Original Article
Day–Night Pattern of Sudden Death in Obstructive Sleep Apnea
N Engl J Med 2005; 352:1206-1214March 24, 2005
- Abstract
Background
The risk of sudden death from cardiac causes in the general population peaks from 6 a.m. to noon and has a nadir from midnight to 6 a.m. Obstructive sleep apnea is highly prevalent and associated with neurohormonal and electrophysiological abnormalities that may increase the risk of sudden death from cardiac causes, especially during sleep.
Methods
We reviewed polysomnograms and the death certificates of 112 Minnesota residents who had undergone polysomnography and had died suddenly from cardiac causes between July 1987 and July 2003. For four intervals of the day, we compared the rates of sudden death from cardiac causes among people with obstructive sleep apnea and the following: the rates among people without obstructive sleep apnea, the rates in the general population, and the expectations according to chance. For each interval, we assessed the median apnea–hypopnea index and the relative risk of sudden death from cardiac causes. We similarly analyzed sudden death from cardiac causes during three time intervals that correlate with usual sleep–wake cycles.
Results
From midnight to 6 a.m., sudden death from cardiac causes occurred in 46 percent of people with obstructive sleep apnea, as compared with 21 percent of people without obstructive sleep apnea (P=0.01), 16 percent of the general population (P<0.001), and the 25 percent expected by chance (P<0.001). People with sudden death from cardiac causes from midnight to 6 a.m. had a significantly higher apnea–hypopnea index than those with sudden death from cardiac causes during other intervals, and the apnea–hypopnea index correlated directly with the relative risk of sudden death from cardiac causes from midnight to 6 a.m. For people with obstructive sleep apnea, the relative risk of sudden death from cardiac causes from midnight to 6 a.m. was 2.57 (95 percent confidence interval, 1.87 to 3.52). The analysis of usual sleep–wake cycles showed similar results.
Conclusions
People with obstructive sleep apnea have a peak in sudden death from cardiac causes during the sleeping hours, which contrasts strikingly with the nadir of sudden death from cardiac causes during this period in people without obstructive sleep apnea and in the general population.
Media in This Article
Figure 1
Day–Night Pattern of Sudden Death from Cardiac Causes in 78 Persons with and 34 Persons without Obstructive Sleep Apnea (OSA) and in the General Population.Figure 2
The Apnea–Hypopnea Index for Persons with Sudden Death from Cardiac Causes during Six-Hour Intervals (Panel A) and the Relative Risk of Sudden Death from Cardiac Causes from Midnight to 6 a.m. for Persons with Mild-to-Moderate Obstructive Sleep Apnea and for Persons with Severe Obstructive Sleep Apnea (Panel B).Article Activity
- Article
The risk of sudden death from cardiac causes in the general population is significantly greater during the morning hours after waking (i.e., from 6 a.m. to noon) than during the other six-hour intervals of the day.1 Also, there is a marked nadir in the risk of sudden death from cardiac causes during sleep (i.e., from midnight to 6 a.m.).1 This same day–night pattern has been shown for the incidence of sudden death from cardiac causes in patients with heart failure2 and for the incidence of acute myocardial infarction.1 The increase in risk in the morning may in part be due to changes in sympathetic activity,3 baroreflex sensitivity,4 coagulability,5 and electrophysiological abnormalities6-8 during the waking morning hours, all of which may predispose persons to cardiac ischemia and fatal arrhythmias.
Obstructive sleep apnea affects 17 to 24 percent of North American adults.9 In people with obstructive sleep apnea, nocturnal repetitive episodes of acute apnea elicit hypoxemia, hypercapnia, increased sympathetic drive,10 surges in blood pressure,10 increases in cardiac-wall stress,11 and cardiac arrhythmias.12-14 Obstructive sleep apnea is also associated with hypercoagulability, vascular oxidative stress, systemic inflammation, and endothelial dysfunction.15 Thus, people with obstructive sleep apnea have severe perturbations of autonomic, hemodynamic, humoral, and vascular regulation during sleep that contrast with the physiology of normal sleep. It is not known whether these nocturnal abnormalities are associated with an increased risk of sudden death from cardiac causes during the night, a time when the risk of sudden death from cardiac causes is at its lowest level for the general population.1
We tested the hypothesis that people with obstructive sleep apnea are more likely to have sudden death from cardiac causes from midnight to 6 a.m. than during the other six-hour intervals of the day. We also tested the hypothesis that the frequency of sudden death from cardiac causes from midnight to 6 a.m. is higher in people with obstructive sleep apnea than in people without obstructive sleep apnea, the general population, and what is expected by chance (i.e., 25 percent per six-hour interval).
Methods
Study Population
We included subjects who authorized their records to be used for research, and the institutional review board of the Mayo Foundation approved the study. We identified Minnesota residents who underwent diagnostic polysomnography at the Mayo Clinic Sleep Disorders Center from July 1, 1987, to July 31, 2003, and confirmed their vital status (available for 99.6 percent) with the use of records from the Minnesota Department of Health and the Mayo Clinic. We then manually reviewed the deceased persons' death certificates (available for 83.8 percent) and included in our study those who died of sudden death from cardiac causes before July 31, 2003 (112 people).
Classification of Sudden Death from Cardiac Causes
Manual review of death certificates and data from the Minnesota Department of Health provided the immediate and underlying causes of death, time of death, and time interval from onset of symptoms to death. A state nosologist used the methods of the National Center for Health Statistics to assign causes of death. We classified the following causes of death as sudden death from cardiac causes: “sudden cardiac death,” “cardiac dysrhythmia,” “cardiac arrhythmia,” “cardiac arrest,” “cardiorespiratory arrest,” or “coronary heart disease” or “myocardial infarction” in which the interval from symptoms to death was an hour or less.
Persons were excluded if the time of sudden death from cardiac causes was not stated or if the death certificate provided information that explicitly contradicted the following definition of sudden death from cardiac causes: “natural death due to cardiac causes, heralded by abrupt loss of consciousness within one hour of the onset of acute symptoms; preexisting heart disease may have been known to be present but the time and mode of death are unexpected”16 and nontraumatic.16 The occurrence of sudden death from cardiac causes during sleep was an exception to the criteria for “loss of consciousness within one hour of the acute onset of symptoms,”16 since some instances of sudden death from cardiac causes occurring during sleep may preclude awakening and the development of symptoms, or the witnessing of these events by others. The death certificates of six people stated that sudden death from cardiac causes was unwitnessed or presumed, but their time of death was noted, and these people were included in the study. The death certificates of all other persons did not state whether sudden death from cardiac causes was witnessed or unwitnessed. Thirty-six death certificates (32 percent) provided specific information about the time interval from symptoms to death.
