Why don't all heavy snorers have obstructive sleep apnea?

Patients with obstructive sleep apnea (OSA) and heavy snorers without apnea both show intrathoracic suction pressures during sleep that exceed their static upper airway closing pressures. Complete airway occlusion, however, occurs only in the former patient group. We hypothesized that the kinetic properties of the airflow would be different in these two types of patients because of differences in upper airway morphology. The pharyngeal computed tomography (CT) was used to measure the cross-sectional areas of the upper airways in 15 patients with OSA, 25 nonapneic heavy snorers, and 14 control subjects while they were awake. Nocturnal breathing was monitored with the static charge-sensitive bed (SCSB). The patients with OSA had a narrower airspace at the velopharyngeal (VP) level than the controls (p less than 0.01); the nonapneic snorers did not differ from the other groups. At the tongue base (TB) and the hyoid bone (HB) levels there was no difference between the OSA and the control groups, but the nonapneic snorers had narrower airways at both of these levels compared with control subjects (p less than 0.01) and at the hyoid bone level compared with the OSA group (p less than 0.05). The VP/HB ratio was the parameter that best distinguished the patients with OSA from the nonapneic snorers (lower in the OSA group, p less than 0.001). We suggest that airway collapse during sleep is favored by a narrow velopharynx associated with large hypopharynx. Some heavy snorers may not have an oropharyngeal collapse because the peak inspiratory suction pressure could already be damped down at the level of the relatively narrow hypopharyngeal airways.     

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.     

Flow-volume curves in snoring patients with and without obstructive sleep apnea

To examine the usefulness of flow-volume curves as a screening test for the diagnosis of obstructive sleep apnea (OSA), we studied 405 consecutive patients referred for evaluation of possible OSA. All patients had full pulmonary function studies, which included measurements of maximal inspiratory and expiratory flow-volume curves, and nocturnal polysomnography, including continuous monitoring of snoring sounds. When the results were analyzed, of the 405 patients studied, 207 had OSA (apnea/hypopnea index [AHI] greater than 10) and 198 did not. Flow-volume curves were examined for the presence of upper airway obstruction defined as midvital capacity flow ratio (MVCFR = ratio of the maximal expiratory flow at 50% of vital capacity to maximal inspiratory flow at 50% of vital capacity) greater than 1.0. We found no significant difference in the values of MVCFR between the two groups: MVCFR was equal to 0.69 +/- 0.31 for nonapneic snorers, and 0.68 +/- 0.29 for the apneic snorers. Furthermore, we redefined the apneic and nonapneic groups using different cutoff values of AHI: 20, 30, 40, and 50. Independently of the AHI cutoff used, we found no significant difference in the MVCFR between the two groups. Linear regression analysis for the entire group of 405 patients revealed no significant correlation between MVCFR and the AHI or the snoring indices. We calculated the sensitivity, specificity, and predictive values of MVCFR for the diagnosis of OSA. We found that this test had 12% sensitivity, 86% specificity, 47% positive predictive value, and 46% negative predictive value.(ABSTRACT TRUNCATED AT 250 WORDS)     

Roentgenographic dimensions of the upper airway in snoring patients with and without obstructive sleep apnea

The purpose of this study was to examine whether a simple test, such as routine roentgenographic views of the upper airway, is useful in identifying anatomic narrowing of the airway in patients with sleep apnea. To accomplish this, we prospectively studied a group of 117 patients (95 male and 22 female subjects) referred for evaluation of heavy snoring and possible obstructive sleep apnea. All patients had full nocturnal polysomnography, including measurements of snoring. Lateral view of the airway obtained after swallowing contrast material was used to measure pharyngeal diameters at three sites along the airway. All measurements were performed with the patients standing and supine. We used three different definitions of sleep apnea (apnea/hypopnea index of 10, 20, and 40), and compared airway diameters between the apneic and nonapneic snorers. Only when sleep apnea was defined as greater than 40 apneas plus hypopneas per hour of sleep was there a significant difference in airway diameter at the tip of the palate and 1 cm distal to it between apneic and nonapneic snorers. Both groups of patients demonstrated a significant reduction in the retropalatal distance on assumption of the supine posture. Stepwise, forward, multiple linear regression analysis showed that the retropalatal distance and airway diameter at the tip of the palate and 1 cm distal to it were significant predictors of snoring, but not apnea. We conclude that (1) airway diameters account for some of the variability in snoring, and (2) they do not differentiate between apneic and nonapneic snorers.     

