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Obstructive sleep apnea: Not just a sleep disorder N RajagopalanDepartment of Pulmonary and Critical Care Medicine and Sleep Medicine, University of Massachusetts, Worcester, Massachusetts, USA
Correspondence Address: Source of Support: None, Conflict of Interest: None DOI: 10.4103/0022-3859.81866
Obstructive sleep apnea (OSA) has long been recognized as a disorder characterized by snoring and frequent cessations of breathing resulting in fragmentation of sleep, which eventually leads to cumulative sleep debt in affected patients. Until two decades ago, snoring and apneas drew attention mainly as a social curiosity and sleep apnea was not thought of as a serious disorder with multisystem involvement. Impairment of quality of work and high incidence of motor vehicle accidents associated with OSA were recognized toward the end of the last century. Since the turn of this millennium physicians have become increasingly aware of the various cardiovascular complications, metabolic disturbances, and neuropsychologic deficits. It has become very clear in the last decade that patients with OSA have a high recurrence of atrial fibrillation after elective cardioversion if their sleep apnea is not treated with continuous positive airway pressure (CPAP). Poor control of diabetes mellitus and resistant hypertension in the setting of OSA has also been recognized and significant progress in our understanding in this area has been accomplished. Unless physicians include sleep in their system review, many cases will go undiagnosed, which will eventually result in cardiovascular complications. Patients are also not readily forthcoming with the symptoms of sleep apnea, as they often assume that symptoms, such as snoring and daytime sleepiness, are not something serious to be discussed with their physician. In this review, the characteristics, the pathophysiology, and epidemiology of OSA are discussed. Furthermore, the mechanisms by which OSA affects the cardiovascular, endocrine, and metabolic functions have been explored. Keywords: CPAP, obstructive sleep apnea, OSA, sleep disorder
Obstructive sleep apnea (OSA) is a type of sleep disorder that affects people of all ages, but predominantly affecting obese middle-aged men. There does not seem to be any gender difference over the age of 50 years and there is no significant effect of body mass index (BMI) on the incidence of OSA over the age of 60 years. [1] There seems to be a higher prevalence of OSA with increasing age. [1] As the symptoms of OSA are often subtle in the beginning, they are either unrecognized or ignored. Lack of significant progress at work and disharmony in married life ensue as the disorder gets worse in its severity. There is increasing evidence of impairment of neurologic, psychometric, endocrine, and most important of all cardiovascular functions in OSA. An extensive search of clinical material relating to sleep apnea and its complications was made using Medline search over the last 20 years using terms, such as obstructive sleep apnea, sleep apnea, and sleep-related breathing disorders (SRBD).
Apneas are characterized by the cessation of airflow for more than 10 s. A hypopnea among adults is characterized by a reduction in nasal pressure by at least 30% of baseline for a duration of at least 10 s accompanied by oxygen desaturation ≥ 4%. In patients of 18 years or younger, a hypopnea is defined by a reduction in nasal pressure amplitude of at least 50% compared with baseline, associated with an arousal, awakening, or oxygen desaturation of at least 3%, that lasts for a duration of at least two missed breaths. [2] In OSA, continuing muscular efforts to overcome the obstructed upper airway result in EEG arousals and frequently result in overall arousals that typically follow apneas. Even though it is clear that sleep fragmentation and chronic sleep deprivation cause the sleepiness in OSA, it is not very clear as to what causes and perhaps predicts long-term cardiovascular complications. Potential contenders are repetitive surges in epinephrine secondary to sympathetic activation and recurrent oxygen desaturations. Interestingly, some patients have frequent apneas but do not show any significant desaturations. On the other hand, there are patients who only have hypopneas but have significant desaturations. From our current knowledge it is not clear as to which of these groups carry a higher risk of cardiovascular complications. In most cases of OSA there is a functional impairment of the upper airway dilator muscle as shown by the fact that obstruction is evident only during sleep. Both tonic and phasic activation of the upper airway dilator muscle are important in the pathogenesis of OSA. It is a well-known fact that there is an inspiration-linked phasic activity of genioglossus and upper airway dilator muscle. This is somewhat attenuated in sleep even in normal people but is more pronounced in patients with sleep apnea. According to Poiseuille's law, whenever there is a decrease in the radius of a tube, the flow rate of either a gas or a liquid can only be maintained if there is an increase in the differential pressure. This is shown by the following formula:  where P = pressure drop, μ = viscosity, L = length of the tube, Q = flow, π = constant, r = radius. In the case of airflow through the upper airway, the increasing differential pressure can only be accomplished by creating a more negative intrathoracic pressure. This results in further narrowing of the already compromised upper airway. Thus a vicious cycle is set off, which ultimately results in complete occlusion of the upper airway. There is a relatively higher prevalence of OSA in North American, European, and Asian nations. Approximately 20% of adults have mild OSA with an Apnea Hyperpnoea Index (AHI > 5/h) and 7% of adults have moderate-to-severe OSA (AHI > 15/h). [3] There is a higher prevalence of OSA in men before the age 50 years. After 50 years, the prevalence of OSA is the same in men and women. Interestingly, the prevalence of OSA is influenced by an increase in BMI only before the age 60 years. However, it should be said that obesity at any age makes a pre-existing sleep apnea worse.