Classification of Obstructive Sleep Apnea
The sleep evaluations of all 112 persons were conducted by a sleep specialist at the Mayo Clinic Sleep Disorder Center. We reviewed each person's first diagnostic polysomnogram, which included measures of the electroencephalogram, electro-oculogram, electromyogram, electrocardiogram, thoracoabdominal excursions, pulse oximetry, and naso-oral airflow.
An apnea was defined as cessation of airflow for at least 10 seconds in the presence of thoracoabdominal ventilatory efforts, and a hypopnea as a reduction in airflow of at least 30 percent with a decrease in oxygen saturation of 2 percent or more for at least 10 seconds in the presence of thoracoabdominal ventilatory efforts. The apnea–hypopnea index was calculated as the sum of apneas and hypopneas per hour of sleep. According to American Academy of Sleep Medicine criteria, an apnea–hypopnea index of 5 or more established the diagnosis of obstructive sleep apnea.17
We collected data on the demographics, coexisting conditions, height, and weight of each person at the time of polysomnography. We considered that continuous positive airway pressure had been used if it was prescribed after the sleep study (which was noted by the sleep-medicine physician reviewing the study results and plan of care) and if a subsequent note in the medical record stated that continuous positive airway pressure was being used. The personnel who collected data from polysomnograms and confirmed sleep diagnoses were different from those who collected data from death certificates and confirmed death diagnoses, and the procedures were performed in a masked fashion.
Statistical Analysis
Characteristics of the study population were described as means ±SD and counts (with percentages) and were compared according to the status of obstructive sleep apnea and the time of sudden death from cardiac causes with the use of the two-tailed t-test, Fisher's exact test, and analysis of variance. The frequency distribution of sudden death from cardiac causes for the four six-hour intervals was compared between persons with and persons without obstructive sleep apnea with the use of Fisher's exact test. The proportion of people with obstructive sleep apnea who had sudden death from cardiac causes during each time interval was compared, with the use of the binomial distribution, with the proportion of people who had sudden death from cardiac causes during the same time interval in a historical control population (from a meta-analysis of 19,390 persons with sudden death from cardiac causes in the general population)1 and with the proportion that was expected by chance to have sudden death from cardiac causes during each quarter of the day (i.e., 25 percent).
The apnea–hypopnea indexes of persons who had sudden death from cardiac causes during each time interval were expressed as medians (with interquartile ranges) and compared with the use of the Kruskal–Wallis test. For persons with and without obstructive sleep apnea, we calculated the relative risk and 95 percent confidence interval of sudden death from cardiac causes during each 6-hour interval as compared with the remaining 18 hours of the day.
We also performed similar analyses of sudden death from cardiac causes in persons with and persons without obstructive sleep apnea for three eight-hour intervals of the day (6 a.m. to 2 p.m., 2 p.m. to 10 p.m., and 10 p.m. to 6 a.m.). These intervals better represent usual sleep–wake cycles.
Results
Patient Characteristics
Characteristics of the study population are described in Table 1Table 1
Characteristics of the Study Population at the Time of Polysomnography, According to the Status of Obstructive Sleep Apnea (OSA) and the Time of Sudden Death from Cardiac Causes.. The diagnoses for the 34 persons without obstructive sleep apnea were no sleep disorder (53 percent), central sleep apnea (23 percent), periodic leg movement disorder (9 percent), obesity–hypoventilation syndrome (6 percent), narcolepsy (6 percent), and hypoventilation due to neuromuscular disease (3 percent). There was a higher proportion of men in the group with obstructive sleep apnea than in the group without obstructive sleep apnea, but the two groups were similar in terms of age, body-mass index, and coexisting conditions. There were no differences in characteristics, or reported use of continuous positive airway pressure, between persons with sudden death from cardiac causes during the various intervals of the day. The use of continuous positive airway pressure was reported in 15 percent of patients with an apnea–hypopnea index of 5 to 19, 39 percent of patients with an apnea–hypopnea index of 20 to 39, and 58 percent of patients with an apnea–hypopnea index of 40 or more (P<0.001).Time Distribution of Sudden Death from Cardiac Causes
Figure 1Figure 1
Day–Night Pattern of Sudden Death from Cardiac Causes in 78 Persons with and 34 Persons without Obstructive Sleep Apnea (OSA) and in the General Population. shows the primary results. From midnight to 6 a.m., the frequency of sudden death from cardiac causes was significantly higher in persons with obstructive sleep apnea than in persons without obstructive sleep apnea (46 percent vs. 21 percent, P=0.01), than in the general population (46 percent vs. 16 percent, P<0.001), and than was expected by chance (46 percent vs. 25 percent, P<0.001). From 6 a.m. to noon, the frequency of sudden death from cardiac causes was significantly lower in persons with obstructive sleep apnea than in persons without obstructive sleep apnea (20 percent vs. 41 percent, P=0.04). From noon to 6 p.m., the frequency of sudden death from cardiac causes was significantly lower in persons with obstructive sleep apnea than in persons without obstructive sleep apnea (9 percent vs. 26 percent, P=0.02), than in the general population (9 percent vs. 29 percent, P<0.001), and than was expected by chance (9 percent vs. 25 percent, P<0.001).Severity of Obstructive Sleep Apnea
Persons with sudden death from cardiac causes from midnight to 6 a.m. had a significantly higher median apnea–hypopnea index than those with sudden death from cardiac causes from 6 a.m. to noon (39 vs. 8, P<0.001) and noon to 6 p.m. (39 vs. 11, P<0.001), and a similar median apnea–hypopnea index to that in persons with sudden death from cardiac causes from 6 p.m. to midnight (39 vs. 41) (Figure 2AFigure 2
The Apnea–Hypopnea Index for Persons with Sudden Death from Cardiac Causes during Six-Hour Intervals (Panel A) and the Relative Risk of Sudden Death from Cardiac Causes from Midnight to 6 a.m. for Persons with Mild-to-Moderate Obstructive Sleep Apnea and for Persons with Severe Obstructive Sleep Apnea (Panel B).). As compared with persons without obstructive sleep apnea, the relative risk of sudden death from cardiac causes from midnight to 6 a.m. was 1.87 (95 percent confidence interval, 0.86 to 4.04) for persons with mild-to-moderate obstructive sleep apnea (apnea–hypopnea index, 5 to 39) and 2.61 (95 percent confidence interval, 1.27 to 5.38) for persons with severe obstructive sleep apnea (apnea–hypopnea index, ≥40) (Figure 2B).Relative Risk of Sudden Death from Cardiac Causes