Impairment of vascular endothelial function and left ventricular filling : association with the severity of apnea-induced hypoxemia during sleep

STUDY OBJECTIVE: To investigate whether a dose-effect relationship exists between the severity of obstructive sleep apnea (OSA) and subclinical indicators of myocardial or vascular dysfunction. DESIGN: Cross-sectional study using correlation analysis. PARTICIPANTS: Twenty subjects referred to our sleep laboratory for screening or therapy of OSA but without regular medication and without known cardiovascular disease. MEASUREMENTS: Severity of OSA was quantified by polysomnography. Moreover, nocturnal excretion of norepinephrine was determined. Left ventricular (LV) myocardial function was assessed with Doppler echocardiography. Using ultrasonographic measurements, endothelium-dependent and endothelium-independent conduit artery dilation were measured as flow-mediated and glyceryltrinitrate-induced changes in brachial artery diameter. RESULTS: Worsening nocturnal hypoxemia, measured as nocturnal oxygen saturation nadir or percentage of sleep time spent in hypoxemia (< 90% hemoglobin oxygen saturation), predicted increased interventricular septum thickness (corrected for age and body mass index), prolonged isovolumetric relaxation time, decreased ratio between peak early and late mitral flow velocities, as well as reduced endothelium-dependent dilatory capacity of the brachial artery (all relationships corrected for cofactor age and with p < 0.05) were observed. Associations between these cardiovascular function markers and nocturnal excretion of norepinephrine followed the same trend, but relations with interventricular septum thickness and flow-mediated artery dilation missed significance (p = 0.064 and p = 0.061, respectively). LV posterior wall thickness, measures of LV systolic function, early mitral flow deceleration time, and endothelium-independent artery dilation were not significantly related to the degree of nocturnal hypoxemia or norepinephrine excretion. None of the correlations with apnea-hypopnea index were statistically significant. CONCLUSIONS: The severity of apnea-related hypoxemia is associated with a gradual deterioration of LV diastolic function as well as large-artery endothelial function.     

A Hypertensive Response to Exercise Is Prominent in Patients With Obstructive Sleep Apnea and Hypertension: A Controlled Study

Blood pressure (BP) behavior during exercise is not clear in hypertensive patients with obstructive sleep apnea (OSA). The authors studied 57 men with newly diagnosed essential hypertension and untreated OSA (apnea‐hypopnea index [AHI] ≥5) but without daytime sleepiness (Epworth Sleepiness Scale score ≤10), and an equal number of hypertensive controls without OSA matched for age, body mass index, and office systolic BP. All patients underwent ambulatory BP measurements, transthoracic echocardiography, and exercise treadmill testing according to the Bruce protocol. A hypertensive response to exercise (HRE) was defined as peak systolic BP ≥210 mm Hg. Patients with OSA and control patients had similar ambulatory and resting BP, ejection fraction, and left ventricular mass. Peak systolic BP was significantly higher in patients with OSA (197.6±25.6 mm Hg vs 187.8±23.6 mm Hg; P=.03), while peak diastolic BP and heart rate did not differ between groups. Furthermore, an HRE was more prevalent in patients with OSA (44% vs 19%; P=.009). Multiple logistic regression revealed that an HRE is independently predicted by both the logAHI and minimum oxygen saturation during sleep (odds ratio, 3.94; confidence interval, 1.69–9.18; P=.001 and odds ratio, 0.94; confidence interval, 0.89–0.99; P=.02, respectively). Exaggerated BP response is more prevalent in nonsleepy hypertensives with OSA compared with their nonapneic counterparts. This finding may have distinct diagnostic and prognostic implications.     

