriers, 9.88% had sleep apnea and are APOE ε4 non‐carriers, 59.45% did not have sleep apnea and are APOE ε4 non‐carriers. Logistic regression showed that sleep apnea was not significantly associated with APOE gene after adjusting age, gender and BMI. The mean levels of CSF amyloid beta among APOE ε4 carriers (mean± SD: 414.7±241.7) were lower than APOE ε4 non‐carriers (mean± SD: 500.9±150.5), and the mean levels of CSF amyloid beta among sleep apnea subjects (mean± SD: 434.6±90.1) were lower than subjects without sleep apnea (mean± SD: 504.9±194.3). However, the differences were not statistically significant.ConclusionIn this study, sleep apnea was not significantly associated with APOE in the NACC sample and the mean levels of CSF amyloid beta did not depend on sleep apnea or APOE gene in cognitively normal subjects.

Sex differences in sleep apnea and comorbid neurodegenerative diseases

Sleep apnea is a disorder, which increasingly affects people worldwide. Whether the associated hypoxic events during sleep are central or obstructive in origin, the end result is excessive daytime sleepiness and an increased risk for several comorbidities, such as cardiovascular and neurodegenerative disorders. Sleep apnea is diagnosed more frequently in men than women, suggesting a role of sex hormones in the pathology of the disease. Furthermore, there are sex differences in the development and progression of comorbid diseases associated with sleep apnea. Therefore, treatment of sleep apnea may be clinically relevant for prevention of subsequent sex-specific comorbid disorders. While the impact sleep apnea has on cardiovascular events has been the subject of many research studies, the role of sleep apnea in neurodegeneration is less established. Here we review known risk factors for sleep apnea and the implications of the observed sex differences in this disease. We also summarize the evidence and mechanisms for how sleep apnea may contribute to the onset of neurodegenerative disorders, such as Alzheimer’s disease and Parkinson’s disease.

Author response: Long-term cerebral white and gray matter changes after preeclampsia.

We thank Dr. Culebras for the comment on our article.1 Sleep apnea might be among the pathophysiologic pathways linking preeclampsia with increased risk of cerebrovascular disease in previously preeclamptic women. In fact, research recently focused on the role of sleep apnea in the etiopathogenesis of cerebrovascular and cardiovascular disease and demonstrated an increased stroke risk in patients with obstructive sleep apnea (OSA).2,3 Intermittent hypoxia with consecutive vascular dysregulation has been identified as a possible mechanism whereby OSA increases risk of stroke. This might be relevant to previously preeclamptic mothers in whom autonomic neurovascular dysfunction, inter alia mediated by functional changes to the sympathetic nervous system, was also demonstrated.4 It remains to be answered whether this similarity among pathologies indeed points to a causative link between preeclampsia and cerebrovascular disease.

Prevalence of Sleep Apnea in patients Treated for an Abdominal Aortic Aneurysm

Objectives: The prevalence of abdominal aortic aneurysms (AAA) in France is between 0.8% and 7.5%. The risk of rupture of an AAA is strongly related to the evolution of its diameter. However the factors influencing the evolution of the diameter are little known. The role of sleep apnea (SA) remains still discussed. The objective of this study was to study the prevalence of SA in the patients presenting with an AAA requiring surgery in comparison with the general population as well as the relation between the AAA diameter and the severity of SA. Materials and Methods: Between June 2012 and December 2014, we included all the patients referred for the treatment of an AAA. All the patients gave their consent for the realization of a preoperative polysomnography. An apnea/hypopnea index (AHI)>10/h was chosen for the diagnosis of SA. For each patient, the age, the gender, the body mass index (BMI), the AHI, the duration of desaturation (saturation 60mm). The prevalence of SA, the AHI, and the duration of desaturation were compared between the groups. Results: 59 patients (52 men, 7 women) were included. The mean age was 71 years (48-88). The average diameter of the AAAwas 58.3mm (45-95). 61.5% of the patients presented SA a prevalence significantly higher than in the general population (61.5 vs 7.5%, p<0.001). The distribution of the groups was: group 1, n1⁄4 9 patients, group 2, n1⁄4 20 patients, group 3, n1⁄416 patients and group 4, n1⁄414 patients. The prevalence of SA increased with the diameter of the AAA (group 1: 20%; group 2: 35%; group 3: 72% and group 4: 77%; p1⁄40.015). SA was more severe in group 4 than in the other groups (AHI was 35 in group 4 vs. 17 in group 3 [p1⁄40.0043], 17 in group 2 [(p1⁄40.01], and 5.4 in group 1 [p1⁄40.0003]). Conclusion: The prevalence of sleep apnea in patients with an AAA seems to be significantly higher than in the general population, independently of the BMI. The growth of the aneurysm seems to be linked to the severity of SAS.

