U. Koehler

Obstructive Sleep Apnea as a Risk Marker in Coronary Artery Disease

Study Objectives: Obstructive sleep apnea (OSA) is associated with a range of cardiovascular sequelae and increased cardiovascular mortality. The aim of our study was to assess the prevalence of OSA in patients with symptomatic angina and angiographically verified coronary artery disease (CAD). In addition, we analyzed the association of OSA and other coronary risk factors with CAD and myocardial infarction. Methods: Overnight non-laboratory-monitoring-system recordings for detection of OSA was performed in 223 male patients with angiographically verified CAD and in 66 male patients with exclusion of CAD. A logistic regression analysis was performed to assess associations between risk factors and CAD and myocardial infarction. Results: CAD patients were found to have OSA in 30.5%, whereas OSA was found in control subjects in 19.7%. The mean apnea/hypopnea index (AHI) was significantly higher (p < 0.01) in CAD patients (9.9 ± 11.8) than in control subjects (6.7 ± 7.3). Body-mass-index (BMI) was significantly higher in patients with CAD and OSA than in patients with CAD without OSA (28.1 vs. 26.7 kg/m2; p < 0.001). No significant difference was found with regard to other risk factors and left ventricular ejection fraction (LVEF) between both groups. Hyperlipidemia (OR 2.3; CI 1.3–3.9; p < 0.005) and OSA defined as AHI ≥20 (OR 2.0; CI 1.0–3.8, p < 0.05) were independently associated with myocardial infarction. Conclusions: There is a high prevalence of OSA among patients with angiographically proven CAD. OSA of moderate severity (AHI ≥20) is independently associated with myocardial infarction. Thus, in the care of patients with CAD, particular vigilance for OSA is important.

Heart block in patients with obstructive sleep apnoea: pathogenetic factors and effects of treatment

Heart block during sleep has been described in up to 10% of patients with obstructive sleep apnoea. The aim of this study was to determine the relationship between sleep stage, oxygen desaturation and apnoea-associated bradyarrhythmias as well as the effect of nasal continuous positive airway pressure (nCPAP)/nasal bi-level positive airway pressure (nBiPAP) therapy on these arrhythmias in patients without electrophysiological abnormalities. Sixteen patients (14 males and two females, mean age 49.6+/-10.4 yrs) with sleep apnoea and nocturnal heart block underwent polysomnography after exclusion of electrophysiological abnormalities of the sinus node function and atrioventricular (AV) conduction system by invasive electrophysiological evaluation. During sleep, 651 episodes of heart block were recorded, 572 (87.9%) occurred during rapid eye movement (REM) sleep and 79 (12.1%) during nonrapid eye movement (NREM) sleep stages 1 and 2. During REM sleep, the frequency of heart block was significantly higher than during NREM sleep: 0.69+/-0.99 versus 0.02+/-0.04 episodes of heart block x min(-1) of the respective sleep stage (p<0.001). During apnoeas or hypopnoeas, 609 bradyarrhythmias (93.5%) occurred with a desaturation of at least 4%. With nCPAP/ nBiPAP therapy, apnoea/hypopnoea index (AHI) decreased from 75.5+/-39.6 x h(-1) to 3.0+/-6.6 x h(-1) (p<0.01) and the number of arrhythmias from 651 to 72 (p<0.01). We conclude that: 1) 87.9% of apnoea-associated bradyarrhythmias occur during rapid eye movement sleep; 2) the vast majority of heart block episodes occur during a desaturation of at least 4% without a previously described threshold value of 72%; and 3) nasal continuous positive airway pressure or nasal bi-level positive airway pressure is the therapy of choice in patients with apnoea-associated bradyarrhythmias.

Outcome of patients with sleep apnea–associated severe bradyarrhythmias after continuous positive airway pressure therapy

Twenty-nine patients in whom severe bradyarrhythmias occurred exclusively during obstructive sleep apnea and in whom advanced sinus node disease or atrioventricular conduction system dysfunction had been excluded by invasive electrophysiologic evaluation were prospectively followed on nasal continuous positive airway pressure. During 54 +/- 10 months follow-up, no syncope and no sudden deaths were observed, suggesting that patients with sleep apnea-associated bradyarrhythmias and a normal electrophysiologic study appear to have a favorable prognosis with continuous positive airway pressure.