Funktionelle Dynamik des rechten Ventrikels und des Lungenkreislaufes bei obstruktiver Schlafapnoe

Obstructive sleep apnea (OSA) is common with an incidence of at least 500,000 patients in the German population. Typical symptoms are daytime sleepiness, headache in the morning, and snoring. Presumably obstructive sleep apnea via various mechanisms increases cardiovascular morbidity. Hypoxemia causes nocturnal hypertension in most of the patients. Nevertheless, about 20% of the patients develop daytime pulmonary hypertension and right heart dysfunction. Clinical and animal studies demonstrated right ventricular hypertrophy as a consequence of intermittent hypoxemia and pulmonary hypertension. Right ventricular hemodynamics differ essentially from left ventricular hemodynamics. Right ventricular function is substantially influenced by right ventricular afterload, which is mainly determined by pulmonary vascular resistance, and slightly influenced by preload. Application of continuous positive airway pressure (CPAP) via a nose mask normalizes nocturnal breathing disorders and reduces pre- and afterload, especially in patients with cardiomegaly. Therefore, CPAP generates positive effects on the myocardium.     

Chronic lung disease in the sleep apnea syndrome

Several well controlled epidemiologic and hemodynamic studies suggest that about 20% of sleep apnea syndrome (SAS) patients will have chronic obstructive pulmonary disease (COPD), and the majority of these patients (with combined diseases) will have pulmonary hypertension. Indeed it has been suggested that only patients with underlying hypoxemia, such as that from COPD, will develop right heart failure in the OSA setting. Experience shows that apnea/COPD patients will have severe hypersomnolence associated with the OSA, cough and dyspnea with the airways disease, and edema and plethora related to chronic hypoxemia. Many patients present with respiratory failure and are diagnosed at the time of initial intubation and mechanical ventilation. Episodic nocturnal hypoxemia may be worsened by a steeper rate of desaturation due to lower alveolar and blood oxygen stores, and longer apneas perhaps contributed to by depressed chemosensitivity. Daytime hypoxemia may also add to the severe hemodynamic disturbances. Since COPD cannot be cured, aggressive treatment of SAS is critical. Past studies have shown that tracheostomy or nasal CPAP in this setting not only leads to resolution of episodic nocturnal desaturation but may lead to rapid improvement in daytime oxygenation in many patients. Pulmonary hypertension and other measures of cardiopulmonary function improve when apnea is cured. Elimination of the SAS may disclose nonapneic REM related desaturation that could require supplemental oxygen therapy in addition to tracheostomy or nasal CPAP. Pulmonary function testing in SAS patients with smoking histories, followed by aggressive treatment of SAS, is recommended.     

Sustained effect of continuous positive airway pressure on baroreflex sensitivity in congestive heart failure patients with obstructive sleep apnea

BACKGROUND: Patients with either heart failure or obstructive sleep apnea have a reduced baroreflex sensitivity for heart rate, a sign of poor prognosis. We previously demonstrated that nocturnal application of continuous positive airway pressure to heart failure patients with obstructive sleep apnea increased baroreflex sensitivity acutely, but it is not known whether these effects persist into wakefulness. OBJECTIVE: To determine whether treating obstructive sleep apnea in heart failure patients with continuous positive airway pressure improves baroreflex sensitivity during wakefulness. METHODS: Spontaneous baroreflex sensitivity was assessed during wakefulness in 33 heart failure patients (left ventricular ejection fraction < or = 45%) with obstructive sleep apnea (apnea-hypopnea index > or = 20). Subsequently, baroreflex sensitivity was reassessed 1 month after patients were randomly allocated to nocturnal continuous positive airway pressure treatment or no treatment (control). RESULTS: Compared with the 14 control patients, the 19 continuous positive airway pressure-treated patients experienced a greater increase in baroreflex sensitivity [median, (25%, 75%)] [from 5.4 (2.2, 8.3) to 7.9 (4.4, 9.4) ms/mmHg; P = 0.01] and left ventricular ejection fraction (P < 0.001). In addition, daytime systolic blood pressure and heart rate decreased more in the continuous positive airway pressure group (from 122 +/- 15 to 113 +/- 12 mmHg; P = 0.02, and from 66 +/- 8 to 62 +/- 8 bpm; P < 0.001, respectively) than in the control group. CONCLUSION: Treatment of coexisting obstructive sleep apnea by continuous positive airway pressure in heart failure patients improves baroreflex sensitivity during wakefulness in addition to improving left ventricular ejection fraction and lowering blood pressure and heart rate. These data indicate that the improved autonomic regulation of heart rate in heart failure patients treated for obstructive sleep apnea during sleep persists into wakefulness.     