The most common symptoms of OSA are sleepiness and tiredness during the daytime and in practically all cases disruptive snoring. There are a number of clinical models that predict the probability of OSA in patients. These models take into account oropharyngeal narrowing (Mallampati classification), neck circumference, and BMI. Definitive diagnosis and management requires a baseline polysomnography followed by a CPAP titration study. Overnight oximetry has been used as a screening test. However, absence of either 3% or 4% desaturation does not necessarily rule out OSA. Home studies with a few channels are increasingly being used as a screening test for the diagnosis of OSA. Even though they have some role, especially as a screening test, they cannot totally replace laboratory-based polysomnography. The most profound effects of OSA are on the cardiovascular system. Even though sleep apnea is a phenomenon seen only in sleep, repeated hypoxemic events, sympathetic activation, and systemic inflammatory mediator release bring about changes that carry over into the daytime. Researchers have often noticed limitations in studying the association of OSA and cardiovascular complications because most of the patients with OSA are also obese and have pre-existing cardiovascular diseases. [4],[5],[6] Ideally, studies looking at this association should have as control obese subjects who have had sleep studies done and proved not to have OSA. To complicate this issue is the fact that some of these obese subjects may have what we know as occult OSA. Despite these shortcomings, a number of studies have convincingly shown striking acute cardiovascular changes with apneic events and disturbed homeostatic mechanisms even during the daytime in OSA patients. There is clearly a perturbation of autonomic system in sleep apnea that may play a significant part in the pathogenesis of cardiovascular complications. The act of breathing suppresses thoracic efferent sympathetic outflow. Absence of breathing results in disinhibition of the sympathetic outflow. Sympathetic activation is potentiated by increased sensitivity of both peripheral and central chemoreceptors by both hypoxemia and hypercarbia. [7] The sympathetic vasoconstriction that results from the apneas and the increase in cardiac output following the apneas results in precipitous increase in blood pressure. Augmented sympathetic activity during awake periods during the daytime has been recognized in normotensive newly diagnosed sleep apnea patients. [8] Sleep apnea patients often have tachycardia, decreased heart rate variability with respiration, and increased blood pressure variability. [9] This predisposes the patient to increased risk of future hypertension. [10] Vascular responses in OSA have been well studied. Endothelin, a potent vasoconstrictor, has been found to be elevated in untreated OSA patients. [11] Endothelial dysfunction secondary to decreased nitric oxide production has been recognized in OSA patients. This affects both resistance and the conduit vessels. [12],[13] Improvement in brachial artery dilation with use of CPAP has been noted in some studies. [14],[15] Repetitive "hypoxemia-reperfusion" injury associated with apneic events can result in increased levels of free radicals in OSA patients. This has been observed in OSA patients with cardiovascular disease. [16],[17] However, this has not been observed in OSA patients without cardiovascular disease. [18],[19] The heart is subjected to a tremendous degree of mechanical disadvantage during periods of upper airway obstruction. Intrathoracic pressure up to −60 to−80 mmHg has been recorded during apneic events. After load of the left ventricle is significantly increased during apnea, as shown by Laplace's law, the wall tension of a chamber becomes directly proportional to the transmural pressure and the radius of the chamber and inversely proportional to the thickness of the wall of the chamber as shown by the following equation: T = (P × R)/M Repeated mechanical effects of this nature translate into structural changes resulting in left ventricular hypertrophy and diastolic dysfunction. [20] Abrupt changes in the intramural pressure stretch and eventually dilate the atria. [21] These mechanical changes may also contribute to the occurrence of atrial fibrillation. Data on the effects of OSA on coagulation are limited and inconclusive. Increased levels of fibrinogen, plasminogen activator inhibitor-1, hematocrit, and increased platelet aggregability have been consistently noted in OSA patients. [22],[23],[24],[25],[26] Systemic inflammatory mediators, such as adhesion molecules and cytokines, are increased in OSA patients. [27],[28] These substances result in adhesion of leukocytes to the endothelium. Endothelial damage ensues eventually resulting in atherosclerosis. C-reactive protein and serum amyloid A [29],[30] are increased in OSA patients. Elevated levels of these factors are linked to poor cardiovascular