Daytime Pulmonary Hypertension Research Articles

PS-C29-5: PULMONARY HYPERTENSION AND RIGHT VENTRICULAR REMODELING IN OBSTRUCTIVE SLEEP APNEA

Background and Objective: Acute pulmonary artery (PA) pressure changes during sleep have been extensively reported in obstructive sleep apnea (OSA). However, the role of OSA as an independent risk factor for the day-time pulmonary hypertension (PH) is not well known. The present study was conducted to examine whether OSA is associated with PH and right ventricular (RV) remodeling. Methods: 423 OSA patients without chronic obstructive pulmonary disease or left ventricular dysfunction {age: 55 ± 13 years old, mean apnea-hypopnea index (AHI): 41 ± 22 /h} were enrolled in this study. All patients were performed polysomnography, echocardiography and spirometry. Pulmonary artery systolic pressure (PASP) was determined by continuous-wave Doppler using the simplified Bernoulli equation. For this study, PH was defined as an estimated PASP of greater than 30 mmHg. Patients were divided into two groups: mild-moderate OSA group (n = 153) (AHI = 5–30 /h) and severe OSA group (n = 270)(AHI over 30/h). Results: The prevalence of PH among all OSA patients was 19%. No significant differences were found in PASP, tricuspid annular velocity and tricuspid annular plane systolic excursion (TAPSE) between mild-moderate OSA group and severe OSA group. However, RV diastolic diameter (28.7 ± 3.4 vs 27.7 ± 3.0 mm, respectively, P < 0.01) and main PA diameter (26.2 ± 3.7 vs 24.8 ± 3.9 mm, respectively, P < 0.05) were significantly higher in severe OSA group than those in mild-moderate OSA group. Conclusions: The severity of OSA was significantly associated with RV and PA diameters independently PASP. These results suggested that OSA may directly affects RV and PA remodeling independently PH.

THE ASSOCIATION OF SLEEP APNEA WITH INVASIVE CARDIOPULMONARY HEMODYNAMICS

Sleep apnea increases pulmonary artery pressure at night, but whether sleep apnea causes persistent daytime pulmonary hypertension is less clear. Adults who underwent an overnight sleep study within our large heath care system between 3/1999 and 12/2017 were eligible for inclusion if they also

Sleep Apnea is not Associated with Elevations in Pulmonary Artery Pressure in a Clinical Cohort

Introduction Pulmonary hypertension (PH) is associated with adverse patient outcomes. Apneic events during sleep cause transient elevations in pulmonary artery pressure, however the association between sleep apnea and persistent daytime PH is less clear. Hypothesis We hypothesized that sleep apnea would be associated with elevated pulmonary artery systolic pressure (PASP) through both direct effects of hypoxia and indirect effects on left ventricular function. Methods We examined the electronic medical records of patients age ≥ 18 years undergoing sleep study within our large multisite hospital system between March 1999 and December 2015 who had an echocardiogram within 12 months of sleep study. Patients with severe left-sided valve disease (n=33), missing PASP (n=736), or missing apnea hypopnea index (AHI) (n=9) were excluded. An AHI ≥15 events/hour was used to define sleep apnea. PASP was noninvasively estimated by Doppler interrogation of the tricuspid regurgitant jet. Multivariable linear regression was used to examine associations between AHI and measures of left ventricular function and PASP. Results A total of 5,075 patients (age 58.2 ± 14.4 years; 53.0% female) were included. Sleep apnea was found in 45.4% of patients. Mean PASP was 33 ± 15 mm Hg with 34.8% having PASP ≥ 36 mmHg. Patients with higher AHI were older, more likely to be male, and had higher body mass index (BMI). Compared to patients without sleep apnea, those with sleep apnea had lower ejection fraction (EF) (53.6 vs 55.4%), higher left ventricular mass index (LVMI) (105 vs 92 g/m 2 ), and higher early mitral inflow to early diastolic mitral annual velocity ratio (E/e’) (11.9 vs 10.8). After adjustment for age, sex, site, and BMI, EF was 0.9 percentage points lower (95% CI [0.4, 1.4]), LVMI was 7.0 g/m 2 higher [5.1, 8.9], and E/e’ was 0.6 higher [0.1, 1.0] in patients with sleep apnea. In contrast, patients with and without sleep apnea had similar PASP (33.9 vs 33.2 mmHg; p=0.08). These findings persisted when limiting analysis to the 1,784 patients who underwent sleep study prior to echocardiogram. Conclusions In this analysis of real world patients referred for sleep study and echocardiogram, although sleep apnea was associated with markers of left ventricular dysfunction, we found no association between sleep apnea and PASP. This finding suggests sleep apnea does not directly elevate daytime pulmonary artery pressure. Elevations in PASP from left ventricular dysfunction may take time to develop and may not be apparent on cross-sectional analysis. Longitudinal follow-up of pulmonary artery pressure trajectories in patients with sleep apnea will provide greater insights on the impact of sleep apnea on PH.