PP.37.06

Objective: Normal diurnal variation of both peripheral and central blood pressure (BP) in healthy subjects is characterized by the increase from morning to evening and nocturnal dipping. Obstructive sleep apnea (OSA) is commonly associated with the inverse 24-hour BP profile and nocturnal and morning BP elevation. However, the diurnal changes of central BP and arterial stiffness are not well investigated. Thus, we conducted a pilot study to assess the evening-to-morning variation of central BP and arterial stiffness in hypertensive patients with moderate-severe OSA. Design and method: Eighteen hypertensive patients (15 males, mean age 53.7 ± 12.0 years old) with moderate-severe OSA [median apnea-hypopnea index (AHI) 65.4 (17.4–115.0) episodes/hour] verified by full polysomnography (Embla, Natus, USA). The patients were overweight or obese [body mass index (BMI) 37.7 ± 4.9 kg/m2), and did not have concomitant cardiovascular diseases. All subjects underwent applanation tonometry (Sphygmocor, Australia) in the morning after awakening and in the evening before going to bed at night in sleep laboratory. Results: OSA patients had higher morning central diastolic BP (91.0 ± 8.1 vs. 86.4 ± 11.6 mmHg; p = 0,040) along with higher morning “office” peripheral diastolic BP (90.0 ± 8.1 vs. 85.1 ± 11.8; p = 0.024) compared to the evening values. Augmentation index (AI) was also slightly higher in the morning [26.1 (2.0; 53.0) vs. 17.0(−4; 35)%; p = 0.05]. Central systolic BP and pulse wave velocity (PWV) did not change significantly from evening to morning (p > 0.05). Correlation analysis showed a moderate association between evening central diastolic BP and AHI (rs = 0.56;p = 0.038) as well as with desaturation index (rs = 0.60;p = 0.023) that weakened after adjustment for age, BMI, peripheral BP, prescribed antihypertensive therapy. An inverse strong association between evening PWV and nocturnal O2 saturation level (rs = −0.81;p = 0.003) remained significant after adjustment for possible confounders. However, the morning parameters were not associated with OSA severity but only with confounding factors (age, “office” BP, therapy). Conclusions: The pilot study demonstrated an inverse diurnal variation of central diastolic BP and arterial stiffness (AI) in hypertensive patients with moderate-to-severe OSA that corresponds to the common impairment of 24-hour ambulatory BP profile in these patients. The role of sleep apnea per se requires further investigation in a controlled study.

Expressions of angiotensin and cytokine receptors in the paracrine signaling of the carotid body in hypoxia and sleep apnea

Arterial chemoreceptors in the carotid body are central to the chemical control of breathing in the chemotransduction of physiological stimuli in the arterial blood for eliciting the chemoreflex, which mediates the respiratory, cardiovascular and autonomic responses to hypoxia, hypercapnia and acidosis. Recent evidence suggests that signaling molecules locally produced in the carotid body, including angiotensin II and pro-inflammatory cytokines play an important role in the modulation of the activity of carotid chemoreceptors, via the angiotensin and cytokine receptors expressed in the chemosensitive cells in an autocrine–paracrine manner. The carotid chemoreceptor activity is augmented in subjects at high altitude and in patients with sleep-disordered breathing. Maladaptive responses of the paracrine signaling to hypoxia in the carotid body have been proposed to play a pathogenic role in sleep apnea. Specifically, recent findings show significant increases in expressions of angiotensin receptors and components of a local angiotensin-generating system in the carotid body in sustained or intermittent hypoxia, which augments the chemoreceptor activity and also mediates the inflammatory response of the carotid body to hypoxia. In addition, inflammation of the carotid body involves an increased local expression of cytokine receptors and pro-inflammatory cytokines in sustained or intermittent hypoxia. This review aims to summarize the evidence supporting that the upregulated expression of the angiotensin receptors and cytokine pathways in the carotid body leads to augmented activities of the carotid chemoreceptor in hypoxic conditions, which could play a role in the pathophysiology of sleep apnea.

The role of local renin-angiotensin system in arterial chemoreceptors in sleep-breathing disorders.