outcomes. Interestingly, nasal CPAP treatment in OSA patients has been shown to decrease the levels of some of these systemic mediators. [31] A double-blind placebo-controlled study showed that Etanercept, a tumor necrosis factor antagonist decreased sleepiness in patients with OSA suggesting that tumor necrosis factor may be one of the factors causing sleepiness in OSA. [32] OSA has been found to be associated with a number of cardiovascular conditions that are discussed in the following sections. Systemic hypertension The first study that found the association of OSA and hypertension was the Wisconsin sleep cohort study. Normotensive OSA patients at baseline were followed for 4 years, looking at the incidence of new hypertension 4 years later, independent of obesity and other comorbidities. [33] Since then several randomized controlled studies have shown the association of sleep apnea and hypertension. [34],[35] Consistent decrease in both systolic and diastolic blood pressure has been noted as early as 1 week of CPAP treatment in OSA patients. [34],[35] It has been observed that the association of hypertension and OSA is stronger with increasing age. [36] Enhanced sympathetic tone may be the main reason in the causation of hypertension in OSA patients. Other factors may also be involved in the pathogenesis of hypertension in OSA patients. Subjects at high risk for sleep apnea have twice the risk of primary hyperaldosteronism and have been shown to have increased 24-h urinary aldosterone excretion compared with subjects at low risk for OSA. [37] Genetic factors may also contribute to the association of hypertension and OSA. [38],[39] The importance of OSA in the causation of hypertension has been highlighted by the recognition of OSA as a treatable cause of hypertension by the Seventh Joint National Committee of Hypertension guidelines. [40] Based on the current evidence, patients with resistant hypertension should be screened for OSA and treated with CPAP. Atrial fibrillation There are a number of mechanisms operating in OSA that can result in atrial fibrillation. Even though an association of atrial fibrillation and OSA has been shown by a number of studies, it has not been proven beyond doubt that OSA causes atrial fibrillation. From the mechanical standpoint sudden stretches in the atria and pulmonary veins resulting from drastic changes in transmural pressure may result in atrial dilation and possibly atrial fibrillation. Other factors that may contribute to the high incidence of atrial fibrillation are high sympathetic activity, sudden surges in blood pressure, hypoxemia, hypercarbia, acidosis, and systemic inflammation. Guilleminault et al. using Holter monitoring found that 3% of 400 OSA patients he studied had atrial fibrillation. [41] This is much higher than the estimated prevalence of atrial fibrillation in the general population. To look at the flip side of the coin there are data indicating that a high percentage of patients with atrial fibrillation have a high incidence of OSA. [42] There is a high incidence of recurrence of atrial fibrillation in the first year following cardioversion in sleep apnea patients not being treated with CPAP. [43] Heart failure It has been well known that nocturnal increase in sympathetic activity and elevated blood pressure create left ventricular pressure overload, which leads to left ventricular hypertrophy and impaired ventricular relaxation. It has also been shown that augmented inspiratory effort resulting from upper airway closure leads to increased negative intrathoracic pressure, which in turn increases the transmural pressure of the left ventricle and there by increases the afterload. [44] Also the increase in venous return during these augmented inspiratory phases distends the right ventricle and pushes the interventricular septum toward the left ventricle, which impairs the left ventricular diastole. [45] Comorbid factors, such as obesity, hypertension, and type 2 diabetes mellitus, also add to the diastolic dysfunction of the left ventricle. The treatment of OSA with nasal CPAP has been shown by some studies to increase the ejection fraction of the left ventricle in patients with left ventricular systolic dysfunction and by lowering the sympathetic activity decrease the left ventricular irritability and cardiac arrhythmias. [46],[47],[48] Conduction abnormalities Sleep apnea is associated with prolonged episodes of hypoxemia. A physiologic reflex similar to the diving reflex is seen during these periods of apnea. The physiologic advantage of diving reflex is to conserve oxygen to the most important vital organs, such as brain and heart, while cutting down blood flow to the periphery. This essentially consists of a sympathetic vasoconstriction affecting the periphery and vagal response affecting the heart. A number of conduction abnormalities have been noted in patients with OSA. [49] Sinoatrial block, sinus arrest, AV conduction abnormalities, and even asystole are