Right ventricular geometry and mechanics in patients with obstructive sleep apnea living at high altitude.

Repetitive obstruction of larynx during sleep can lead to daytime pulmonary hypertension and alterations in right ventricular morphology and function in a small fraction of obstructive sleep apnea syndrome (OSAS) patients. Environmental effects, particularly high altitude, can modify the effects of OSAS on pulmonary circulation, since altitude-related hypoxia is related with pulmonary vasoconstriction. This potential interaction, however, was not investigated in previous studies. A total of 41 newly diagnosed OSAS patients were included in this study after pre-enrolment screening. Two-dimensional, three-dimensional, and Doppler echocardiographic data were collected after polysomnographic verification of OSAS. Three-dimensional echocardiograms were analyzed to calculate right ventricular volumes, volume indices, and ejection fraction. Systolic pulmonary artery pressure (38.35 ± 8.60 vs. 30.94 ± 6.47 mmHg; p = 0.002), pulmonary acceleration time (118.36 ± 16.36 vs. 103.13 ± 18.42 ms; p = 0.001), right ventricle (RV) end-diastolic volume index (48.15 ± 11.48 vs. 41.48 ± 6.45 ml; p = 0.009), and RV end-systolic volume index (26.50 ± 8.11 vs. 22.15 ± 3.85; p = 0.01) were significantly higher in OSAS patients, with similar RV ejection fraction (EF) between groups. No significant differences were noted in other two-dimensional, Doppler or speckle-tracking strain, measurements. Both RVEF and pulmonary acceleration time were predictors of disease severity. A greater degree of RV structural remodeling and higher systolic pulmonary pressure were observed in OSAS patients living at high altitude compared to healthy highlanders. The reversibility of these alterations with treatment remains to be studied.

SEVERE PULMONARY HYPERTENSION DUE TO SLEEP-DISORDERED BREATHING IN AN ACHONDROPLASIC CHILD

Achondroplasia is the most common skeletal dysplasia in children. Achondroplasic patients often have respiratory problems associated with upper respiratory tract obstruction and craniofacial dysmorphology. Chronic hypoxemia in these patients can result in pulmonary hypertension. In this report an achondroplasic child with severe day-time pulmonary hypertension is presented.

Pulmonary hypertension in obstructive sleep apnea hypopnea syndrome

BackgroundThere has been uncertainty until recently whether OSA, is sufficient to cause persistent daytime pulmonary hypertension and right ventricular dysfunction. ObjectivesThe aims of this study, were to investigate whether OSA by itself without any other cardiac or lung disease can lead to pulmonary hypertension, and to assess the effect of CPAP therapy on pulmonary artery pressure. Subjects and methodsThe study was performed on 54 OSA patients. All patients were subjected to thorough history taking including Epworth sleepiness scale and Berlin questionnaire, physical examinations, calculation of BMI, plain chest X-ray pulmonary function tests, polysomnography and echocardiography. Ten patients out of 24 patients of OSA with PH have been treated with CPAP for six months. ResultsPulmonary hypertension (PH) was present in (44.4%) of OSA patients. There were significantly higher PASP and mPAP in severe OSA patients versus non severe OSA patients. There were significant higher BMI, neck circumference, AHI and ODI in OSA patients with PH compared to OSA patients without PH. Awake SaO2 and minimum SaO2 were significantly lower in OSA patients with PH compared to OSA patients without PH. There were significant reduction in both mPAP and PASP after 6months of CPAP treatment (p=0.007, 0.005 respectively). ConclusionOSA is associated with pulmonary hypertension, improvement of pulmonary hypertension through controlling OSA by CPAP therapy signifies that OSA plays a crucial role in the pathogenesis of pulmonary hypertension. RecommendationsCPAP therapy should be advised to all OSA patients with pulmonary hypertension.