For persons with obstructive sleep apnea, the relative risk of sudden death from cardiac causes from midnight to 6 a.m. (as compared with the remaining 18 hours of the day) was 2.57 (95 percent confidence interval, 1.87 to 3.52), from 6 a.m. to noon was 0.77 (95 percent confidence interval, 0.49 to 1.21), from noon to 6 p.m. was 0.30 (95 percent confidence interval, 0.15 to 0.61), and from 6 p.m. to midnight was 0.97 (95 percent confidence interval, 0.64 to 1.46). For persons without obstructive sleep apnea, the relative risk of sudden death from cardiac causes from midnight to 6 a.m. (as compared with the remaining 18 hours of the day) was 0.77 (95 percent confidence interval, 0.36 to 1.66), from 6 a.m. to noon was 2.10 (95 percent confidence interval, 1.14 to 3.85), from noon to 6 p.m. was 1.08 (95 percent confidence interval, 0.54 to 2.16), and from 6 p.m. to midnight was 0.40 (95 percent confidence interval, 0.15 to 1.08) (Figure 3Figure 3
Relative Risk of Sudden Death from Cardiac Causes during Six-Hour Intervals as Compared with the Remaining 18 Hours of the Day, for 78 Persons with and 34 Persons without Obstructive Sleep Apnea (OSA).).Sleep–Wake Cycles
The sleep–wake cycles are described in Figure 4Figure 4
Sudden Death from Cardiac Causes According to Usual Sleep–Wake Cycles.. Included are the day–night pattern of sudden death from cardiac causes (Figure 4A), the severity of obstructive sleep apnea (Figure 4B), and the relative risk of sudden death from cardiac causes during the three time intervals that represent usual sleep–wake cycles (Figure 4C).Discussion
This study shows that persons with obstructive sleep apnea have a significantly increased risk of sudden death from cardiac causes during the sleeping hours, which is in striking contrast to the nadir of sudden death from cardiac causes during this time in persons without obstructive sleep apnea and in the general population. In the analysis of sudden death from cardiac causes from midnight to 6 a.m. (which allows for the comparison of our results to results of large studies in the general population) and in the analysis of sudden death from cardiac causes from 10 p.m. to 6 a.m. (which is more relevant to sleep-related pathophysiology), a marked nocturnal peak in sudden death from cardiac causes was observed in persons with obstructive sleep apnea. In more than half of persons with obstructive sleep apnea, sudden death from cardiac causes occurred between 10 p.m. and 6 a.m. By contrast, the persons without obstructive sleep apnea in our study sample had a day–night pattern of sudden death from cardiac causes very similar to that in the general population, with a peak in sudden death from cardiac causes from 6 a.m. to noon.
Furthermore, our analysis showed that the severity of obstructive sleep apnea correlated directly with the risk of nocturnal sudden death from cardiac causes, such that the relative risk of sudden death from cardiac causes during the sleeping hours was 40 percent higher in persons with severe obstructive sleep apnea (apnea–hypopnea index, ≥40) than in those with mild-to-moderate obstructive sleep apnea (apnea–hypopnea index, 5 to 39).
The mean age at which sudden death from cardiac causes occurred in persons with obstructive sleep apnea was similar to the mean age of sudden death from cardiac causes in persons without obstructive sleep apnea and in the general population.18 Our findings should not be generalized to younger persons with obstructive sleep apnea. Also, this finding suggests that obstructive sleep apnea does not hasten sudden death from cardiac causes; however, our study cannot address whether obstructive sleep apnea increases the overall risk of sudden death from cardiac causes.
Our data may also provide insights into the conventional understanding of the day–night pattern of sudden death from cardiac causes in the general population. First, obstructive sleep apnea may be implicated in some of the 16 percent of cases of sudden death from cardiac causes that occur between midnight and 6 a.m. in the general population,1 since obstructive sleep apnea affects at least 25 million adult Americans9 and remains undiagnosed in the vast majority of these people.19 Second, the risk of sudden death from cardiac causes from 6 a.m. to noon in persons without obstructive sleep apnea may be even greater than the risk that is currently supported by data from the general population, since those data include people with and people without obstructive sleep apnea, and we showed that the presence of obstructive sleep apnea is associated with a lower risk during this period.
The marked nocturnal nadir of sudden death from cardiac causes in the general population probably reflects the normal physiology of sleep, in which sympathetic activity is decreased3 and cardiac dysrhythmias are uncommon.20 The unique day–night pattern of sudden death from cardiac causes that we observed in persons with obstructive sleep apnea is consistent with their exposure during sleep to critical mechanisms that could promote sudden death from cardiac causes.
Obstructive sleep apnea is characterized by repetitive collapse of the pharyngeal airway during sleep, resulting in complete or partial cessation of airflow, sometimes hundreds of times nightly. The resultant hypoxemia can lead to nocturnal cardiac ischemia21 and ventricular arrhythmias.22 Apneic episodes elicit increased sympathetic activity,10 blood-pressure elevations,10 and platelet aggregation.23 Obstructive sleep apnea is associated with abnormalities in cardiac autonomic and electrophysiological factors, including heart rate variability,24 the duration of the QT interval,25 baroreflex function, and chemoreceptor sensitivity.26 Serious and potentially fatal arrhythmias occur during sleep in patients with obstructive sleep apnea12-14,22,27-31 and are attenuated by effective treatment.14,29-32 Thus, multiple pathophysiological mechanisms occur during sleep in persons with obstructive sleep apnea and may explain an increased risk of nocturnal sudden death from cardiac causes.
Two previous studies evaluated the day–night pattern of sudden death from cardiac causes in persons with sleep disorders.33,34 Neither study specifically examined obstructive sleep apnea. The first study obtained histories of snoring from the cohabitants of 321 men who had sudden death from cardiac causes. It found that habitual snorers were more likely than occasional snorers or nonsnorers to have sudden death from cardiac causes during sleep and between 4 a.m. and 8 a.m.33 The second study reported that among 13 persons with sleep-disordered breathing (not just obstructive sleep apnea) and sudden death from cardiac causes, none died during sleep.34 In contrast, our study assessed the day–night pattern of sudden death from cardiac causes in a large group of nonselected persons with or without confirmed obstructive sleep apnea as determined by the gold standard of diagnostic tests.
One limitation of the present study relates to the recognized difficulty of establishing the diagnosis and timing of sudden death from cardiac causes. Our use of data from death certificates to identify sudden death from cardiac causes has precedent in previous epidemiologic studies35,36 and has been validated in large populations,37-40 including our regional population.39,40 Furthermore, we used information from the death certificates about the time interval from the onset of symptoms to death in order to corroborate the diagnosis of sudden death from cardiac causes on the basis of current definitions.16 For example, we were able to exclude persons who were diagnosed with sudden death from cardiac causes on the basis of old criteria that allowed a 24-hour interval between symptoms and death.