well known to occur during apneas in patients with OSA. No structural or anatomic abnormalities have been noted in the conduction apparatus in these patients. It has been proven beyond doubt that these conduction abnormalities result from increased parasympathetic tone and hypoxemia. Reversal of these conduction abnormalities have also been studied by the use of nasal CPAP. [49] Arrhythmias during sleep and in obstructive sleep apnea Ventricular arrhythmias demonstrate a diurnal variation with highest incidence in the early morning. This may in fact be related to diurnal variation in sympathetic activity. Ventricular premature contractions and other arrhythmias have been noted to occur with prolonged desaturations in OSA. These are more common in post myocardial infarction situation and also in the postoperative period following coronary artery bypass graft surgery. There is a high prevalence of sudden cardiac death in patients with OSA. However, the timing of this event is between midnight and 6 am rather than between 6 am and noon as in the general population. [50] A higher prevalence of OSA has been noted in patients with Marfan syndrome. This may be related to the higher incidence of cranial facial abnormalities and lax connective tissue of the upper airway structures. [51] Sudden changes in the aortic transmural pressure secondary to changes in intrathoracic pressure, which are well known to occur in OSA possibly contribute to the aortic dilation seen in Marfan syndrome, who classically have cystic medial necrosis. Increased aortic transmural pressure has also been implicated in the causation of aortic dissection. Patients with aortic dissection are more likely to have OSA independent of hypertension. [52] Nocturnal ST-segment changes suggestive of myocardial ischemia have been noted in OSA patients who did not have any other clinically significant symptoms of coronary artery disease. [53] In a 7-year follow-up study, a higher likelihood of cardiovascular events in patients with OSA was noted. [54] More than 50% of untreated OSA patients had cardiovascular events compared with <10% of those treated with CPAP. [55] In a small study of patients with at least one coronary artery disease (more than 70% occlusion) and moderate-to-severe OSA (AHI more than 15/h), CPAP treatment was accompanied by an estimated risk reduction of 76% for a composite endpoint (cardiovascular death, acute coronary syndrome, hospitalization for heart failure, and coronary revascularization). [56] In a 10-year follow-up study, Marin and colleagues studied healthy men, primary snores, subjects with mild-to-moderate OSA, untreated severe OSA patients, and severe OSA patients treated with CPAP. The risk of fatal and nonfatal cardiovascular events significantly reduced in severe OSA patients who were treated. [56] Pulmonary hypertension Hypoxia whether it is acute or chronic has been a well-recognized factor in the causation of pulmonary hypertension. This is probably the most likely mechanism of pulmonary arterial hypertension in chronic obstructive pulmonary disease (COPD). However, it is not clear whether this is the mechanism for Pulmonary Artery Hypertension (PAH) sometimes observed in OSA. Hypoxia-inducible factors (HIF)-one alpha and HIF-2 mediate certain adaptive mechanisms in hypoxic conditions. These factors have been shown to induce synthesis of mRNA, which protect the cells from apoptosis. Even though reversible pulmonary arterial hypertension has been noted in both acute and chronic hypoxic conditions, it is not clear whether chronic remodeling occurs in these situations. 5-Hydroxy tryptamine has been implicated in the pathogenesis of pulmonary arterial hypertension in the setting of COPD. 5-HTs exert its effect via transporter 5-HTT and receptors 5-HTA1, 5-HTA2, 5-HTB1, and 5-HTB2. Animals lacking 5-HT transporter gene are protected against hypoxia-induced PAH. Patients with COPD with LL genotype (associated with higher levels of 5-HTT expression in pulmonary artery smooth muscle cell (PASMC) have more severe PAH than the SS genotype or heterozygotes. [57] So far there is no convincing data as to the role of 5-HT or its transporter in the pathogenesis of PAH in OSA patients. Mitochondria of PASMC play a role in hypoxia-induced pulmonary vasoconstriction. Mitochondrial reactive oxygen species decreases in hypoxic conditions. This inhibits oxygen-sensitive ATP-dependent voltage-gated potassium channel and causes membrane depolarization and activation of voltage-gated L-type calcium channel. This is followed by calcium influx and smooth muscle contraction. HIF-one alpha activation downregulates oxygen-sensitive potassium channels and causes more muscle contraction in pulmonary vascular system. Patients with pulmonary arterial hypertension tend to have lower PaO 2 and higher PaCO 2 , lower forced vital capacity and lower forced expiratory volume in 1 s. The presence of PAH has not been recognized to be associated with the severity of