Mal-effects of obstructive sleep apnea on the heart

Objective

This study aims to examine the impact of chronic intermittent hypoxia on hearts in patients with obstructive sleep apnea (OSA).

Methods

Two hundred twenty patients were divided into groups based on (1) severity of the disease, (2) years of disease history, and (3) with or without secondary hypertension. All subjects underwent blood pressure measurements, polysomnogram monitoring, and cardiac Doppler ultrasound examinations.

Results

The left ventricular ejection fraction (LVEF), fractional shortening (FS), and the ratio of early to late diastolic filling (E/A) in patients with severe OSA were lower than in those with moderate OSA and in healthy controls. The inner diameters of the main pulmonary artery (inD of MPA), the inner diameters of the right cardiac ventricle (inD of RV), and the thickness of anterior wall of the right ventricle (TAW of RV) were increased in patients with severe OSA compared to those with moderate disease and worsened as a function of time with disease. The tissue Doppler imaging-derived Tei index and pulmonary artery systolic pressure were also increased along with the severity of OSA. LVEF and FS in patients who had suffered from OSA for >10?years were decreased compared with those suffering from OSA for a shorter time. LVEF and FS in patients with secondary hypertension were decreased significantly relative to non-hypertensive OSA patients and healthy controls. E/A was decreased in OSA patients whether they had secondary hypertension or not.

Conclusion

OSA affected the left ventricular diastolic function in the early stage of the disease. Extended exposure to OSA resulted in left ventricular dysfunction with increased hypertension. Right ventricle dysfunction and abnormalities became more severe as the disease progressed.     

Does obstructive sleep apnea increase hematocrit?

This study assessed the relationship between hematocrit levels and severity of obstructive sleep apnea (OSA) and examined how this relationship was affected by the degree of hypoxia as well as by possible confounding factors. Two-hundred sixty three subjects (189 men and 74 women) underwent nocturnal polysomnography with oximetry and had measurements of hematocrit, hemoglobin, white blood cell count, body mass index (BMI), blood pressure (BP), and 24-h urine norepinephrine (NE). Patients with severe OSA [respiratory disturbance index (RDI) >30] had significantly higher hematocrit values than patients with mild to moderate OSA or nonapneic controls (p<0.01). However, only one patient had a hematocrit in the range of clinical polycythemia. Hematocrit levels were significantly correlated with BMI, BP, urinary NE, RDI, percent of time spent at oxygen saturation <90%, and with mean oxygen saturation. Multiple linear regression analysis revealed that mean oxygen saturation, RDI, and percent of time spent at oxygen saturation <90% were significant predictors of hematocrit level, even after controlling for gender, ethnicity, 24-h urine NE, BMI, and BP (p<0.05). The severity of OSA is significantly associated with increased hematocrit, even after controlling for possible confounding variables. However, nocturnal hypoxemia in OSA does not usually lead to clinical polycythemia.     

Cardiovascular diseases in obstructive sleep apnea

Obstructive sleep apnea (OSA) affects approximately 5% of women and 15% of men in the middle-aged adults, and associated with adverse health outcomes. Cardiovascular disturbances are the most serious complications of OSA. These complications include heart failure, left/right ventricular dysfunction, acute myocardial infarction, arrhythmias, stroke, systemic and pulmonary hypertension. All these cardiovascular complications increase morbidity and mortality of OSA. Several epidemiologic studies have demonstrated that sleep related breathing disorders are an independent risk factor for hypertension, probably resulting from a combination of intermittent hypoxia and hypercapnia, arousals, increased sympathetic activity, and altered baroreflex control during sleep. Arterial hypertension, obesity, diabetes mellitus and coronary artery disease (CAD) which are independent predictors of left ventricular dysfunction, often have co-existence with OSA. Especially severe OSA patients having diastolic dysfunction might have an increased risk of heart failure, since diastolic dysfunction might be combined with systolic dysfunction. Early recognition and appropriate therapy of ventricular dysfunction is advisable to prevent further progression to heart failure and death. Patients with acute myocardial infarction, especially if they had apneas and hypoxemia without evident heart failure should be evaluated for sleep disorders. So, patients with CAD should be evaluated for OSA and vice versa. Early recognition and treatment of OSA may improve cardiovascular functions. Continuous positive airway pressure (CPAP) applied by nasal mask, is still the gold standard method for treatment of the disease and prevention of complications.     