Functional impact of pulmonary hypertension due to hypoventilation and changes under noninvasive ventilation

We aimed to characterise the association of pulmonary hypertension due to hypoventilation and exercise capacity, and the haemodynamic and functional changes under noninvasive ventilation. A retrospective analysis was carried out to assess haemodynamics and functional capacity in 18 patients with daytime pulmonary hypertension, due to hypoventilation, at baseline and after 3 months of noninvasive ventilation. Patients presented with a mean±SD pulmonary artery pressure of 49±13 mmHg, preserved cardiac index (3.2±0.66 L·min(-1)·m(-2)), 6-min walking distance of 303±134 m and severely elevated N-terminal pro-brain natriuretic peptide (NT-proBNP) levels. Mean pulmonary artery pressure correlated negatively with maximum work rate (R= -0.72; p=0.03) and 6-min walking distance (R= -0.62; p=0.01). Following noninvasive ventilation we found a significant reduction of mean pulmonary artery pressure (-18 mmHg; p<0.001) and NT-proBNP levels (-2110 pg·mL(-1); p=0.001), and improvement in the 6-min walking distance (+66 m; p=0.008) and maximum work rate (+18 W; p=0.028). Changes in work rate correlated inversely with pulmonary artery pressure (R= -0.75; p=0.031). In this specific cohort with hypoventilation and severe pulmonary hypertension, pulmonary hypertension was associated with reduced exercise capacity. Following noninvasive ventilation, haemodynamics and exercise capacity improved significantly.

Pulmonary function and pulmonary hemodynamics in obstructive sleep apnea syndrome

The prevalence and mechanisms of daytime pulmonary hypertension were examined in 24 cases of obstructive sleep apnea syndrome (OSAS). All patients were free from chronic lung disease. They underwent pulmonary function tests and blood gas analysis in the sitting and supine position, hypercapnic ventilatory response test, exercise test and right heart catheterization. Elevation of mean pulmonary arterial pressure (m-PAP) above 20 mmHg was observed in 5 out of 24 cases (20.8%). The group with pulmonary hypertension (PG+: m-PAP = 22.2 +/- 2.7 mmHg) showed marked obesity (p < 0.001), significant decrease of supine FRC/TLC (p < 0.05), increase of supine CC/FRC (p < 0.01), decrease of supine PaO2 (p < 0.02) and desaturation during exercise (p < 0.05) in comparison with the group without pulmonary hypertension (PH-: 13.9 +/- 3.1 mmHg). m-PAP was positively correlated with %IBW and desaturation during exercise (p < 0.01, p < 0.02) and negatively correlated with supine PaO2 (p < 0.01). Various changes in pulmonary function and pulmonary hemodynamics due to obesity seem to lead to daytime pulmonary hypertension of OSAS.

Nocturnal pulmonary hypertension in patients with obstructive sleep apnea associated with daytime pulmonary hypertension

We investigated the effect of state-specific changes associated with REM sleep on pulmonary artery pressure in patients with obstructive sleep apnea (OSAS). Six male patients with OSAS (age; 40 +/- 12 SD yrs, BMI; 39.0 +/- 8.6 kg/m2, AHI; 51.5 +/- 28.5) were examined throughout the night by polysomnography, while monitoring pulmonary artery pressure via right cardiac catheterization. All patients had pulmonary hypertension (PH) during periods of wakefulness, and their mean pulmonary artery pressure (PAPm) was 31.1 +/- 7.4 mmHg. PAPm was analyzed at two different points in each apneic episode. PAPbase was the baseline value when inspiratory effects during apnea were not elicited, and PAPpeak was the peak value observed just after the cessation of OSA. PAPpeak was higher in REM (56.3 +/- 12.4) than in NREM (41.4 +/- 6.9 mmHg; P < 0.01), and both values were significantly higher than those observed during periods of wakefulness. The magnitude of elevation of PAP (delta PAP; PAPpeak-PAPbase) in REM and NREM were 11.6 +/- 2.0 and 6.9 +/- 2.8 mmHg, respectively. Relative ratios in the response of PAP to a decrease in O2 desaturation (delta PAP/delta SpO2) showed almost the same value for REM (-0.57 +/- 0.27) and NREM sleep (-0.57 +/- 0.26 mmHg/%). The values of PAPm at SpO2 75% were significantly higher in REM than in NREM (48.7 +/- 11.2 vs. 41.6 +/- 6.2 mmHg). We conclude that transient pulmonary hypertension could be caused not only by hypoxia, but also by state-specific responses (which are unrelated to hypoxia) that occur during REM sleep.