OSA as measured by AHI. A number of retrospective and a few prospective studies have found the incidence of PAH to be between 19% and 42%. [58] A number of these studies did not exclude other coexisting lung conditions, including COPD. Most of the studies used mean pulmonary artery pressure (MPAP) of 20 mm mercury as cutoff point for calling it pulmonary arterial hypertension. Bady and colleagues using right heart catheterization data found 12/44 (27%) had MPAP greater than 20 mm mercury. [59] All these patients had normal pulmonary capillary occlusion pressure. These patients were found to have more severe nocturnal hypoxemia, higher BMI, lower daytime PaO 2 and higher PaCO 2 . Taken together, these data suggest that the frequency of PAH in patients with OSA is low and often mild. There are a few patients who have significant elevation in pulmonary artery pressure in association with OSA. It is not clear whether these are instances of incidental idiopathic pulmonary arterial hypertension or not. In support of the notion that OSA is responsible for pulmonary artery hypertension in those patients with mild PAH is observation that CPAP treatment normalizes their pulmonary arterial pressures. [60],[61] Cerebrovascular events and obstructive sleep apnea The association of OSA and cerebrovascular events has long been recognized. However, the etiologic link has been difficult to establish. Studies have reported a higher prevalence of OSA in patients with recent stroke. [62],[63] OSA is being recognized as a modifiable risk factor for cerebrovascular disease. It is believed that the circadian influence on stroke incidence may be related to the effect of sleep on cerebral blood flow and blood rheology. Sleep state has a profound effect on cerebral hemodynamics. Several studies using transcranial Doppler ultrasonography, Xenon-133 inhalation method, and single photon emission computerized tomography have shown 5%-28% reduction in cerebral blood flow during non-REM sleep and a 4%-41% increase in REM sleep compared to wakefulness in normal persons. [64],[65] Changes in cerebral blood flow normally reflect changes in metabolic rate and oxygen consumption in both non-REM and REM sleep. The exception to this is during translation to and from sleep. These cerebral blood flow changes are independent of extracerebral hemodynamic factors. Several studies have shown large fluctuations in cerebral blood flow during and after apnea. Reduction in cerebral blood flow during awake period has been noted in OSA patients compared with normal subjects. [66] Significant reductions in cerebral blood flow, particularly to the brainstem-cerebellum regions during non-REM sleep has been reported by many studies in OSA. [67] Simultaneous monitoring of intracranial pressure, intraarterial pressure, and central venous pressure during sleep in OSA patients has shown marked increase in intracranial pressure, resulting in decrease in the cerebral blood flow during periods of apneas. The magnitude of the increased intracranial pressure was found to be correlated with duration of apneas. Impaired cerebral autoregulation has been shown by abnormalities in cerebrovascular responses to hypercapnia. The cerebral under perfusion during sleep apnea was found to be associated with cerebral oxygen desaturation by near-infrared spectroscopy, suggesting cerebral ischemia during apneas. [68] These abnormalities have been shown by studies to be corrected by CPAP treatment indicating functional impairment rather than structural changes. The observed high frequency of OSA in patients with Transient Ischemic Attack (TIA) suggests pre-existing OSA in patients with strokes rather than a consequence of it. Carotid intimal-medial thickness often considered a surrogate for stroke risk has been found to be increased in patients with OSA. [69] Paroxysmal atrial fibrillation in combination with prothrombotic tendency may also account for the increased risk of stroke in sleep in OSA patients. Increase in right heart pressure secondary to sleep apnea can also result in shunting through a patent foramen ovale and result in paradoxical embolism. [70] Sleep Heart Health Study [71] reported an odds ratio of 1.6 and Wisconsin Sleep Cohort Study [72] reported an odds ratio of 4.3 for stroke in OSA patients compared with normal controls. A more recent longitudinal study showed an association of OSA with stroke even after controlling for other confounding variables. [73] Metabolic dysregulation Leptin is a hormone produced by fat cells. Leptin plays an important regulatory role in metabolism and in respiration. Leptin levels have been found to be high in obese people and also in OSA patients without obesity. Increased resistance to leptin has been proposed as a reason for decreased activity of leptin in both obese people and OSA patients. [74] Genetic factors may contribute to the high levels of leptin seen in OSA patients as shown by linkage of leptin levels and families with OSA. [75] Increased