Impact of obstructive sleep apnea on left ventricular mass and diastolic function

We wished to determine if obstructive sleep apnea (OSA) is associated with increased left ventricular mass (LVM) and impaired left ventricular diastolic function (LVDF) independently of coexisting obesity, hypertension (HTN), and diabetes mellitus (DM). Patients without primary cardiac disease, referred for evaluation of OSA (n = 533), had overnight polysomnography and Doppler echocardiography while awake. Patients were divided, according to the apnea-hypopnea index (AHI), into an OSA group (AHI > or = 5/h, n = 353) and a non-OSA group (AHI < 5/h, n = 180). In men, LVM was greater in the OSA group (98.9 +/- 25.6 versus 92.3 +/- 22.5 g/m, p = 0.023) despite exclusion of those with HTN and DM. A similar trend was noted in women. Regression analysis revealed that LVM was correlated with body mass index (BMI) (beta = 0.480, p < 0.0005), age (beta = 0.16, p = 0.001), and the presence of HTN (beta = 0.137, p = 0.003) in men and with BMI (beta = 0.501, p < 0.0005) in women, but not with AHI or oxygen saturation during sleep. The ratio of peak early filling velocity to peak late filling velocity (E/A), an index of LVDF, was similar in both groups (1.28 +/- 0.32 versus 1.34 +/- 0.31, p = 0.058); it was correlated with age (beta = -0.474, p < 0.0005), but not with AHI or oxygen saturation during sleep. We conclude that OSA is not associated with increased LVM or impaired LVDF independently of obesity, HTN, or advancing age.     

Impact of obstructive sleep apnea on left ventricular diastolic function

The aim of this study was to investigate the impact of obstructive sleep apnea (OSA) on left ventricular (LV) functional changes by using tissue Doppler imaging-derived indexes in patients with OSA. We studied 62 patients classified into 3 groups, namely 18 with mild to moderate OSA, 24 with severe OSA, and 20 control subjects without OSA according to the apnea-hypopnea index (AHI) on complete overnight polysomnogram. All underwent conventional and tissue Doppler echocardiographies. Only early diastolic velocity (Ea; -6.2 +/- 0.3 vs -7.1 +/- 0.3 vs -7.3 +/- 0.3 cm/s, respectively, for the 3 groups, p = 0.023) was significantly decreased in the severe OSA group. Other echocardiographic parameters of diastolic function such as isovolumic relaxation time, deceleration time, mitral inflow early/late wave velocity ratio, and pulmonary vein systolic/diastolic pulmonary vein velocity ratio were comparable among the 3 groups. AHI was correlated only with tissue Doppler imaging-derived indexes of LV diastolic function (Ea r = -0.382, p = 0.002; Ea/late diastolic velocity r = -0.329, p = 0.009), but not with conventional Doppler indexes. AHI remained a significant predictor of Ea after adjusting for age, heart rate, fasting glucose level, blood pressure, body mass index, and LV mass index in a multiple stepwise linear regression model (p = 0.007). In conclusion, only patients with severe OSA showed a greater impairment of LV diastolic function. Of all echocardiographic parameters of diastolic dysfunction investigated, only Ea was identified as the best index to demonstrate an association between LV diastolic dysfunction and severity of OSA independently of body mass index, diabetes mellitus, and hypertension.     

Influence of obstructive sleep apnea on left ventricular mass and global function: sleep apnea and myocardial performance index

Obstructive sleep apnea (OSA) is associated with cardiovascular mortality and morbidity. It may predispose patients to left ventricular hypertrophy and heart failure. The aim of this study was to determine the left ventricular mass (LVM) and myocardial performance index (MPI) reflecting left ventricular global function in uncomplicated OSA patients. Sixty-four subjects without hypertension, diabetes mellitus, and any cardiac or pulmonary disease referred for evaluation of OSA underwent overnight polysomnography and complete echocardiographic assessment. According to the apnea hypopnea index (AHI), subjects were divided into three groups: group 1, control subjects with nonapneic snorers (AHI < 5, n = 18); group 2, patients with mild to moderate OSA (AHI: 5–30, n = 25); and group 3, severe OSA (AHI > 30, n = 21). Basic echocardiographic measurements, LVM, and LVM index were measured. Left ventricular MPI was calculated as (isovolumic contraction time+isovolumic relaxation time)/aortic ejection time by Doppler echocardiography. There were no significant differences in age, sex, body mass index, heart rate, and systolic and diastolic blood pressure among the three groups. Left atrium, interventricular septum, left ventricular posterior wall, left ventricular end-diastolic and end-systolic diameters, LVM mass, and LVM index were not significantly different among the three groups. Left ventricular MPI was significantly higher in severe OSA patients (0.64 ± 0.18) than in controls (0.49 ± 0.18; P < 0.05). There was no significant difference between controls (0.49 ± 0.18) and mild to moderate OSA (0.61 ± 0.16; P = 0.08) and between mild to moderate OSA (0.61 ± 0.16) and severe OSA (0.64 ± 0.18; P = 0.84). The present study demonstrates that patients with severe OSA have global left ventricular dysfunction.     