Our methods also improve on past studies that searched databases of diagnostic codes to identify potential cases, since we identified persons with sudden death from cardiac causes by our direct review of every available death record from the larger population. Qualifiers such as “witnessed,” “unwitnessed,” and “presumed” were infrequently noted on the death certificates. Therefore, we included all cases of sudden death from cardiac causes regardless of these statements. Thus, persons with sudden death from cardiac causes during sleep, which may preclude the development of symptoms or the witnessing of the event by others, were exceptions to the criteria that required timing of symptoms and a change in consciousness, and they were included in the study when a time of death was noted. It is important to note that we collected sleep data and death data independently of one another, and in a masked fashion, in order to avoid diagnostic suspicion bias.
Another limitation of the study relates to the ascertainment and interpretation of treatment with continuous positive airway pressure. During the years of this study, continuous-positive-airway-pressure devices that stored the time of use were rarely used. The medical records lacked objective data regarding frequency, duration, or effectiveness of continuous positive airway pressure. Therefore, we could not verify whether continuous positive airway pressure was used in the days before sudden death from cardiac causes or during the event.
That continuous positive airway pressure may have been generally ineffective is suggested by the finding that the risk of nocturnal sudden death from cardiac causes increased with increasing severity of obstructive sleep apnea despite more reported use of continuous positive airway pressure with increasing severity of obstructive sleep apnea. Because of the lack of objective data from continuous-positive-airway-pressure devices, subjective data regarding their use were necessary. This is an important limitation of retrospective assessments of treatment of obstructive sleep apnea.
This study shows that persons with obstructive sleep apnea have a significant alteration in the well-established day–night pattern of sudden death from cardiac causes evident in the general population. Our study cannot address the question of whether obstructive sleep apnea increases the overall risk of sudden death from cardiac causes. Given our findings and the relatively high prevalence of obstructive sleep apnea in Western populations, this is an important question that remains to be answered.
Supported by grants (HL61560, HL65176, HL73211, and M01 R-00585) from the National Institutes of Health, by the Dana Foundation, and by the Mayo Clinic College of Medicine. Dr. Gami is also supported by the Dr. Ralph and Marian C. Falk Medical Research Trust Fellowship for Clinical Research.
Source Information
From the Divisions of Cardiovascular Diseases (A.S.G., V.K.S.), Pulmonary and Critical Care Medicine (E.J.O.), and Hypertension (V.K.S.), Department of Internal Medicine (A.S.G., D.E.H., E.J.O., V.K.S.), Mayo Clinic College of Medicine, Rochester, Minn.
Address reprint requests to Dr. Somers at the Division of Cardiovascular Diseases, Mayo Clinic College of Medicine, 200 First St. SW, Rochester, MN 55905, or at somers.virend@mayo.edu.
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Citing Articles
1
Christine H. Won, Hyung J. Chun, Suparna M. Chandra, Priscilla S. Sarinas, Rajinder K. Chitkara, Paul A. Heidenreich. (2012) Severe obstructive sleep apnea increases mortality in patients with ischemic heart disease and myocardial injury. Sleep and Breathing
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Athanasia Pataka, Euphemia Daskalopoulou, Stefanos Papastefanou, Chousein Baltatzi, Petros Aggelopulos, Emmanuel Vlachogiannis. (2012) Multiple heart pauses during sleep in a patient with obstructive sleep apnoea syndrome. Sleep and Breathing
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Abraham Otero, Paulo Félix, Senén Barro, Carlos Zamarrón. (2012) A structural knowledge-based proposal for the identification and characterization of apnoea episodes. Applied Soft Computing 12:1, 516-526
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Richard B. Berry. 2012. Consequences of Obstructive Sleep Apnea and the Benefits of Treatment. , 281-298.
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H. Klar Yaggi, Paul Dieffenbach. 2012. Sleep-Disordered Breathing and Cerebrovascular Disease. , 647-655.
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Richard L. Verrier, Murray A. Mittleman. 2012. Sleep-Related Cardiac Disorders. , 585-594.
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Richard L. Horner. 2012. Neural Control of the Upper Airway: Integrative Physiological Mechanisms and Relevance for Sleep Disordered Breathing. .
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Bruce J. Swihart, Brian S. Caffo, Ciprian M. Crainiceanu, Naresh M. Punjabi. (2012) Mixed effect Poisson log-linear models for clinical and epidemiological sleep hypnogram data. Statistics in Medicinen/a-n/a
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V. Areias, J. Romero, K. Cunha, R. Faria, J. Mimoso, V. Gomes, U. Brito. (2012) Sleep Apnea–Hypopnea Syndrome and Acute Coronary Syndrome – An association not to forget. Revista Portuguesa de Pneumologia (English Edition) 18:1, 22-28
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Sanjaya Gupta, Todd Arnedt. 2011. Sleep and Cardiovascular Disease. , 135-152.
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Jorge Rey de Castro, Edmundo Rosales-Mayor, Jenny Ferreyra-Pereyra. (2011) Using a generic measure of quality of life in patients with obstructive sleep apnea. Sleep and Breathing 15:4, 729-735
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Hrayr Attarian, Mari Viola-Saltzman, Walter M. Jay. (2011) Ophthalmic and Neuro-Ophthalmic Complications of Obstructive Sleep Apnoea. Neuro-Ophthalmology 35:5-6, 236-241
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David A. Ehrmann. (2011) Metabolic Dysfunction in PCOS: Relationship to Obstructive Sleep Apnea. Steroids
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Ulrich Koehler, Sandra Apelt, Werner Cassel, Olaf Hildebrandt, Christoph Nell, Stephan Ranft, Wolfram Grimm. (2011) Schlafbezogene Atmungsstörungen und maligne ventrikuläre Arrhythmien bei Patienten mit chronischer Herzinsuffizienz. Wiener klinische Wochenschrift
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Prabhakaran Gopalakrishnan, Tahir Tak. (2011) Obstructive Sleep Apnea and Cardiovascular Disease. Cardiology in Review 19:6, 279-290
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Yasuhiko Nakagawa, Ken Kishida, Tohru Mazaki, Hiroyoshi Yokoi, Masakiyo Nobuyoshi, Tohru Funahashi, Iichiro Shimomura. (2011) Impact of Sleep-Disordered Breathing, Visceral Fat Accumulation and Adiponectin Levels in Patients with Night-Time Onset of Acute Coronary Syndrome. The American Journal of Cardiology 108:9, 1266-1271
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Richard L. Horner. 2011. Autonomic consequences of arousal from sleep and neural mechanisms of arousal. , 128-156.
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Nalaka S. Gooneratne. 2011. Sleep apnea in older adults. , 399-417.
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Julio A. Chirinos, Frederick F. Samaha, Mark H. Sanders. 2011. Other cardiovascular consequences of sleep apnea. , 251-285.