Nocturnal myocardial ischemia and cardiac arrhythmia in patients with sleep apnea with and without coronary heart disease

SummaryTo study the effect of apnea and hypoventilation-induced hypoxemia on the heart, we carried out polysomnographic recordings over; 4 nights with electrocardiographic tracings in 30 patients with and without coronary heart disease. Evaluations of the data were based on the 2nd and 4th nights. In six subjects, five with coronary heart disease, we found 85 episodes of nocturnal ischemia, mainly during REM sleep (83.5%), high apnea activity, and sustained and progressive hypoxemia. Complex ventricular ectopy was observed in 14/13 patients (nights 2/4) and repetitive ventricular ectopy in 5/3. There was no significant difference in the quality and quantity of ventricular ectopy during wake and sleep states between the CHD group and the control group. In one patient ventricular bigeminy was observed only at a threshold of SaO2 below 60%. Bradyarrhythmia was made evident in four subjects from the CHD group and correlated mainly with apnea activity. We suppose that patients with sleep apnea and CHD are at cardiac risk because coronary heart disease can be aggravated by insufficient arterial oxygen supply due to cumulative phases of apnea and hypoventilation. The reduced hypoxic tolerance of the heart may lead to myocardial ischemia: and increased electrical instability.

Relations among hypoxemia, sleep stage, and bradyarrhythmia during obstructive sleep apnea

BACKGROUND Obesity, apneic hypoxemia, and rapid eye movement (REM) sleep are supposed to be the major causes for bradyarrhythmia in patients with obstructive sleep apnea. The aims of this study were to compare clinical findings and diagnoses in patients with obstructive sleep apnea with and without nocturnal bradyarrhythmia and to analyze the relations among hypoxemia, sleep stage, and bradyarrhythmia. METHODS During a 17-month period 239 patients were found to have sleep apnea in an ambulatory study. Patients with nocturnal bradyarrhythmia were hospitalized for 3 days and polysomnographies were performed over 2 successive nights. A Holter electrocardiogram was recorded for 48 hours. RESULTS Nocturnal episodes of bradyarrhythmia were identified in 17 (7%) of 239 patients. Body mass index (39 +/- 7 vs 31 +/- 5 kg/m(2)) and respiratory disturbance index (90 +/- 36 per hour vs 24 +/- 24 per hour) were significantly different (P <.01) between patients with (n = 17) and without bradyarrhythmia (n = 222). Bradyarrhythmia occurred significantly more often during REM than non-REM sleep (P <.01). There was a significant difference in end-apneic oxygen saturation in apnea/hypopnea episodes with and without bradyarrhythmia (71% +/- 9% vs 75% +/- 10%; P <.01). A linear relation between end-apneic oxygen saturation and number of sinus arrests and heart blocks could not be found. CONCLUSIONS Patients with apnea-associated bradyarrhythmia are more overweight than patients without bradyarrhythmia. The higher respiratory disturbance index measurements found in these patients may be caused by this difference. Bradyarrhythmia occurs predominantly during REM sleep and occurred independently from decrease in oxygen saturation; a threshold value as an upper limit could not be found.

Pulmonary haemodynamics in obstructive sleep apnoea: time course and associated factors