Pulmonale Hypertonie und schlafbezogene Atmungsstörungen

Pulmonary hypertension (PH), i. e. an increase of mean pulmonary artery pressure above 20 mm Hg under resting conditions, can be observed in different forms of sleep-disordered breathing (SDB). In obstructive sleep apnea (OSA) the apnea-associated triggers of hypoxia and intrathoracic pressure swings lead to repetitive rises of pulmonary artery pressure during sleep. In 20 - 30 % of these patients daytime PH occurs. PH in the setting of OSA is usually mild and rarely causes clinically evident cor pulmonale. Effective CPAP therapy has a beneficial influence on pulmonary hemodynamics in OSA. Severe congestive heart failure (i. e. with a LVEF < 40 %) might provoke pulmonary venous hypertension and thereby stimulation of pulmonary stretch and irritant receptors. The ensuing hyperventilation leads to a decrease of pCO (2) levels below the apneic threshold and thus contributes to the emergence of Cheyne Stokes respiration (CSR) in up to one half of the affected patients. Patients suffering from advanced idiopathic pulmonary arterial hypertension (IPAH) might show a similar breathing pattern while asleep. Possible pathogenetic factors of the nocturnal periodic breathing occurring in end-stage IPAH are prolonged circulation times and hypocapnia. In conclusion, SDB might cause PH (OSA-associated PH). On the other hand, PH might lead to the development of SDB (CSR in congestive heart failure, periodic breathing in IPAH).

Functional dynamics of the right ventricle and pulmonary circulation in obstructive sleep apnea. Therapeutic consequences

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.

Prevalence of pulmonary hypertension and its association with respiratory disturbances in obese patients living at moderately high altitude.

To determine the point prevalence of pulmonary hypertension (PH) and its relationship with respiratory disturbances in obese patients living at moderate altitude. A total of 57 obese patients comprised the final sample and consisted of 34 women and 23 men, with a mean age of 42.7+/-12.1 ys and a mean body mass index (BMI) 47.1+/-10.6 kg/m(2) (range from 30.1 to 76.1). The mean living altitude was 2248.7 m, range 2100-2400 m above sea level. Doppler echocardiography, pulmonary function tests, arterial blood gas analysis, and polysomnography were performed. Data showed that 96.5% of the studied sample had daytime PH defined as calculated systolic pulmonary artery pressure (PSAP) >30 mmHg (mean PSAP=50, s.d.=13 mmHg). The severity of diurnal PH was found to be related to the presence of alveolar hypoventilation and BMI. The main risk factor for severity of diurnal PH was hypoventilation with a significant odds ratio (OR) 7.96, 95% CI 1.35-46.84, BMI was (OR 1.12, 95% CI 1.02-1.25) and apnea/hypopnea index was not a predictor of pulmonary hypertension severity (OR 0.99, 95% CI 0.97-1.02). We concluded that prevalence of diurnal PH is high in obese patients living at moderate altitude, and that hypoventilation is the main risk factor associated with the severity of pulmonary hypertension.

Pulmonary hemodynamics in obstructive sleep apnea: frequency and causes of pulmonary hypertension.

The association between nocturnal apneas and transient pulmonary hypertension (PHT) has been well documented. However, there is controversy over the frequency and pathophysiological mechanisms of daytime pulmonary hypertension in patients with obstructive sleep apnea (OSAS). The present study sought to evaluate frequency and mechanisms of pulmonary hypertension in patients with OSAS. It included 49 consecutive patients with polysomnographically proven OSAS without pathological lung function testing. All patients performed daytime measurements of pulmonary hemodynamics at rest and during exercise (50-75W). Six patients (12%) had resting PHT mean pulmonary of artery pressure (PAPM) of >20 mmHg), whereas 39 patients (80%) showed PHT during exercise (PAPM >30 mmHg). Multiple regression analysis revealed 3 independent contributing factors for mean pulmonary artery pressure during exercise (PAPMmax): body mass index, age and total lung capacity % of predicted. Twenty-five of the 39 patients with pathologically high PAPMmax (64%) showed elevated pulmonary capillary wedge pressures (PCWPmax > 20 mmHg), whereas no patient had elevated pulmonary vascular resistance (PVRmax > 120 dynes x s x cm(-5)). In conclusion, daytime PHT during exercise is frequently seen in patients with OSAS and normal lung function testing and is mainly caused by abnormally high PCWP, whereas PVR seems to play a minor role.