The renin-angiotensin system (RAS) plays pivotal roles in the regulation of cardiovascular and renal functions to maintain the fluid and electrolyte homeostasis. Experimental studies have demonstrated a locally expressed RAS in the carotid body, which is functional significant in the effect of angiotensin peptides on the regulation of the activity of peripheral chemoreceptors and the chemoreflex. The physiological and pathophysiological implications of the RAS in the carotid body have been proposed upon recent studies showing a significant upregulation of the RAS expression under hypoxic conditions relevant to altitude acclimation and sleep apnea and also in animal model of heart failure. Specifically, the increased expression of angiotensinogen, angiotensin-converting enzyme and angiotensin AT1 receptors plays significant roles in the augmented carotid chemoreceptor activity and inflammation of the carotid body. This review aims to summarize these results with highlights on the pathophysiological function of the RAS under hypoxic conditions. It is concluded that the maladaptive changes of the RAS in the carotid body plays a pathogenic role in sleep apnea and heart failure, which could potentially be a therapeutic target for the treatment of the pathophysiological consequence of sleep apnea.

Role of Sleep Apnea and Continuous Positive Airway Pressure Therapy in the Incidence of Stroke or Coronary Heart Disease in Women

It is unknown whether obstructive sleep apnea (OSA) may be a risk factor for incident cardiovascular events in women. We sought to investigate whether OSA increases the incidence of a composite of stroke or coronary heart disease (CHD) in women, and the role of continuous positive airway pressure (CPAP) treatment on this association. This was a prospective, observational study conducted in two Spanish teaching hospitals between 1998 and 2007. Consecutive women referred for suspected OSA and free of previous stroke and CHD were analyzed. Women with an apnea-hypopnea index (AHI) less than 10 comprised the control group, and those with an AHI greater than or equal to 10 were diagnosed with OSA and classified as CPAP-treated (adherence ≥ 4 h/d) or untreated (adherence < 4 h/d or not prescribed). The follow-up ended in December 2010. A total of 967 women were studied (median follow-up, 6.8 yr; interquartile range, 5.2-8.2). The untreated OSA group showed a greater incidence rate of the composite outcome than the control group (2.19 vs. 0.54 per 100 person-years; P < 0.0005). Compared with the control group, the fully adjusted hazard ratios for the composite outcome incidence were 2.76 (95% confidence interval [CI], 1.35-5.62) for the untreated OSA group, and 0.91 (95% CI, 0.43-1.95) for the CPAP-treated group. When the type of cardiovascular event was separately assessed, untreated OSA showed a stronger association with incident stroke (adjusted hazard ratio, 6.44; 95% CI, 1.46-28.3) than with CHD (adjusted hazard ratio, 1.77; 95% CI, 0.76-4.09). In women, untreated OSA is associated with increased incidence of serious cardiovascular outcomes, particularly incident stroke. Adequate CPAP treatment seems to reduce this risk.

Abstract P102: Risk of Incident Hypertension and Diabetes Mellitus in Habitual Snorers and Sleep Apneic Individuals; The Multiethnic Study of Atherosclerosis

Background: Data regarding temporal association of sleep apnea and snoring with incident hypertension (HTN) and diabetes mellitus(DM) are limited. Hypothesis: We hypothesized that sleep apnea and snoring are associated with incident HTN and DM. Methods: Participants of age 45 - 65 years from 4 ethnicities (Asian, Hispanic, African American and Caucasian) without known cardiovascular disease from Multi Ethnic Study of Atherosclerosis (MESA) were administered a sleep questionnaire. HTN was defined as being on antihypertensive medication or blood pressure ≥140/90 mmHg. DM was defined as fasting blood glucose ≥126 mg/dL or use of antidiabetic medications. Participants with baseline HTN and DM were excluded. Cox proportional hazard models were constructed to evaluate the association of habitual snoring (defined as snoring on ≥3 days of week) and sleep apnea (self-report of diagnosis by doctor) with hypertension or diabetes. The analysis was adjusted for age, gender, race, body mass index (BMI), exercise, education. Two separate analyses were performed after excluding hypertensives and diabetics at baseline. Results: Out of 6618 participants, 6206 responded to the sleep questionnaire. There were 213 (3.4%) participants with sleep apnea and 1481 (23.8%) were categorized as habitual snorers. 98% of participants reporting sleep apnea also reported snoring. There were 1364 (38.7%) cases of incident hypertension and 619 (11.3%) incident DM over a period of 10 years. Habitual snoring and sleep apnea both were not associated with incident HTN. Habitual snoring was also not associated with incident DM. Sleep apnea was independently associated with incident DM (see table). Conclusion: Despite potential misclassification of sleep apnea due to self -report, our study shows a strong association between sleep apnea and incident DM but not with incident hypertension. The findings support future research addressing role of sleep apnea in development of DM.