Changes in pulmonary artery pressure within an obstructive apnoea and elevations of transmural pulmonary artery pressure (Ppa,tm) towards the end of apnoea are well known. The purpose of our study was to examine which factors contribute to the increase of Ppa,tm in an apnoea. In addition, the time course of Ppa,tm and associated factors during a sleep study was investigated. We analysed the association of changes in arterial oxygen saturation (Sa,O2), oesophageal pressure (Poes) to estimate intrathoracic pressure, systolic blood pressure (BPsys) to estimate left ventricular afterload, apnoea duration and the change in Ppa,tm (deltaPpa,tm) during the course of obstructive apnoeas. Consecutive apnoeas in nonrapid eye movement (NREM)-sleep at the beginning, the middle and the end of the sleep study were analysed in six patients with obstructive sleep apnoea. The mean systolic Ppa,tm was 28.0+/-12.1 mmHg at the beginning of apnoea and 38.6+/-15.5 mmHg at the end (deltaPpa,tm 10.5+/-7.4 mmHg; p<0.0001). DeltaSa,O2 (p<0.0001; odds ratio (OR) 1.45; confidence interval (CI) 1.20-1.76) and deltaPoes (p<0.0001; OR 1.22; CI 1.11-1.34) were independently associated with deltaPpa,tm in a multiple regression analysis. Apnoea duration as well as deltaPoes, deltaPpa,tm and deltaSa,O2 were all significantly higher (p<0.05) in apnoeas at the middle of the sleep study than at the beginning or the end. In conclusion, hypoxaemia and mechanical factors as an increase in negative thoracic pressure contribute to elevations of the transmural pulmonary artery pressure during an obstructive apnoea. The time course of pulmonary haemodynamics within a steep study reveals that the highest transmural pulmonary artery pressure occurs in the middle of the night with no progressive increase towards the end of the sleep study.

A Prospective Polysomnographic Study on the Evolution of Complex Sleep Apnoea

Complex sleep apnoea (CompSA) may be observed following continuous positive airway pressure (CPAP) treatment. In a prospective study, 675 obstructive sleep apnoea patients (mean age 55.9 yrs; 13.9% female) participated. Full-night polysomnography was performed at diagnosis, during the first night with stable CPAP and after 3 months of CPAP. 12.2% (82 out of 675 patients) had initial CompSA. 28 of those were lost to follow-up. Only 14 out of the remaining 54 patients continued to satisfy criteria for CompSA at follow-up. 16 out of 382 patients not initially diagnosed with CompSA exhibited novel CompSA after 3 months. 30 (6.9%) out of 436 patients had follow-up CompSA. Individuals with CompSA were 5 yrs older and 40% had coronary artery disease. At diagnosis, they had similar sleep quality but more central and mixed apnoeas. On the first CPAP night and at follow-up, sleep quality was impaired (more wakefulness after sleep onset) for patients with CompSA. Sleepiness was improved with CPAP, and was similar for patients with or without CompSA at diagnosis and follow-up. CompSA is not stable over time and is mainly observed in predisposed patients on nights with impaired sleep quality. It remains unclear to what extent sleep impairment is cause or effect of CompSA.

Sleep-disordered breathing in patients with implantable cardioverter-defibrillator

AIMS To assess the prognostic significance of screening for sleep-disordered breathing in patients with implantable cardioverter-defibrillator (ICD) with regard to appropriate ICD therapy and total mortality. METHODS AND RESULTS Overnight sleep studies were performed in 204 ICD recipients not known to have sleep apnoea and with no history of daytime sleepiness. Sleep-disordered breathing was diagnosed in the presence of an apnoea-hypopnea index of five or more events per hour. Seventy patients (34%) had no sleep apnoea, 105 patients (51%) had central sleep apnoea, and 29 patients (14%) had obstructive sleep apnoea. During 38 ± 26 months follow-up, 80 patients (39%) received appropriate ICD therapy for ventricular tachycardia (VT) or ventricular fibrillation (VF), and 54 patients (26%) died. On multivariate Cox regression analysis, age, left ventricular (LV) end-diastolic diameter, secondary prevention ICD indication, use of diuretics, and absence of aldosterone antagonist therapy but not sleep apnoea were associated with appropriate ICD therapy for VT or VF. In addition, multivariate Cox analysis identified age and LV ejection fraction but not sleep apnoea as predictors of total mortality. CONCLUSION Undiagnosed sleep-disordered breathing is common in ICD recipients. The presence and severity of previously unknown sleep apnoea in ICD recipients, however, does not appear to be an independent predictor of appropriate ICD therapy or morality during follow-up.