Evidence for left ventricular dysfunction in patients with obstructive sleep apnoea syndrome.

There is limited information on the development of left ventricular (LV) dysfunction in patients with obstructive sleep apnoea (OSA) in the absence of lung and cardiac comorbidity. This study aimed to investigate whether OSA patients without heart morbidity develop LV dysfunction, and to assess the effect of continuous positive airway pressure (CPAP) on LV function. Twenty-nine OSA patients and 12 control subjects were studied using technetium-99m ventriculography to estimate LV ejection fraction (LVEF), LV peak emptying rate (LVPER), time to peak emptying rate (TPER), peak filling rate (LVPFR) and time to peak filling rate (TPFR) before and after 6 months of treatment with CPAP. A significantly lower LVEF was found in OSA patients, compared to control subjects, (53+/-7 versus 61+/-6%) along with a reduced LVPER (2.82+/-0.58 versus 3.82+/-0.77 end-diastolic volumes x s(-1)). Furthermore, OSA patients had significantly lower LVPFR (2.67+/-0.71 versus 3.93+/-0.58 end-diastolic volumes x s(-1)) and delayed TPFR (0.19+/-0.04 versus 0.15+/-0.03 s) in comparison with the control group. Six-months of CPAP treatment was effective in significantly improving LVEF, LVPER, LVPFR and TPFR. In conclusion, obstructive sleep apnoea patients without any cardiovascular disease seem to develop left ventricular systolic and diastolic dysfunction, which may be reversed, either partially or completely, after 6 months of continuous positive airway pressure treatment.     

Impact of obstructive sleep apnea on right ventricular global function: sleep apnea and myocardial performance index

BACKGROUND: Obstructive sleep apnea (OSA) is characterized by repetitive upper airway obstructions during sleep, and it might cause cardiovascular complications such as heart failure, arrhythmias, myocardial infarction, systemic and pulmonary hypertension. OBJECTIVES: To determine right ventricular diameters and myocardial performance index (MPI) reflecting ventricular global function in uncomplicated OSA patients. METHODS: 49 subjects without hypertension, diabetes mellitus, or any cardiac or pulmonary disease referred for evaluation of OSA had overnight polysomnography and complete echocardiographic assessment. According to the apnea-hypopnea index (AHI), subjects were divided into three groups: group 1: control subjects (AHI <5, n = 20), group 2: patients with mild OSA (AHI: 5-14, n = 11), and group 3: moderate-severe OSA (AHI > or = 15, n = 18). Right ventricular free wall diameter was measured by M mode, and right ventricular MPI was calculated as (isovolumic contraction time + isovolumic relaxation time)/pulmonary ejection time. RESULTS: There were no differences of age, body mass index, heart rates, systolic and diastolic blood pressures among the groups (p > 0.05). Right ventricular end-diastolic and end-systolic diameters were not statistically different between the groups, and were within normal limits. Also, right ventricular free wall diameter was not significantly different between the groups of control, mild OSA and moderate-severe OSA (6.7 +/- 0.9, 6.9 +/- 1.0, 7.1 +/- 1.1 mm, p > 0.05). Right ventricular diastolic dysfunction was shown only in group 3 patients. Right ventricular MPI was statistically higher in group 3 (0.62 +/- 0.18) than in group 2 patients (0.50 +/- 0.10), and group 1 patients (0.48 +/- 0.08, p < 0.001). CONCLUSIONS: It was suggested that patients with moderate-severe OSA had a right ventricular global dysfunction, in addition to the presence of a diastolic dysfunction.     

Effect of obstructive sleep apnea on aortic elastic parameters: relationship to left ventricular mass and function.