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Silje K. Namtvedt, Anna Randby, Gunnar Einvik, Harald Hrubos-Strøm, Virend K. Somers, Helge Røsjø, Torbjørn Omland. (2011) Cardiac Arrhythmias in Obstructive Sleep Apnea (from the Akershus Sleep Apnea Project). The American Journal of Cardiology 108:8, 1141-1146
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KUN-TA CHOU, YU-TIEN CHANG, YUH-MIN CHEN, KANG-CHENG SU, DIANG-WANG PERNG, SHI-CHUAN CHANG, GUANG-MING SHIAO. (2011) The minimum period of polysomnography required to confirm a diagnosis of severe obstructive sleep apnoea. Respirology 16:7, 1096-1102
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Hala A. Shaheen, Ann A. Abd El-Kader, Amira M. Gohary, Neveen M. El-Fayoumy, Lamia M. Afifi. (2011) Obstructive sleep apnea in epilepsy: a preliminary Egyptian study. Sleep and Breathing
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Kavita Mundey, Shilpa Guggali, B. Tucker Woodson. (2011) Use of Portable Monitoring for Diagnosis and Follow-Up of Sleep-Disordered Breathing Treated With Upper Airway Surgery. Sleep Medicine Clinics 6:3, 341-347
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V. Areias, J. Romero, K. Cunha, R. Faria, J. Mimoso, V. Gomes, U. Brito. (2011) Síndrome da Apneia-Hipopneia do Sono e Síndrome Coronária Aguda – Uma associação a não esquecer. Revista Portuguesa de Pneumologia
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Osamu Shirasaki, Mitsuo Kuwabara, Minako Saito, Kayoko Tagami, Sumio Washiya, Kazuomi Kario. (2011) Development and clinical application of a new technique for detecting ‘sleep blood pressure surges’ in sleep apnea patients based on a variable desaturation threshold. Hypertension Research 34:8, 922-928
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Ryujiro Sasanabe, Toshiaki Shiomi. (2011) Improved accuracy for the detection of sleep apnea-related surges in blood pressure. Hypertension Research 34:8, 909-909
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Denis Martinez, Cristini Klein, Laura Rahmeier, Roberto Pacheco Silva, Cintia Zappe Fiori, Cristiane Maria Cassol, Sandro Cadaval Gonçalves, Angelo Jose Goncalves Bos. (2011) Sleep apnea is a stronger predictor for coronary heart disease than traditional risk factors. Sleep and Breathing
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RUI CHEN, KANG-PING XIONG, JUAN-YING HUANG, YI-XIN LIAN, FA JIN, ZHEN-HUA LI, MIN-YAN ZHAO, CHUN-FENG LIU. (2011) Neurocognitive impairment in Chinese patients with obstructive sleep apnoea hypopnoea syndrome. Respirology 16:5, 842-848
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Kishor Gandhi, James W. Heitz, Eugene R. Viscusi. (2011) Challenges in Acute Pain Management. Anesthesiology Clinics 29:2, 291-309
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A. I. Vinik, R. E. Maser, D. Ziegler. (2011) Autonomic imbalance: prophet of doom or scope for hope?. Diabetic Medicine 28:6, 643-651
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U. Koehler, M. Augsten, S. Apelt, P. Boehm, S. Noeske, V. Groß, C. Nell, F. Dette. (2011) Autonome Regulation und nächtliche Arrhythmien bei Patienten mit schlafbezogener Atmungsstörung. Somnologie - Schlafforschung und Schlafmedizin 15:2, 105-110
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Paolo Alboni, Marco Alboni, Lorella Gianfranchi. (2011) Diving bradycardia: a mechanism of defence against hypoxic damage. Journal of Cardiovascular Medicine 12:6, 422-427
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Tawfiq Zeidan-Shwiri, Doron Aronson, Khalid Atalla, Miry Blich, Mahmoud Suleiman, Ibrahim Marai, Lior Gepstein, Lena Lavie, Peretz Lavie, Monther Boulos. (2011) Circadian pattern of life-threatening ventricular arrhythmia in patients with sleep-disordered breathing and implantable cardioverter-defibrillators. Heart Rhythm 8:5, 657-662
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Satya Krishna Ramachandran, Naeem Haider, Kelly A. Saran, Michael Mathis, Joyce Kim, Michelle Morris, Michael O'Reilly. (2011) Life-threatening critical respiratory events: a retrospective study of postoperative patients found unresponsive during analgesic therapy. Journal of Clinical Anesthesia 23:3, 207-213
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Puja Kohli, Jay S. Balachandran, Atul Malhotra. (2011) Obstructive Sleep Apnea and the Risk for Cardiovascular Disease. Current Atherosclerosis Reports 13:2, 138-146
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Shiro Yamada, Mamoru Sakakibara, Shouji Matsushima, Akimichi Saito, Tsuneaki Homma, Arata Fukushima, Yoshihiro Masaki, Masaya Watanabe, Hirofumi Mitsuyama, Hisashi Yokoshiki, Hiroyuki Tsutsui. (2011) Successful termination of recurrent ventricular arrhythmias by adaptive servo-ventilation in a patient with heart failure. Journal of Cardiology Cases 3:2, e57-e61
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Antonia Barceló, Javier Piérola, Mónica de la Peña, Guillem Frontera, Aina Yañez, Alberto Alonso-Fernández, Olga Ayllon, Alvar G. N. Agusti. (2011) Impaired circadian variation of platelet activity in patients with sleep apnea. Sleep and Breathing
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A.P. Vaz, M. Drummond, P. Caetano Mota, M. Severo, J. Almeida, J. Carlos Winck. (2011) Tradução do Questionário de Berlim para língua Portuguesa e sua aplicação na identificação da SAOS numa consulta de patologia respiratória do sono. Revista Portuguesa de Pneumologia 17:2, 59-65
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A.P. Vaz, M. Drummond, P. Caetano Mota, M. Severo, J. Almeida, J.C. Winck. (2011) Translation of Berlin Questionnaire to Portuguese language and its application in OSA identification in a sleep disordered breathing clinic. Revista Portuguesa de Pneumologia (English Edition) 17:2, 59-65
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, Jing Feng, Quan-ying He, Xi-long Zhang, Bao-yuan Chen. (2011) Epworth Sleepiness Scale may be an indicator for blood pressure profile and prevalence of coronary artery disease and cerebrovascular disease in patients with obstructive sleep apnea. Sleep and Breathing
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Rui Chen, Kang-ping Xiong, Yi-xin Lian, Juan-ying Huang, Min-yan Zhao, Jian-xiang Li, Chun-feng Liu. (2011) Daytime sleepiness and its determining factors in Chinese obstructive sleep apnea patients. Sleep and Breathing 15:1, 129-135
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Yasuhiko Nakagawa, Ken Kishida, Shinji Kihara, Ryoko Yoshida, Tohru Funahashi, Iichiro Shimomura. (2011) Nocturnal Falls of Adiponectin Levels in Sleep Apnea with Abdominal Obesity and Impact of Hypoxia-Induced Dysregulated Adiponectin Production in Obese Murine Mesenteric Adipose Tissue. Journal of Atherosclerosis and Thrombosis 18:3, 240-247
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Virend K. Somers, Shahrokh Javaheri. 2011. Cardiovascular Effects of Sleep-Related Breathing Disorders. , 1370-1380.