Cardiovascular Abnormalities in Sleep-Disordered Breathing

The role of sleep-disordered breathing (SDB) in the development of persistent daytime pulmonary hypertension (PH) and cor pulmonale is controversial and has not been extensively studied. In this review we discuss the physiological changes that occur during SDB in the cardiovascular system, as well as review the most recent literature examining the relationship between SDB and PH/cor pulmonale. The literature suggests that much of the PH and right heart dysfunction seen in SDB is related to concurrent obesity and underlying lung disease, although it does appear that isolated SDB (in the form of obstructive sleep apnea) may be responsible for a small but significant degree of PH. The clinical consequences of this, however, remain unclear.

Pulmonary hypertension in patients with severe obstructive sleep apnea.

Thirty-seven patients (35 men and two women) with obstructive sleep apnea-hypopnea syndrome (OSAHS) without any known cardiovascular and lung diseases were examined by Doppler echocardiography. Eight of the 37 (21.6%) patients experienced daytime pulmonary hypertension (PH), and all of them had severe OSAHS with an apnea-hypopnea index of > 30. The study suggested that one-third of patients with severe OSAHS had daytime PH.

Daytime Pulmonary Hypertension in Patients with Obstructive Sleep Apnea

Background: Limited information exists regarding the development of pulmonary hypertension in patients with obstructive sleep apnea (OSA) in the absence of lung and heart comorbidity. Objectives: The aims of this study were to investigate whether OSA patients without any other cardiac or lung disease develop pulmonary hypertension, and to assess the effect of continuous positive airway pressure (CPAP) treatment on pulmonary artery pressure (P_PA). Methods: Twenty-nine patients aged 51 ± 10 years with OSA and 12 control subjects were studied with pulsed-wave Doppler echocardiography for estimation of P_PA before and after 6-month effective treatment with CPAP. Results: A significantly higher mean P_PA was found in OSA patients as compared to control subjects (17.2 ± 5.2 vs. 12.1 ± 1.9 mm Hg, p < 0.001). Six out of the 29 OSA patients had mild pulmonary hypertension (P_PA ≧ 20 mm Hg). Significant differences were observed between pulmonary hypertensive and normotensive OSA patients with respect to age (62 ± 4 vs. 48 ± 15 years, respectively, p < 0.05), body mass index (41 ± 7 vs. 32 ± 4 kg/m², p < 0.02) and daytime P_aO₂ (81 ± 9 vs. 92 ± 9 mm Hg, p < 0.05). CPAP treatment was effective in reducing mean P_PA in both groups of pulmonary hypertensive and normotensive OSA patients (decreases in P_PA from 25.6 ± 4.0 to 19.5 ± 1.5 mm Hg, p < 0.001; from 14.9 ± 2.2 to 11.5 ± 2.0 mm Hg, respectively, p < 0.001). Conclusions: A proportion (20.7%) of OSA patients without any other lung or heart disease and characterized by older age, greater obesity and lower daytime oxygenation develop mild pulmonary hypertension which has been partially or completely reversed after 6-month CPAP treatment. In conclusion, OSA alone constitutes an independent risk factor for the development of pulmonary hypertension.

Manifestation of Pulmonary Hypertension During REM Sleep in Obstructive Sleep Apnea Syndrome

The effect of sleep stage change on pulmonary circulation has not been well documented in patients with obstructive sleep apnea syndrome (OSAS). We investigated whether or not stage-specific change can affect pulmonary artery pressure (Ppa) in patients with OSAS. Thirty-one patients with OSAS underwent right cardiac catheterization in the daytime and the following night, including 19 patients in whom Ppa could be measured throughout non-rapid eye movement (NREM) and rapid eye movement (REM) sleep. Ten of the 19 patients had daytime pulmonary hypertension (PH) defined by a mean Ppa (Ppa) >/= 20 mm Hg. Then we analyzed Ppa response to hypoxia spontaneously occurring during the period of sleep apnea. The slopes of the regression lines between arterial oxygen saturation measured by pulse oximeter (SpO2) and Ppa curves were almost the same in both NREM and REM patient groups with or without daytime PH, whereas the response curve was significantly shifted upward in REM compared with NREM patients with daytime PH. Furthermore, Ppa was elevated more markedly in association with REM burst, phasic REM, compared with tonic REM. We conclude that vascular tone of pulmonary artery could be elevated in association with REM sleep which is independent of the degree of hypoxia, and that this state-specific change is manifested in patients with daytime PH.