Respiratory disturbance during sleep in COPD patients without daytime hypoxemia

Chronic obstructive pulmonary disease (COPD) is associated with significant morbidity and mortality. Its possible association with obstructive sleep apnea is a major cause of concern for clinicians. As the prevalence of both COPD and sleep apnea continues to rise, further investigation of this interaction is needed. In addition, COPD patients are at risk for hypoventilation during sleep due to the underlying respiratory dysfunction. In this study, 13 COPD subjects and 13 non-COPD control subjects were compared for the presence and severity of obstructive sleep apnea and nocturnal hypoventilation. All 26 subjects had presented to a sleep clinic and showed no signs of daytime hypoxemia. After matching for BMI and age, COPD subjects had a similar prevalence of sleep apnea with a lower degree of severity compared to the control subjects. However, less severe events, such as RERA, occurred at similar rates between the two groups. There was no significant difference between groups in the magnitude of oxyhemoglobin desaturation during sleep. Interestingly, severity and presence of nocturnal hypoxemia correlated with that of sleep apnea in the control group, but not in the COPD subjects. In conclusion, COPD without daytime hypoxemia was not a risk factor for sleep apnea or nocturnal hypoventilation in this study.     

Severe obstructive sleep apnea is associated with left ventricular diastolic dysfunction

INTRODUCTION: Hypertension is common in patients with obstructive sleep apnea (OSA). However, the effect of OSA on ventricular function, especially diastolic function, is not clear. Therefore, we have assessed the prevalence of diastolic dysfunction in patients with OSA and the relationship between diastolic parameters and severity of OSA. METHODS: Sixty-eight consecutive patients with OSA confirmed by polysomnography underwent echocardiography. Diastolic function of the left ventricle was determined by transmitral valve pulse-wave Doppler echocardiography. Various baseline characteristics, severity of OSA, and echocardiographic parameters were compared between patients with and without diastolic dysfunction. RESULTS: There were 61 male and 7 female patients with a mean age of 48.1 +/- 11.1 years, body mass index of 28.5 +/- 4.3 kg/m(2), and apnea/hypopnea index (AHI) of 44.3 +/- 23.2/h (mean +/- SD). An abnormal relaxation pattern (ARP) in diastole was noted in 25 patients (36.8%). Older age (52.7 +/- 8.9 years vs 45.1 +/- 11.3 years, p = 0.005), hypertension (56% vs 20%, p = 0.002), and a lower minimum pulse oximetric saturation (SpO(2)) during sleep (70.5 +/- 17.9% vs 78.8 +/- 12.9%, respectively; p = 0.049) were more common in patients with ARP. By multivariate analysis, minimum SpO(2) < 70% was an independent predictor of ARP (odds ratio, 4.34; 95% confidence interval, 1.23 to 15.25; p = 0.02) irrespective of age and hypertension. Patients with AHI > or = 40/h had significantly longer isovolumic relaxation times than those with AHI < 40/h (106 +/- 19 ms vs 93 +/- 17 ms, respectively; p = 0.005). CONCLUSION: Diastolic dysfunction with ARP was common in patients with OSA. More severe sleep apnea was associated with a higher degree of left ventricular diastolic dysfunction in this study.     

Associated factors for sleep apnea in heart failure

Objective

Genesis of sleep apnoea syndrome (SAS) in chronic heart failure (CHF) is not well known. The aim of our study was to find associated factors to SAS in heart failure (HF) and to look for differences between central sleep apnea (CSA) and obstructive sleep apnea (OSA).

Patients and methods

We realised a cross-sectional and retrospective study. Thirty patients with stable heart failure under medical optimal therapy were included. Polygraphy, echocardiography and cardiopulmonary exercise were systematically performed.

Results

Men were predominant (80%) in the group. Mean age, left ventricular ejection fraction (LVEF) were respectively 64.1 ± 13.8 years and 40 ± 9.8%. SAS was present in 60% of patients (33.3% were classified as central sleep apnoea [CSA] and 26.7% as obstructive sleep apnoea [OSA]). Body mass index, blood pressure and left ventricular pressures estimated by the E/Ea ratio were significantly higher in the group with SAS (P < 0.05) compared to the non SAS group. New York Heart Association class was significantly higher (P = 0.04) and the predicted peak VO₂ was significantly lower in CSA patients compared to OSA patients.