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T. Bitter, N. Westerheide, C. Prinz, M. S. Hossain, J. Vogt, C. Langer, D. Horstkotte, O. Oldenburg. (2011) Cheyne-Stokes respiration and obstructive sleep apnoea are independent risk factors for malignant ventricular arrhythmias requiring appropriate cardioverter-defibrillator therapies in patients with congestive heart failure. European Heart Journal 32:1, 61-74
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Taeko SASAI, Yuichi INOUE, Akira MATSUO, Masato MATSUURA, Eisuke MATSUSHIMA. (2011) Changes in respiratory disorder parameters during the night in patients with obstructive sleep apnoea. Respirology 16:1, 116-123
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Jan Hedner, Karl A. Franklin, Yüksel Peker. 2011. Coronary Artery Disease and Obstructive Sleep Apnea. , 1393-1399.
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Barbara S. Gold. (2011) Preoperative Evaluation of the Adult Outpatient. ASA Refresher Courses in Anesthesiology 39:1, 57-64
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Robin J. Trupp, Elizabeth J. Corwin, Karen L. Ahijevych, Thomas Nygren. (2010) The Impact of Educational Message Framing on Adherence to Continuous Positive Airway Pressure Therapy. Behavioral Sleep Medicine 9:1, 38-52
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Hiromitsu Sekizuka, Naohiko Osada, Keisuke Kida, Kihei Yoneyama, Yu Eguchi, Fumihiko Miyake. (2010) Relationship between chronic kidney disease and sleep blood pressure in patients with sleep apnea syndrome. Hypertension Research 33:12, 1278-1282
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Meredith A. Brisco, Lee R. Goldberg. (2010) Sleep Apnea in Congestive Heart Failure. Current Heart Failure Reports 7:4, 175-184
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Francoise J. Roux, Meir H. Kryger. (2010) Therapeutics for Sleep-disordered Breathing. Sleep Medicine Clinics 5:4, 647-657
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MARGHERITA PADELETTI, SIMONE VIGNINI, GIUSEPPE RICCIARDI, PAOLO PIERAGNOLI, VALERIO ZACÀ, MICHELE EMDIN, STEFANO FUMAGALLI, SANJA JELIC. (2010) Sleep Disordered Breathing and Arrhythmia Burden in Pacemaker Recipients. Pacing and Clinical Electrophysiology 33:12, 1462-1466
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Péter Torzsa, László Kalabay, Ágnes Ádám, Márta Novák, István Mucsi. (2010) Az obstruktív alvási apnoe klinikai jelentősége, a családorvos szerepe a betegek kezelésében, valamint gondozásában. Orvosi Hetilap 151:42, 1725-1733
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Jacek Wolf, Dagmara Hering, Krzysztof Narkiewicz. (2010) Non-dipping pattern of hypertension and obstructive sleep apnea syndrome. Hypertension Research 33:9, 867-871
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Dashiell GANTNER, Ji-Yong GE, Li-Hua LI, Nick ANTIC, Sam WINDLER, Keith WONG, Emma HEELEY, Shao-Guang HUANG, Ping CUI, Craig ANDERSON, Ji-Guang WANG, Doug MCEVOY. (2010) Diagnostic accuracy of a questionnaire and simple home monitoring device in detecting obstructive sleep apnoea in a Chinese population at high cardiovascular risk. Respirology 15:6, 952-960
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David E. Green, David A. Schulman. (2010) Obstructive Sleep Apnea and Cardiovascular Disease. Current Treatment Options in Cardiovascular Medicine 12:4, 342-354
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S. Steiner, R. Willinghöfer. (2010) Kardiale Auswirkungen der obstruktiven Schlafapnoe. Der Internist 51:7, 857-862
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Christian Prinz, Thomas Bitter, Cornelia Piper, Dieter Horstkotte, Lothar Faber, Olaf Oldenburg. (2010) Sleep apnea is common in patients with coronary artery disease. Wiener Medizinische Wochenschrift 160:13-14, 349-355
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Kim H Chan, Ian Wilcox. (2010) Obstructive sleep apnea: novel trigger and potential therapeutic target for cardiac arrhythmias. Expert Review of Cardiovascular Therapy 8:7, 981-994
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Bernardo Selim, Christine Won, H. Klar Yaggi. (2010) Cardiovascular Consequences of Sleep Apnea. Clinics in Chest Medicine 31:2, 203-220
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Susumu Kashine, Ken Kishida, Tohru Funahashi, Yasuhiko Nakagawa, Michio Otuki, Kohei Okita, Hiromi Iwahashi, Shinji Kihara, Tadashi Nakamura, Yuji Matsuzawa, Iichiro Shimomura. (2010) Characteristics of sleep-disordered breathing in Japanese patients with type 2 diabetes mellitus. Metabolism 59:5, 690-696
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David Vearrier, Barbara Phillips, Michael I. Greenberg. (2010) Addressing obstructive sleep apnea in the emergency department. The Journal of Emergency Medicine
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Silvia Perotti, Marzia Vassalini. (2010) Sudden death due to a hypopharyngeal mass during sleep: A case report. Legal Medicine 12:2, 90-93
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M. Augsten, J.E.S. Nolte, L. Jerrentrup, S. Apelt, H.F. Becker, U. Koehler. (2010) Kardiale Arrhythmien bei obstruktiver Schlafapnoe. Somnologie - Schlafforschung und Schlafmedizin 14:1, 56-60
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Luca Tomaello, Luisa Zanolla, Corrado Vassanelli, Vincenzo LoCascio, Marcello Ferrari. (2010) Sleep Disordered Breathing is Associated with Appropriate Implantable Cardioverter Defibrillator Therapy in Congestive Heart Failure Patients. Clinical Cardiology 33:2, E27-E30
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Mehmood Butt, Girish Dwivedi, Omer Khair, Gregory Y.H. Lip. (2010) Obstructive sleep apnea and cardiovascular disease. International Journal of Cardiology 139:1, 7-16
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Susanna S.S. NG, Tat-On CHAN, Kin-Wang TO, Jenny NGAI, Alvin TUNG, Fanny W.S. KO, David S.C. HUI. (2010) Validation of Embletta portable diagnostic system for identifying patients with suspected obstructive sleep apnoea syndrome (OSAS). Respirology 15:2, 336-342