Long-Term Compliance with Continuous Positive Airway Pressure in Patients with Obstructive Sleep Apnea Syndrome

A ten-year retrospective analysis of the clinical features and survival of 60 Saudi children with systemic lupus erythematosus (SLE) was made. All the patients fulfilled the 1982 American College of Rheumatologyâs revised criteria for SLE and had had the disease at or before the age of 16 years. The female to male ratio was 5:1, the mean age of onset was 12.1 years (range 1.6-16 years), and the mean duration of follow-up was 4.7 years (range 2.2-11). Thirty-eight patients (63%) were diagnosed correctly before referral to KFSH&RC or KKUH. The mode of presentation was as follows: 55 patients had musculoskeletal involvement (91.6%), 49 patients had skin involvement (81.6%), 40 patients had hematological abnormalities (66.6%), 39 patients had renal disease (65%), 10 patients had pulmonary involvement (16%), 23 patients had cardiovascular disease (38%) and 18 patients had central nervous system involvement. During the study period four patients died (6.6%)âtwo of renal failure, one from meningitis and one from severe sepsis. This is the largest collection of childhood systemic lupus erythematosus from the Middle East and it shows that SLE is more common in Saudis than was hitherto believed, and that it has a high rate of organ involvement.

Pulmonary Hypertension, Hypoxemia, and Hypercapnia in Obstructive Sleep Apnea Patients

To define the parameters of respiratory insufficiency in OSA, 114 consecutive patients (108 men, six women) were prospectively studied. In addition to standard polysomnography, they underwent pulmonary function tests, right heart catheterization, and ventilatory response tests to hypercapnia. Nineteen patients (19 percent) had a resting PAP greater than or equal to 20 mm Hg. Multiple regression analysis showed that FEV1 and PaO2 (both with a negative coefficient) and PaCO2 (with a positive coefficient) significantly contributed to PAP. Thirteen patients (12 percent) had a PaCO2 greater than or equal to 45 mm Hg. A multiple regression analysis showed that FEV1 and the minute ventilation at PETCO2 = 60 mm Hg (both with a negative coefficient) and the cumulative apnea duration (with a positive coefficient) significantly contributed to PaCO2. Thirty-seven patients (33 percent) had a PaO2 less than or equal to 65 mm Hg. A multiple regression analysis showed that FEV1 (with a positive coefficient) and the hypopnea + apnea index (with a negative coefficient) significantly contributed to PaO2. These data confirm that impaired daytime pulmonary function (diffuse airway obstruction) contributes to the development of daytime pulmonary hypertension, hypoxemia, and hypercapnia in OSA patients. They show that the amount of sleep-related breathing disorders also plays a significant role.

Daytime pulmonary hypertension in patients with obstructive sleep apnea syndrome.

The frequency of daytime pulmonary hypertension (PH) in patients with obstructive sleep apnea syndrome (OSAS) has not been well established and its mechanisms are still under debate. We have thus performed right heart catheterization, in addition to standard spirography and arterial blood gas measurements, in a series of 46 consecutive patients in whom OSAS was firmly diagnosed by whole-night polysomnography. Only 9 of the 46 patients (20%) had PH defined by a mean resting pulmonary arterial pressure (Ppa) greater than or equal to 20 mm Hg. Among the patients without resting PH, 14 had exercising PH (defined by a Ppa greater than 30 mm Hg during 40-watt, steady-state exercise). Patients with resting PH differed from the others by a lower daytime PaO2 (60.8 +/- 7.6 versus 76.2 +/- 9.4 mm Hg; p less than 0.001), a higher daytime PaCO2 (44.6 +/- 4.2 versus 38.0 +/- 4.0 mm Hg; p less than 0.001), and lower VC and FEV1 (p less than 0.001). There was no difference between the 2 groups with regard to apnea index (62 +/- 34 versus 65 +/- 40) or the lowest sleep SaO2 (59 +/- 21 versus 66 +/- 18%) or the time spent in apnea. For the group as a whole, there was a good correlation between Ppa and daytime PaO2 (r = -0.61; p less than 0.001), PaCO2 (r = 0.55; p less than 0.001), and FEV1 (r = -0.52; p less than 0.001), but there was no significant correlation between Ppa and the apnea index, the lowest sleep SaO2, or the time spent in apnea.(ABSTRACT TRUNCATED AT 250 WORDS)