BACKGROUND: Obstructive sleep apnea (OSA) syndrome has a critical association with cardiovascular mortality and morbidity. Aortic elastic parameters are important markers for left ventricular (LV) function and are deteriorated in cardiovascular disease. METHODS AND RESULTS: Aortic elastic parameters and LV functions and mass were investigated in 40 patients with OSA (apnea - hypopnea index (AHI) >or=5) (mean age 51.3 +/-9 years, 32 males) and 24 controls (AHI <5) (mean age 51.9+/-5.2 years, 19 males). All subjects underwent polysomnographic examination and recordings were obtained during sleep. They also underwent a complete echocardiographic examination and systolic and diastolic aortic measurements were noted from M-mode traces of the aortic root. There were no significant differences in the demographic data of the patients with OSA and the controls. Subjects with OSA demonstrated higher values of aortic stiffness (7.1+/-1.88 vs 6.42+/-1.56, p=0.0001), but lower distensibility (9.47+/-1.33 vs 11.8+/-3.36, p=0.0001) than the controls. LV ejection fraction was significantly lower in patients with OSA when compared with the control group (61.3+/-5.2% vs 65.9+/-8.4%, p=0.0001). LV diastolic parameters were also compared and were worse in the subjects with OSA than in the control subjects (mitral E/A: 0.91 +/-0.42 vs 1.35+/-0.66, p=0.001; Em/Am: 0.86+/-0.54 vs 1.23+/-0.59, p=0.021). Respiratory disturbance index had a positive correlation with aortic stiffness (r=0.63, p=0.0001 and negative correlation with distensibility (r=-0.41, p=0.001). CONCLUSION: Aortic elastic parameters are deteriorated in OSA, which has an extremely high association with cardiovascular disease. Increased aortic stiffness might be responsible for the LV systolic and diastolic deterioration in OSA syndrome.     

Impact of CPAP on asthmatic patients with obstructive sleep apnoea.

The impact of continuous positive airway pressure (CPAP) treatment on the airway responsiveness of asthmatic subjects with obstructive sleep apnoea (OSA) has scarcely been studied. A prospective study was performed comparing the changes in airway responsiveness and quality of life in stable asthmatic OSA patients, before and 6 weeks after their nocturnal CPAP treatment. A total of 20 subjects (11 males and nine females) participated in the study. With the nocturnal CPAP treatment, the apnoea/hypopnoea index dropped from 48.1 +/- 23.6 x h(-1) to 2.6 +/- 2.5 x h(-1). There were no significant changes in airway responsiveness after CPAP treatment (provocative concentration causing a 20% fall in forced expiratory volume in one second (FEV(1); PC(20) 2.5 mg x mL(-1) (1.4-4.5)) compared with baseline (PC(20) 2.2 mg x mL(-1) (1.3-3.5)). There was no significant change in FEV(1) either. However, the asthma quality of life of the subjects improved from 5.0 +/- 1.2 at baseline to 5.8 +/- 0.9 at the end of the study. In conclusion, nocturnal continuous positive airway pressure treatment did not alter airway responsiveness or forced expiratory volume in one second in subjects with stable mild-to-moderate asthma and newly diagnosed obstructive sleep apnoea. However, nocturnal continuous positive airway pressure treatment did improve asthma quality of life.     

Changes in left ventricular ejection fraction during REM sleep and exercise in chronic obstructive pulmonary disease and sleep apnoea syndrome.

Nine patients, 4 with chronic obstructive pulmonary disease (COPD) and 5 with obstructive sleep apnoea syndrome (OSAS) were monitored during sleep, rest and exercise. Left ventricular ejection fraction (LVEF) was investigated using gated equilibrium 99mtechnetium ventricular scintigraphy during rapid eye movement (REM) sleep, during exercise, and during wakeful rest. Control wakeful rest periods used for comparison with a study state (either REM sleep or exercise) were always selected during the same circadian segment as that state. Myocardial stress thallium-201 scintigraphy was performed during, and 4 h after, exercise, and results were compared to a daytime rest period. Several patients had myocardial hypoperfusion despite a normal electrocardiographic (ECG) treadmill test. During REM sleep, all patients exhibited a significant change in LVEF (greater than 5%) compared to wakefulness. During exercise, 5 subjects increased their LVEF normally (greater than 5%) and 4 (1 COPD, 3 OSAS) decreased it. All patients had a similar change (increase or decrease) during REM and at maximal exercise. Our results suggest that REM sleep in COPD and in OSAS can produce a myocardial stress as great as that produced by exercise. We conclude that REM sleep, like exercise, is a state in which morbidity may become higher and that it may account for mortality in COPD and OSAS patients with compromised myocardial circulation.     

Platelet function in patients with obstructive sleep apnoea syndrome.