Conclusion

High left ventricular pressures estimated by the E/Ea are significantly associated with SAS in heart failure. CSA patients tend to have a worse functional state than OSA patients.     

Acute and chronic effects of airway obstruction on canine left ventricular performance

We used a canine model of chronic obstructive sleep apnea (OSA) to examine the effects of intermittent airway occlusion during sleep on left ventricular (LV) performance. Studies were performed in four dogs. The effects of acute airway occlusion on LV pressure and volume (on a background of chronic OSA) were determined with an impedance catheter and a high fidelity manometer. In conscious animals (n = 3), experiencing spontaneous episodes of sleep, acute airway occlusion caused significant increases in LV transmural systolic pressure that were associated with increased end-systolic volume and reduced stroke volume. To determine the effects of chronic OSA on baseline LV function, two-dimensional echocardiograms were performed in conscious animals (n = 4) during unobstructed breathing before and after a 1- to 3-mo period of OSA. During chronic OSA, there was a significant decrease in LV ejection fraction as a result of increases in end-systolic volume. We conclude that in chronic OSA acute airway occlusion during sleep is associated with increases in LV afterload and decreases in fractional shortening. Chronic OSA also leads to sustained decreases in LV systolic performance that could be caused by the development of systemic hypertension and/or transient increases in LV afterload during episodes of airway obstruction.     

Prevalence of moderate or severe left ventricular diastolic dysfunction in obese persons with obstructive sleep apnea

We investigated prior to gastric bypass surgery the prevalence of left ventricular diastolic dysfunction (LVDD) by Doppler and tissue Doppler echocardiography in 14 obese women and in 6 obese men, mean age 45 years, with a mean body mass index of 49+/-5 kg/m2 who had nocturnal polysomnography for obstructive sleep apnea (OSA). The Doppler and tissue Doppler echocardiographic data were analyzed blindly without knowledge of the clinical characteristics or whether OSA was present or absent. Of 20 patients, 8 (40%) had no OSA, 4 (20%) had mild OSA, and 8 (40%) had moderate or severe OSA. Moderate or severe LVDD was present in 4 of 8 patients (50%) with moderate or severe OSA and in none of 12 patients (0%) with no or mild OSA (p<0.01). Obese patients with moderate or severe OSA have a higher prevalence of moderate or severe LVDD than obese patients with no or mild OSA.     

Timing of nocturnal ventricular ectopy in heart failure patients with sleep apnea

BACKGROUND: Ventricular ectopy is frequent in heart failure (HF) patients with sleep apnea. A previous report indicated that in HF patients, ventricular premature beats (VPB) occurred more frequently during episodes of recurrent central sleep apnea (CSA) than during normal breathing, and their frequency was greater during hyperpnea than during apnea. We hypothesized that, because respiratory stimuli that might provoke ventricular ectopy are stronger during obstructive apneas than during central apneas, in contrast to CSA, VPBs would be more frequent during apnea than hyperpnea in HF patients with obstructive sleep apnea (OSA). METHODS: HF patients in sinus rhythm who have OSA or CSA (apnea-hypopnea index, > or = 15 events per hour) and with > 30 VPBs per hour were matched for severity of cardiac dysfunction and sleep apnea. The frequency of VPBs was then assessed during stage 2 sleep during the apneic and the hyperpneic phases of recurrent obstructive or central apneas. RESULTS: VPBs occurred more frequently during the apneic phase than during the hyperpneic phase in patients with OSA. In contrast, VPBs occurred more frequently during the hyperpneic phase than the apneic phase in patients with CSA. There was no difference in the degree of apnea-related oxygen desaturation between central and obstructive apneas. CONCLUSIONS: In patients with HF, nocturnal ventricular ectopy oscillates in time with oscillations in ventilation, with VPBs occurring predominantly during apneas in patients with OSA, but during hyperpneas in patients with CSA. This difference in VPB timing between OSA and CSA may be attributable to the differences in timing of arrhythmic stresses in these patients.     