Pathogenic Roles of the Carotid Body Inflammation in Sleep Apnea

Breathing difficulties in sleep are a hallmark of sleep-disordered breathing commonly observed in patients with sleep disorders. The pathophysiology of sleep apnea is in part due to an augmented activity of the carotid body chemoreflex. Arterial chemoreceptors in the carotid body are sensitive to inflammatory cytokines and immunogenic molecules in the circulation, because cytokine receptors are expressed in the carotid body in experimental animals and human. Intriguingly, proinflammatory cytokines are also locally produced and released in the carotid body. Also, there are significant increases in the expression of proinflammatory cytokines, cytokine receptors, and inflammatory mediators in the carotid body under hypoxic conditions, suggesting an inflammatory response of the carotid body. These upregulated cytokine signaling pathways could enhance the carotid chemoreceptor activity, leading to an overactivity of the chemoreflex adversely effecting breathing instability and autonomic imbalance. This review aims to summarize findings of the literature relevant to inflammation in the carotid body, with highlights on the pathophysiological impact in sleep apnea. It is concluded that local inflammation in the carotid body plays a pathogenic role in sleep apnea, which could potentially be a therapeutic target for the treatment of the pathophysiological consequence of sleep apnea.

Sleep Apnea, Heart Failure, and Pulmonary Hypertension

Despite the emergence of sleep apnea (SA) as a significant risk factor for heart failure (HF) mortality, data indicate that SA remains under-diagnosed and under-treated. Less well established, though perhaps more emphasized, is the role of sleep apnea in pulmonary hypertension (PH). SA occurs in approximately 50 % of HF patients, and its consequences include intermittent hypoxemia, arousal, and intra-thoracic pressure swings leading to neurohormonal stimulation, oxidative stress and inflammation. While SA is also considered a cause of PH, severe PH due solely to SA is rare. Combining the results of several studies using Swan-Ganz catheters for diagnosis of PH, approximately 10 % of patients with OSA have PH. Effective treatment of SA in HF is associated with improved survival, while treatment of SA in PH is typically associated with modest hemodynamic improvement.

No snooze button on treating sleep disorders

[thereby] treating the patient’s whole well-being just like [the recommendations for] nutrition and exercise.” Many of the advances of modern life contribute to the different sleep problems clinicians fi nd in an estimated 30% to 40% of Americans. Air travel, shift work, smartphones buzzing and vibrating in the night, television and the internet—all contribute to insomnia, hypersomnia (sleeping during the day), parasomnia (disruptive sleep), circadian rhythm disturbances, narcolepsy, or sleep apnea. One-half of patients have chronic sleep disturbance. For people who sleep for far less than 8 hours each night or who have jobs or lifestyles that require them to sleep during the day, physiologic or psychological problems may ensue eventually in the form of fatigue, headache, irritability, inattentiveness, or narcolepsy. More serious health problems can also develop, including hypertension and other cardiovascular disorders.

Circulating Endothelial Microparticle Levels and Hemodynamic Severity of Pulmonary Hypertension: Is There a Role for Sleep Apnea?

Circulating Endothelial Microparticle Levels and Hemodynamic Severity of Pulmonary Hypertension: Is There a Role for Sleep Apnea?

Circulating Endothelial Microparticle Levels and Hemodynamic Severity of Pulmonary Hypertension: Is There a Role for Sleep Apnea?

Circulating Endothelial Microparticle Levels and Hemodynamic Severity of Pulmonary Hypertension: Is There a Role for Sleep Apnea?

Sleep Apnea Syndrome

Global risk assessment is the standard of care for coronary artery disease management. In this setting, sleep apnea syndrome, which includes obstructive sleep apnea and central sleep apnea, is being increasingly recognized as a potentially modifiable risk factor for coronary artery disease. Emerging evidence points toward a cause and effect relationship between sleep apnea syndrome and medical conditions like insulin resistance, hypertension, heart failure, and myocardial ischemia. The effects of sleep apnea on coronary artery disease can be independent of many traditional risk factors. Continuous positive airway pressure has been shown to decrease inflammatory markers that are elevated in sleep apnea syndrome. Well-designed randomized controlled clinical trials are needed to better establish the role of sleep apnea in the genesis and progression of coronary artery disease.

Cardiovascular Risk Factors and Signs of Subclinical Atherosclerosis in the Heinz Nixdorf Recall Study: Risk Factor Sleep Apnea

This is a very interesting study, but, as a sleep physician, I was surprised to find no mention of sleep apnea as an independent risk factor for the development of atherosclerosis. The role of sleep apnea in promoting the development of atherosclerosis has been demonstrated in a large number of investigations and scientific studies. As a single example, a review article by Dr. Schulz of Giessen (Germany) that appeared in Deutsches Arzteblatt in 2006 presented this relationship quite clearly. In view of the (high) body-mass index of the participants in this study, I suspect that sleep apnea was a common problem among them.