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Andrew D Calvin, Virend K Somers. (2009) Obstructive sleep apnea and cardiovascular disease. Current Opinion in Cardiology 24:6, 516-520
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Ken Monahan, Amy Storfer-Isser, Reena Mehra, Eyal Shahar, Murray Mittleman, Jeff Rottman, Naresh Punjabi, Mark Sanders, Stuart F. Quan, Helaine Resnick, Susan Redline. (2009) Triggering of Nocturnal Arrhythmias by Sleep-Disordered Breathing Events. Journal of the American College of Cardiology 54:19, 1797-1804
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N. Takasugi, K. Nishigaki, T. Kubota, K. Tsuchiya, K. Natsuyama, M. Takasugi, T. Nawa, S. Ojio, T. Aoyama, M. Kawasaki, G. Takemura, S. Minatoguchi. (2009) Sleep apnoea induces cardiac electrical instability assessed by T-wave alternans in patients with congestive heart failure. European Journal of Heart Failure 11:11, 1063-1070
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Ian Wilcox, Christopher Semsarian. (2009) Obstructive Sleep Apnea. Journal of the American College of Cardiology 54:19, 1810-1812
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S. S. S. Ng, T.-O. Chan, K.-W. To, J. Ngai, A. Tung, F. W. S. Ko, D. S. C. Hui. (2009) Validation of a portable recording device (ApneaLink) for identifying patients with suspected obstructive sleep apnoea syndrome. Internal Medicine Journal 39:11, 757-762
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Yuichi J. Shimada, Kazutoshi Sato, Sam Hanon, Paul Schweitzer. (2009) Termination of Recurrent Ventricular Tachycardia by Continuous Positive Airway Pressure Ventilation. Annals of Noninvasive Electrocardiology 14:4, 404-406
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Neomi Shah, Francoise Roux. (2009) The Relationship of Obesity and Obstructive Sleep Apnea. Clinics in Chest Medicine 30:3, 455-465
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SONYA CRAIG, JUSTIN C. T. PEPPERELL, MALCOLM KOHLER, NICKY CROSTHWAITE, ROBERT J. O. DAVIES, JOHN R. STRADLING. (2009) Continuous positive airway pressure treatment for obstructive sleep apnoea reduces resting heart rate but does not affect dysrhythmias: a randomised controlled trial. Journal of Sleep Research 18:3, 329-336
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Kiran Devulapally, Raymond Pongonis, Rami Khayat. (2009) OSA: the new cardiovascular disease. Heart Failure Reviews 14:3, 155-164
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Sanja Jelic, Thierry H. Jemtel. (2009) Sleep-disordered breathing in acute decompensated heart failure. Current Heart Failure Reports 6:3, 169-175
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Neil E. I. Langlois. (2009) Sudden adult death. Forensic Science, Medicine, and Pathology 5:3, 210-232
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Andrew D. Calvin, Felipe N. Albuquerque, Francisco Lopez-Jimenez, Virend K. Somers. (2009) Obstructive Sleep Apnea, Inflammation, and the Metabolic Syndrome. Metabolic Syndrome and Related Disorders 7:4, 271-277
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J-P Baguet, G Barone-Rochette, J-L Pépin. (2009) Hypertension and obstructive sleep apnoea syndrome: current perspectives. Journal of Human Hypertension 23:7, 431-443
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Kazuomi Kario. (2009) Obstructive sleep apnea syndrome and hypertension: mechanism of the linkage and 24-h blood pressure control. Hypertension Research 32:7, 537-541
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JANET H. SMITH, MATHIAS BAUMERT, EUGENE NALIVAIKO, RONALD DOUGLAS McEVOY, PETER G. CATCHESIDE. (2009) Arousal in obstructive sleep apnoea patients is associated with ECG RR and QT interval shortening and PR interval lengthening. Journal of Sleep Research 18:2, 188-195
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Jean-Louis Pépin, Pascal Defaye, Elodie Vincent, Sylvain Christophle-Boulard, Renaud Tamisier, Patrick Lévy. (2009) Sleep apnea diagnosis using an ECG Holter device including a nasal pressure (NP) recording: Validation of visual and automatic analysis of nasal pressure versus full polysomnography. Sleep Medicine 10:6, 651-656
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Yasuhiko Nakagawa, Ken Kishida, Shinji Kihara, Tohru Funahashi, Iichiro Shimomura. (2009) Adiponectin ameliorates hypoxia-induced pulmonary arterial remodeling. Biochemical and Biophysical Research Communications 382:1, 183-188
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Satya Krishna Ramachandran, Lydia A. Josephs. (2009) A Meta-analysis of Clinical Screening Tests for Obstructive Sleep Apnea. Anesthesiology 110:4, 928-939
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Shiroh Isono. (2009) Obstructive Sleep Apnea of Obese Adults. Anesthesiology 110:4, 908-921
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See Meng Khoo, J. J. Mukherjee, Jason Phua, Dong Xia Shi. (2009) Obstructive sleep apnea presenting as recurrent cardiopulmonary arrest. Sleep and Breathing 13:1, 89-92
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Altan Onat, Gülay Hergenç, Hüsniye Yüksel, Günay Can, Erkan Ayhan, Zekeriya Kaya, Dursun Dursunoğlu. (2009) Neck circumference as a measure of central obesity: Associations with metabolic syndrome and obstructive sleep apnea syndrome beyond waist circumference. Clinical Nutrition 28:1, 46-51
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Lucia Cubattoli, Chiara Barneschi, Egidio Mastrocinque, Paola Bonucci, Pier Paolo Giomarelli. (2009) Cardiac Arrest After Intragastric Balloon Insertion in a Super-Obese Patient. Obesity Surgery 19:2, 253-256
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Richard S.T. Leung. (2009) Sleep-Disordered Breathing: Autonomic Mechanisms and Arrhythmias. Progress in Cardiovascular Diseases 51:4, 324-338
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Sudhansu Chokroverty. 2009. Sleep Disturbances in General Medical Disorders. , 550-580.