Patients with obstructive sleep apnoea syndrome (OSAS) are subject to an increased cardiovascular morbidity including myocardial infarction and stroke. Platelets play an important role in the pathogenesis and triggering of acute cardiovascular syndromes. So far, the influence of OSAS on platelet function is not fully understood. Platelet aggregability to epinephrine, collagen, arachidonic acid, and adenosine diphosphate in vitro was measured in 17 consecutive male patients (53.0+/-2.1 yrs) with polysomnographically verified OSAS and compared with that of 15 male controls (50.1+/-3.6 yrs) at 20:00 h, 24:00 h, and 06:00 h. In addition, the long-term effects of continuous positive airway pressure (CPAP) therapy on platelet aggregability was assessed after 6 months. Platelet aggregation in vitro induced by epinephrine showed a slight increase overnight in the untreated OSAS patients (NS) whereas it decreased slightly (NS) in the controls and in the treated OSAS patients. Pretherapeutic platelet aggregability was significantly lowered by CPAP therapy both at 24:00 h (64.0+/-6.5 versus 55.3+/-6.7%, p<0.05) and at 06:00 h (64.1+/-6.5 versus 45.8+/-7.6%; p=0.01). Platelet aggregability during sleep in the controls resembled that found in patients with OSAS during CPAP therapy. The results suggest that obstructive sleep apnoea syndrome contributes, at least in part, to platelet dysfunction and that long-term continuous positive airway pressure treatment may reduce platelet aggregability.     

Obstructive sleep apnoea inhibits the recovery of left ventricular function in patients with acute myocardial infarction.

AIMS: It has been suggested that obstructive sleep apnoea syndrome (OSA) may be a direct cause of left ventricular (LV) systolic dysfunction. This study was designed to examine our hypothesis that OSA inhibits the recovery of LV function in patients with acute myocardial infarction (AMI). METHODS AND RESULTS: Our 86 consecutive first-AMI patients underwent primary percutaneous coronary intervention (PCI). All patients underwent polysomnography and OSA was defined as an apnoea-hypoapnoea index (AHI) > or =15 events/h, of which more than 50% were obstructive. Left ventriculograms immediately after PCI and at 21 days were used to evaluate LV ejection fraction (LVEF), LV end-diastolic volume index, and regional wall motion (RWM) within the infarct area. OSA was observed in 37 patients (43%). All three indices of LV function after primary PCI were comparable between the two groups. Increases in LVEF and RWM during admission were significantly lower in OSA patients than those without OSA (delta LVEF: -0.3+/-9.6 vs. 7.4+/-7.2%, P < 0.001; delta RWM: 0.26+/-1.04 SD/chord vs. 1.16+/-1.20 SD/chord, P = 0.002). Multiple regression analysis showed that AHI correlated negatively with delta LVEF and delta RWM. CONCLUSION: The novel finding is that OSA may inhibit the recovery of LV function in patients with AMI.     

Plasma B-type natriuretic peptide level is associated with left ventricular hypertrophy among obstructive sleep apnoea patients

OBJECTIVES: To examine whether increased plasma levels of B-type natriuretic peptide (BNP) are associated with cardiac structural and functional abnormalities in obstructive sleep apnoea (OSA) patients, taking into consideration the confounding effect of obesity. MEASUREMENTS: In a cross-sectional study, polysomnography, echocardiography and the measurement of the serum levels of BNP were performed in 235 consecutive subjects (age 52 +/- 14 years) visiting our sleep clinic. Left ventricular hypertrophy (LVH) [left ventricular mass index (LVMI) > or = 125 g/m in men, and > or = 110 g/m in women] and cardiac diastolic function (E/A ratio) were determined by echocardiography. RESULTS: The LVMI, prevalence rate of LVH and body mass index (BMI) were higher, and the E/A ratio lower in the subjects with severe OSA (apnoea-hypopnoea index > or = 30/h, n = 146, LVH 80%) than in those with mild to moderate OSA (n = 89, LVH 35%; P < 0.01), although plasma BNP levels were similar in the two groups. Although the log-transformed plasma BNP level showed a negative correlation with BMI, the results of binary logistic regression analysis demonstrated that the quintile value of BNP was an independent significant variable for the identification of LVH (adjusted odds ratio in quintile 5 = 4.01, 95% confidence interval 1.18-13.70, P < 0.01), even after adjusting for obesity and other risk factors. CONCLUSION: An increased likelihood of cardiac structural and functional abnormalities was observed with increasing severity of OSA. Increased plasma levels of BNP do seem to reflect an increased likelihood of LVH in patients with severe OSA.     