Acute and chronic effects of continuous positive airway pressure therapy on left ventricular systolic and diastolic function in patients with obstructive sleep apnea and congestive heart failure

BACKGROUND:

Obstructive sleep apnea (OSA) may contribute to the pathogenesis of congestive heart failure (CHF). Nocturnal continuous positive airway pressure (CPAP) therapy can alleviate OSA and may have a role in the treatment of CHF patients.

OBJECTIVES:

To investigate the acute and chronic effects of CPAP therapy on left ventricular systolic function, diastolic function and filling pressures in CHF patients with OSA.

METHODS:

Twelve patients with stable CHF (New York Heart Association II or III, radionuclide ejection fraction lower than 40%) underwent overnight polysomnography to detect OSA. In patients with OSA (n=7), echocardiography was performed at baseline (awake, before and during acute CPAP administration) and after 6.9±3.3 weeks of nocturnal CPAP therapy. Patients without OSA (n=5) did not receive CPAP therapy, but underwent a baseline and follow-up echocardiogram.

RESULTS:

In CHF patients with OSA, acute CPAP administration resulted in a decrease in stroke volume (44±15 mL versus 50±14 mL, P=0.002) and left ventricular ejection fraction ([LVEF] 34.8±5.0% versus 38.4±3.3%, P=0.006) compared with baseline, but no change in diastolic function or filling pressures (peak early diastolic mitral annular velocity [Ea]: 6.0±1.6 cm/s versus 6.3±1.6 cm/s, P not significant; peak early filling velocity to peak late filling velocity [E/A] ratio: 1.05±0.74 versus 1.00±0.67, P not significant; E/Ea ratio: 10.9±4.1 versus 11.3±4.1, P not significant). In contrast, chronic CPAP therapy resulted in a trend to an increase in stroke volume (59±19 mL versus 50±14 mL, P=0.07) and a significant increase in LVEF (43.4±4.8% versus 38.4±3.3%, P=0.01) compared with baseline, but no change in diastolic function or filling pressures (Ea: 6.2±1.2 cm/s versus 6.3±1.6 cm/s, P not significant; E/A ratio: 1.13±0.61 versus 1.00±0.67, P not significant; E/Ea ratio: 12.1±2.7 versus 11.3±4.1, P not significant). There was no change in left ventricular systolic function, diastolic function or filling pressures at follow-up in CHF patients without OSA.

CONCLUSIONS:

Acute CPAP administration decreased stroke volume and LVEF in stable CHF patients with OSA. In contrast, chronic CPAP therapy for seven weeks improved left ventricular systolic function, but did not affect diastolic function or filling pressures. The potential clinical implications of the discrepant effects of CPAP therapy on left ventricular systolic and diastolic function in CHF patients with OSA warrant further study.     

Systemic hypertension in snorers with and without sleep apnea.

To investigate the impact of sleep-disordered breathing events on daytime hypertension (HT) in patients with increased upper airway resistance during sleep, we studied 191 male snorers aged 49.9 +/- 0.8 years. In 116 of them, an apnea-hypopnea index (AHI) above 10--defined as the presence of obstructive sleep apnea (OSA)--was found; the other 75 subjects had an AHI lower than 10 and were classified as habitual snorers (HSN). Prevalence of HT was not different between OSA (56 of 116 = 48 percent) and HSN (33 of 75 = 44 percent) and there was also no difference in systolic, diastolic, and mean blood pressures between the two groups. Hypertensive OSA patients had higher body mass index (BMI) than normotensive OSA subjects (31.4 +/- 0.7 vs 29.4 +/- 0.6; p less than 0.05), but there was no difference in age, AHI, and nocturnal oxygenation parameters. The same was true for the HSN group, with hypertensive subjects being more obese than normotensive subjects (BMI: 30 +/- 0.8 vs 27.3 +/- 0.8; p less than 0.05), but no difference in age and polysomnographic features. Discriminant analysis with HT as the classification variable and age, BMI, AHI, mean, and lowest nocturnal oxyhemoglobin saturation as independent variables, revealed an independent influence on HT only for BMI (F-prob = 0.001). Thus, our results stand against the hypothesis of a causal relationship between sleep-disordered breathing events and daytime hypertension. We conclude that the high prevalence of HT in male snorers is more directly linked to obesity than to sleep apnea, but an independent effect of snoring per se cannot be excluded.