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T Douglas Bradley, John S Floras. (2009) Obstructive sleep apnoea and its cardiovascular consequences. The Lancet 373:9657, 82-93
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Masahiko Kato, Taro Adachi, Yuki Koshino, Virend K. Somers. (2009) Obstructive Sleep Apnea and Cardiovascular Disease. Circulation Journal 73:8, 1363-1370
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S. Tasci. (2008) Obstruktive Schlafapnoe und kardiovaskuläre Komorbidität. Der Kardiologe 2:6, 513-524
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Satish Bhadriraju, Carlton R. Kemp, Mani Cheruvu, Srinivas Bhadriraju. (2008) Sleep Apnea Syndrome. Critical Pathways in Cardiology: A Journal of Evidence-Based Medicine 7:4, 248-253
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Baha A. Al-Shawwa, Arunkumar N. Badi, Andrew N. Goldberg, B. Tucker Woodson. (2008) Defining common outcome metrics used in obstructive sleep apnea. Sleep Medicine Reviews 12:6, 449-461
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Olaf Oldenburg, Barbara Lamp, Klaus Freivogel, Thomas Bitter, Christoph Langer, Dieter Horstkotte. (2008) Low night-to-night variability of sleep disordered breathing in patients with stable congestive heart failure. Clinical Research in Cardiology 97:11, 836-842
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Naoki Serizawa, Dai Yumino, Katsuya Kajimoto, Yoshimi Tagawa, Atsushi Takagi, Morio Shoda, Hiroshi Kasanuki, Nobuhisa Hagiwara. (2008) Impact of Sleep-Disordered Breathing on Life-Threatening Ventricular Arrhythmia in Heart Failure Patients With Implantable Cardioverter-Defibrillator. The American Journal of Cardiology 102:8, 1064-1068
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Susanne Brenner, Christiane Angermann, Berthold Jany, Georg Ertl, Stefan Störk. (2008) Sleep-Disordered Breathing and Heart Failure. Trends in Cardiovascular Medicine 18:7, 240-247
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APOOR S. GAMI, VIREND K. SOMERS. (2008) Implications of Obstructive Sleep Apnea for Atrial Fibrillation and Sudden Cardiac Death. Journal of Cardiovascular Electrophysiology 19:9, 997-1003
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Virend K. Somers, David P. White, Raouf Amin, William T. Abraham, Fernando Costa, Antonio Culebras, Stephen Daniels, John S. Floras, Carl E. Hunt, Lyle J. Olson, Thomas G. Pickering, Richard Russell, Mary Woo, Terry Young. (2008) Sleep Apnea and Cardiovascular Disease. Journal of the American College of Cardiology 52:8, 686-717
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Wolfram Grimm. (2008) Arrhythmias in patients with obstructive sleep apnea. Sleep Medicine 9:5, 471-472
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Jonathan E. Shaw, Naresh M. Punjabi, John P. Wilding, K. George M.M. Alberti, Paul Z. Zimmet. (2008) Sleep-disordered breathing and type 2 diabetes. Diabetes Research and Clinical Practice 81:1, 2-12
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Francesca Olmetti, Maria Teresa La Rovere, Elena Robbi, Anna Eugenia Taurino, Francesco Fanfulla. (2008) Nocturnal cardiac arrhythmia in patients with obstructive sleep apnea. Sleep Medicine 9:5, 475-480
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Fatima H. Sert Kuniyoshi, Arturo Garcia-Touchard, Apoor S. Gami, Abel Romero-Corral, Christelle van der Walt, Snigdha Pusalavidyasagar, Tomas Kara, Sean M. Caples, Gregg S. Pressman, Elisardo C. Vasquez, Francisco Lopez-Jimenez, Virend K. Somers. (2008) Day–Night Variation of Acute Myocardial Infarction in Obstructive Sleep Apnea. Journal of the American College of Cardiology 52:5, 343-346
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A. G. P. de Sousa, C. Cercato, M. C. Mancini, A. Halpern. (2008) Obesity and obstructive sleep apnea-hypopnea syndrome. Obesity Reviews 9:4, 340-354
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T. Jared Bunch, Roger D. White, Francisco Lopez-Jimenez, Randal J. Thomas. (2008) Association of body weight with total mortality and with ICD shocks among survivors of ventricular fibrillation in out-of-hospital cardiac arrest. Resuscitation 77:3, 351-355
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Won Lee, Swamy Nagubadi, Meir H Kryger, Babak Mokhlesi. (2008) Epidemiology of obstructive sleep apnea: a population-based perspective. Expert Review of Respiratory Medicine 2:3, 349-364
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Joji Ishikawa, Satoshi Hoshide, Kazuo Eguchi, Shizukiyo Ishikawa, Thomas G Pickering, Kazuyuki Shimada, Kazuomi Kario. (2008) Increased low-grade inflammation and plasminogen-activator inhibitor-1 level in nondippers with sleep apnea syndrome. Journal of Hypertension 26:6, 1181-1187
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Yuki Koshino, Makoto Satoh, Yasuko Katayose, Kyo Yasuda, Takeshi Tanigawa, Noriyuki Takeyasu, Shigeyuki Watanabe, Iwao Yamaguchi, Kazutaka Aonuma. (2008) Association of Sleep-Disordered Breathing and Ventricular Arrhythmias in Patients Without Heart Failure. The American Journal of Cardiology 101:6, 882-886
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Kannan Ramar, Christian Guilleminault. (2008) Cardiovascular complications of obstructive sleep apnea. Expert Review of Respiratory Medicine 2:1, 63-74
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Lars Lüthje, Stefan Andreas. (2008) Obstructive sleep apnea and coronary artery disease. Sleep Medicine Reviews 12:1, 19-31
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András Tislér, Alexander G. Logan, Katalin Akócsi, László Tornóci, István Kiss. (2008) Circadian Variation of Death in Hemodialysis Patients. American Journal of Kidney Diseases 51:1, 53-61
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Kihei Yoneyama, Naohiko Osada, Takashi Shimozato, Yuki Ishibashi, Akio Hayashi, Eiji Takahashi, Keisuke Kida, Kengo Suzuki, Masachika Tamura, Koji Inoue, Yoshihiro J. Akashi, Kazuto Omiya, Fumihiko Miyake, Kazuhiro P. Izawa, Satoshi Watanabe. (2008) Relationship Between Sleep-Disordered Breathing Level and Acute Onset Time of Congestive Heart Failure. International Heart Journal 49:4, 471-480
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Paolo Bottini, Stefania Redolfi, Marco L. Dottorini, Claudio Tantucci. (2008) Autonomic Neuropathy Increases the Risk of Obstructive Sleep Apnea in Obese Diabetics. Respiration 75:3, 265-271
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Julio A. Barcena, James C. Fang. (2007) Diagnosis and treatment of sleep apnea in heart disease. Current Treatment Options in Cardiovascular Medicine 9:6, 501-509
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Timo Laitio, Jouko Jalonen, Tom Kuusela, Harry Scheinin. (2007) The Role of Heart Rate Variability in Risk Stratification for Adverse Postoperative Cardiac Events. Anesthesia & Analgesia 105:6, 1548-1560
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