An Apnea-Monitoring Device Based on Variation of Heart Rate and Snoring

Sleep apnea syndromes are complex clinical pictures. The underlying sleep- induced disturbance of the respiratory regulation causes periodic nocturnal haltings of breathing which are defined as apneas when they last longer than 10 s. The therapeutic reduction of sleep apnea activity (SAA) leads to a reversal of the accompanying symptoms and findings if the disease is recognized and treated during its early stages.

Erhöht Schlafapnoe das Risiko für einen Myokardinfarkt im Schlaf

Myocardial infarction shows a circadian pattern with a maximum in the early morning hours. In patients with sleep-related breathing disorders (SRBD), it is assumed that apnea-associated changes of hemodynamics, blood gases, and rheology lead to a higher frequency of myocardial infarction during sleep. This investigation analyzes the circadian pattern of myocardial infarction in patients with and without SRBD. Within a time period of 20 months, 89 male patients with acute myocardial infarction were consecutively admitted to the intensive care unit. A nocturnal long-term registration of oxygen saturation, heart rate, breathing sounds, and body position by means of a 4-channel recording system (MESAM IV) was carried out in 59 of the 89 patients 6 to 10 days (evaluation I) and in 43 of 59 patients 22 to 28 days after infarction (evaluation II). Sleep apnea with a respiratory-disturbance-index (RDI≥10/h was found in 44.1/39.5% of the patients (evaluation I/II). In 22 % of the patients, time of infarction was during a sleeping period. Patients with myocardial infarction during sleep had a clearly higher RDI in comparison to patients with a myocardial infarction during wakefulness (evaluation I: 22.7 versus 9.4/h; p=0.08;evaluationII: 20.3 versus 7.3;p<0.05). 53.6 % of all myocardial infarctions occurred during the time period 5:00–11:00 a.m. Investigations in a larger number of patients are necessary to confirm these results as well as the relevance of sleep apnea as a cardiovascular risk factor. Das Auftreten des Myokardinfarktes zeigt ein zirkadianes Muster mit einem Maximum in den frühen Morgenstunden. Bei Patienten mit schlafbezogenen Atmungsstörungen (SBAS) ist zu mutmaßen, daß diese aufgrund der akuten apnoeassoziierten Veränderungen von Hämodynamik, Blutgasen und Rheologie vermehrt Myokardinfarkte im Schlaf aufweisen. In dieser Untersuchung wird die zirkadiane Verteilung von Myokardinfarkten bei Patienten mit und ohne SBAS analysiert. Bei 59 von 89 männlichen Patienten, die konsekutiv innerhalb eines Zeitraums von 20 Monaten mit akutem Myokardinfarkt auf die Intensivstation aufgenommen wurden, konnte zwischen dem 6. und 10. Tag nach Infarkt (Meßzeitpunkt I), bei 43 der 59 Patienten zwischen dem 22. und 28. Tag nach Infarkt (Meßzeitpunkt II) eine nächtliche Langzeitregistrierung von transkutaner Sauerstoffsättigung, Herzfrequenz, Atemgeräuschen und Körperlage mittels 4-Kanal-Diagnostiksystem (MESAM IV) durchgeführt werden. Eine Schlafapnoe mit einem RDI≥10/h war zum MZP I bei 44,1 % der Patienten nachweisbar, zum MZP II bei 39,5 %. Bei 22 % der Patienten mit sicher festzulegendem Infarktzeitpunkt trat der Infarkt im Schlaf auf. Die Patienten mit Myokardinfarkt im Schlaf hatten im Vergleich zu Patienten mit Myokardinfarkt im Wachzustand einen deutlich höheren RDI (MZP I: 22,7 vs. 9,4/h; p=0,08; MZP II: 20,3 vs. 7,3/h; p<0,05). 53,6 % aller Infarkte waren im Zeitraum von 5.00 bis 11.00 Uhr nachweisbar. Untersuchungen an größeren Patientenkollektiven sind notwendig, um die vorliegenden Ergebnisse sowie die Relevanz des kardiovaskulären Risikofaktors Schlafapnoe zu bestätigen.