leptin levels may also be related to nocturnal hypoxemia and carbon dioxide retention. [76],[77] Differential resistance to leptin may have implications, such as impaired regulation of respiration, increased risk of cardiovascular complications secondary to high levels, platelet aggregation, and cardiovascular events. [78],[79] Neuropeptide Y, an orexigenic hypothalamic peptide plays an important role in regulating body weight, energy balance, and sympathetic tone. Neuropeptide Y levels are increased in OSA and with CPAP treatment, decrease promptly. [80] Ghrelin, a peptide produced in the stomach regulates appetite control and satiety. Levels are increased in OSA and decrease appropriately with CPAP treatment. [81] The characteristic features of metabolic syndrome include increased weight and waist circumference, hypertension, high fasting glucose levels and triglycerides, low high-density lipoprotein, microalbuminuria, systemic inflammation, sympathetic activation, endothelial dysfunction, and physical deconditioning. Metabolic syndrome (syndrome X) has been well recognized as a major risk factor for cardiovascular disease. [82] Comparing patients with and without OSA but with similar BMI, patients with OSA are more likely to have metabolic syndrome. [82] It is debatable whether OSA is a component of metabolic syndrome sharing the same pathophysiology or whether it promotes the development of metabolic syndrome. Erectile dysfunction has been linked to OSA. Two percent of patients with erectile dysfunction have been reported to have OSA. [83] Erectile dysfunction or decreased libido has been reported in 33% of patients with OSA. Different mechanisms have been postulated to explain sexual dysfunction. They are dysregulation of autonomic vascular control, endothelial dysfunction, and sleep deprivation. Nocturnal levels of testosterone have been found to be decreased to levels seen in elderly subjects. Obstructive sleep apnea and diabetes Insulin resistance in association with OSA either as a part of metabolic syndrome or by itself has been well recognized. Sleep-disordered breathing is associated with an increase in sympathetic neural traffic that is manifested by elevated levels of plasma and urinary catecholamines. [84],[85] Sleep deprivation by itself has been associated with altered glucocorticoid regulation and glucose intolerance. [86],[87] Glucose intolerance secondary to hypoxemia is a well-known phenomenon. The association between OSA and insulin resistance and therefore of type 2 diabetes mellitus is so strong that physicians should always investigate for OSA and treat these patients with CPAP, especially in obese patients presenting with other features of metabolic syndrome. Obstructive sleep apnea and other neurologic disorders OSA occurs with increasing frequency with aging. It is a potential etiologic factor for a new onset as well as for worsening of seizure. Sleep fragmentation and chronic sleep deprivation are perhaps the responsible factors. [88],[89] Neuropsychologic deficits in attention span, executive functioning, and fine motor coordination have been linked to OSA. [90] Intelligence, basic verbal, and visual-perceptual abilities do not seem to be affected by OSA. Similarly, not so significant memory disturbances have been recognized in OSA. However, it must be mentioned that job performance has been shown to improve significantly with CPAP treatment. [91] Specific neurologic deficits, such as apraxia of speech associated with seizure disorder in a child, have been described, and definitive treatment for OSA by tonsillectomy and adenoidectomy has been shown to be curative in that child. [92]
Sleep apnea is just not a sleep disorder. In addition to impairment of job performance it also accounts for a big chunk of automobile accidents. [93],[94] Since the time these issues were recognized three decades ago, significant advances have been made in the understanding of other major complications of sleep apnea. The most important of these are cardiovascular, such as atrial fibrillation, diastolic dysfunction, and hypertension. Unless physicians include Sleep in their system review, many cases will go undiagnosed with the resulting cardiovascular complications. Patients are also not readily forthcoming with the symptoms of sleep apnea as they assume that symptoms, such as snoring and daytime sleepiness, are not something serious to be discussed with their physician. With the ever-increasing health care cost, less expensive screening tests are being relied up on for the diagnosis of sleep apnea. Tests, such as overnight oximetry and home study using limited recording are not very sensitive in diagnosing OSA. These issues are definitely of paramount importance in developing countries with limited resources. Hopefully in the next few years we should come up with simple and less expensive tests and treatment for this simple but serious disorder.
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