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

Krieger, J; Sforza, Émilia; Apprill, M; Lampert, Eliane; Weitzenblum, E; Ratomaharo, J.

doi:10.1378/chest.96.4.729

Cited by 166 publications

(97 citation statements)

References 9 publications

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“…Notwhitstanding, the prevalence for PH in the OSAS group (Group-3) was higher than that reported for other European populations with OSAS (17-27%) living at an altitude, on average, 150 m above sea level 4,7,8,13,14 and with mean BMI between 31 and 35, except for the report of Alchanatis et al 13 in which the BMI of the patients was in the lower limit of our sample (4177).…”

Section: Discussioncontrasting

confidence: 77%

“…1-3 A significant proportion of OSAS patients (17-42%) also have elevated daytime pulmonary artery pressure. [4][5][6][7][8] Although transient increases in pulmonary artery pressure during apneas are well recognized, the role of sleep apnea in inducing sustained waking pulmonary hypertension has been controversial. It has been suggested that PH develops in patients with OSAS only in the presence of daytime hypoxemia secondary either to clinically significant chronic obstructive pulmonary disease, a diminished chemosensitivity or to obesity.…”

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confidence: 99%

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

et al. 2004

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OBJECTIVE:To determine the point prevalence of pulmonary hypertension (PH) and its relationship with respiratory disturbances in obese patients living at moderate altitude. SUBJECTS: A total of 57 obese patients comprised the final sample and consisted of 34 women and 23 men, with a mean age of 42.7712.1 ys and a mean body mass index (BMI) 47.1710.6 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. MEASUREMENTS: Doppler echocardiography, pulmonary function tests, arterial blood gas analysis, and polysomnography were performed. RESULTS: Data showed that 96.5% of the studied sample had daytime PH defined as calculated systolic pulmonary artery pressure (PSAP) 430 mmHg (mean PSAP ¼ 50, s.d. ¼ 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). CONCLUSION: 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.

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Section: Discussioncontrasting

confidence: 77%

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confidence: 99%

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

et al. 2004

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“…Another confounding factor is the association of chronic obstructive pulmonary disease (COPD), which may explain certain conflicting results on the role of SAS in the development of daytime alveolar hypoventilation and pulmonary arterial hypertension [9][10][11].…”

Section: Aamentioning

confidence: 99%

“…Obesity is a major confounding factor as it is strongly associated with SAS [7,8], and may yield the same cardiorespiratory complications as SAS. Therefore, observing cardiac and respiratory abnormalities in an obese patient with SAS does not necessarily imply a causal association between nocturnal apnoeas and cardiorespiratory morbidity.Another confounding factor is the association of chronic obstructive pulmonary disease (COPD), which may explain certain conflicting results on the role of SAS in the development of daytime alveolar hypoventilation and pulmonary arterial hypertension [9][10][11].The aim of the present study was to assess the cardiorespiratory consequences of SAS by comparing the results of a comprehensive cardiorespiratory evaluation in apnoeic and nonapnoeic patients with a similar degree of obesity, i.e. massive obesity and without COPD.…”

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Cardiorespiratory consequences of sleep apnoea syndrome in patients with massive obesity

Laaban¹,

Cassuto²,

Orvoen-Frija³

et al. 1998

Eur Respir J

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aaSleep apnoea syndrome (SAS) has been reported to be associated with excess mortality [1,2] and a wide range of cardiac and respiratory sequelae [3][4][5]: daytime alveolar hypoventilation, pulmonary arterial hypertension, systemic arterial hypertension, left ventricular hypertrophy and dysfunction, cardiac arrhythmias and ischaemic heart disease. However, conflicting data have been published on the cardiorespiratory consequences of SAS. This might be due to the fact that most studies did not take sufficient account of the potential effects of confounding variables, such as age, smoking, and obesity [6]. Obesity is a major confounding factor as it is strongly associated with SAS [7,8], and may yield the same cardiorespiratory complications as SAS. Therefore, observing cardiac and respiratory abnormalities in an obese patient with SAS does not necessarily imply a causal association between nocturnal apnoeas and cardiorespiratory morbidity.Another confounding factor is the association of chronic obstructive pulmonary disease (COPD), which may explain certain conflicting results on the role of SAS in the development of daytime alveolar hypoventilation and pulmonary arterial hypertension [9][10][11].The aim of the present study was to assess the cardiorespiratory consequences of SAS by comparing the results of a comprehensive cardiorespiratory evaluation in apnoeic and nonapnoeic patients with a similar degree of obesity, i.e. massive obesity and without COPD. This study investigated the role of SAS in the development of daytime alveolar hypoventilation, pulmonary arterial hypertension, systemic arterial hypertension, left ventricular dysfunction, left ventricular hypertrophy and dilatation, cardiac arrhythmias and coronary artery disease. Patients and methods Study populationThe study population included morbidly obese patients admitted consecutively over a 3 yr period to the Nutrition department of Hôtel-Dieu Hospital for an extensive Nocturnal apnoeas in massive obesity may thus be associated with moderate daytime hypoxaemia, mild pulmonary arterial hypertension and moderate left ventricular hypertrophy, but not with severe cardiorespiratory complications.

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“…Die dort gefundenen Zusammenhänge können jedoch alle durch Über-gewicht, Rauchen und chronisch obstruktive Bronchitis erklärt werden (19 …”

Section: Pulmonale Hypertonieunclassified

Obstructive sleep apnea syndrome - diagnostics

Hader

Sanner²,

Rasche³

2004

Dtsch med Wochenschr

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DefinitionUnter obstruktiver Schlafapnoe/-hypopnoe wird ein periodisches Sistieren (Apnoe) oder eine periodische Reduktion (Hypopnoe) der Atmung bedingt durch eine komplette oder inkomplette Okklusion der oberen Atemwege im Schlaf mit daraus resultierender Weckreaktion (Arousal) bei fortbestehender Aktivität der Atmungsmuskulatur verstanden (Abb.1). Ein obstruktives Schlafapnoe-Syndrom (OSAS) liegt dann vor, wenn aufgrund der schlafbezogenen Atmungsstörung Folgesymptome entstehen. Als Leitsymptome des OSAS finden sich exzessive Tagesschläfrigkeit, lautes und unregelmäßiges Schnarchen und Atemstillstände während des Schlafens (1, 12, 13). Klassifikation schlafbezogener Atmungsstörungen

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

Cited by 166 publications

References 9 publications

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

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

Cardiorespiratory consequences of sleep apnoea syndrome in patients with massive obesity

Obstructive sleep apnea syndrome - diagnostics

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