Sexual function in male patients with obstructive sleep apnoea

Objective: Our objective was to investigate general and functional aspects of sexuality in male patients with a confirmed diagnosis of obstructive sleep apnoea (OSA) and compare the results with normative data. Materials and Methods: We investigated 308 male patients (age 30–69) admitted to a sleep laboratory and receiving a diagnosis of OSA, using questions drawn from two self‐administered questionnaires on sexuality [Fugl‐Meyer Life satisfaction checklist (LiSat) and Brief Sexual Function Inventory (BSFI)]. Results: We found that both general (Fugl‐Meyer LiSat) and functional (BSFI) aspects of sexuality were worse in patients with (untreated) OSA when compared with normative data. Both aspects were dependent on age, obesity, social factors and concomitant medication but not on the severity of OSA as reflected by the apnoea–hypopnoea index or subjective sleepiness. Conclusion: We conclude that although sexual dysfunction is more prevalent in OSA patients than in the general population, it is a complex problem relating more to age, obesity, social factors and comorbidity than to the severity of OSA. Please cite this paper as: Petersen M, Kristensen E, Berg S, Midgren B. Sexual function in male patients with obstructive sleep apnoea. The Clinical Respiratory Journal 2010; 4: 186–191.     

Effects of obesity upon genioglossus structure and function in obstructive sleep apnoea.

Obesity is a common feature of the obstructive sleep apnoea syndrome. It can influence the structure and function of skeletal muscles. However, its effects upon the upper airway muscles have not been explored directly. This study assessed the structure and function of the genioglossus in patients with obstructive sleep apnoea syndrome and in healthy subjects (with and without obesity, defined by a body mass index > 30 kg x m(-2)). Further, to investigate the effects of continuous positive airway pressure (CPAP) treatment, patients with obstructive sleep apnoea syndrome after at least 1 yr under CPAP were also studied. The study found that obese and nonobese patients showed different in vitro geniglossus endurance properties. In obese patients, geniglossus endurance was indistinguishable from normal while, nonobese patients, at diagnosis, showed increased genioglossus fatigability; this was not observed in patients treated with CPAP. By contrast, patients with obstructive sleep apnoea syndrome showed at diagnosis a higher percentage of type II fibres than controls and patients under CPAP treatment independently of obesity. This difference is mainly due to a predominance of subtype IIb fibre. This difference was not observed in the group of patients treated with CPAP. Genioglossus twitch force was normal in all patients. These results suggest that different pathogenic mechanisms may underlie the development of obstructive sleep apnoea syndrome in obese and nonobese patients. This observation may have potential clinical implications.     

Oxidative stress in obstructive sleep apnoea.

AIMS: Any sustained elevation of oxidative stress in patients with obstructive sleep apnoea (OSA) might help explain their increased risk for cardiovascular diseases. We tested the hypothesis that measures of oxidative stress are increased in otherwise healthy subjects with OSA when compared to closely matched OSA-free control subjects. METHODS AND RESULTS: Plasma indices of oxidative stress and lipid peroxidation [thiobarbituric acid-reactive substances (TBARS), oxidized LDL (oxLDL), isoprostanes] were measured in 41 moderate-severe OSA males without other diseases and in 35 matched controls first before sleep, then after 4 h of untreated OSA, and again in the morning after 4 h of effective treatment with continuous positive airway pressure (CPAP). Plasma levels of oxLDL, TBARS, and isoprostanes in OSA patients (n=34, 26, 17, respectively) were comparable to the controls (n=28, 27, 15 for the three markers, respectively). Neither untreated OSA nor CPAP treatment nor normal sleep affected levels of any of the three measures of oxidative stress. There was no association between the severity of sleep apnoea and any measure of oxidative stress. CONCLUSION: Otherwise healthy OSA patients, without any other co-morbidities, do not manifest evidence for higher oxidative stress and lipid peroxidation. Thus, oxidative stress and lipid peroxidation do not appear to be key mediators of increased cardiovascular disease in OSA patients.     

Update on paediatric obstructive sleep apnoea

Obstructive sleep apnoea (OSA) is one of the most common causes of sleep-disordered breathing (SDB) in children. It is associated with significant morbidity, potentially impacting on long-term neurocognitive and behavioural development, as well as cardiovascular outcomes and metabolic homeostasis. The low grade systemic inflammation and increased oxidative stress seen in this condition are believed to underpin the development of these OSA-related morbidities. The significant variance in degree of end organ morbidity in patients with the same severity of OSA highlights the importance of the interplay of genetic and environmental factors in determining the overall OSA phenotype. This review seeks to summarize the current understanding of the aetiology and mechanisms underlying OSA, its risk factors, diagnosis and treatment.