- ICH GCP
- Registre américain des essais cliniques
- Essai clinique NCT02505594
Potential Mechanism of Exercise Impairment in OSA
Pulmonary Vasoreactivity as a Potential Mechanism of Exercise Impairment in Obstructive Sleep Apnea
Aperçu de l'étude
Statut
Les conditions
Description détaillée
Obstructive sleep apnea (OSA) is a common disorder with major cardiovascular sequelae, including increased systemic hypertension and strokes. OSA is highly prevalent among patients with cardiovascular disease (CVD), but OSA remains under-diagnosed, thus under-treated. Furthermore, a recent study confirmed that OSA is associated with impaired exercise capacity and increasing OSA severity predicts worsening exercise capacity, which is a marker of potential increased cardiovascular risk. However, potential mechanisms of decreased exercise capacity caused by OSA remain unclear.
Several pathophysiologic mechanisms of OSA have been proposed to explain this observation. Endothelial dysfunction is one mechanism that may result from OSA-related intermittent hypoxemia, heightened sympathetic activation, and increased blood pressure. Endothelial dysfunction is characterized by alteration of normal endothelial physiology consisting of a reduction in the bioavailability of vasodilators such as nitric oxide leading to impaired endothelium-depended vasodilation. Endothelial dysfunction has been consistently associated with an increased incidence of CVD. Recent evidence also suggests a correlation between endothelial function and exercise capacity.
In addition, endothelial dysfunction of pulmonary vasculature play an integral role in the pathogenesis of pulmonary hypertension (PH), which is defined by a mean pulmonary artery pressure exceeding 25 mm Hg. PH is associated with increased mortality and multiple morbidities including impaired exercise capacity. OSA has been formally recognized as a cause of PH by the World Health Organization (WHO) and the estimated prevalence of PH in patients with OSA is 17%. Repetitive nocturnal hypoxemia, increased sympathetic tone, and diminished endothelial dependent vaso-reactivity contribute to pulmonary artery hypoxic vasoconstriction, subsequently leading to pulmonary vasculature remodeling and PH. Recently, PH induced by exercise was described as part of the PH spectrum and may represent early, mild, PH that is still clinically relevant in many patients. To detect early PH in OSA patients may signify the importance of treatment and compliance for newly diagnosed OSA patients.
In summary, our hypothesis is that OSA patients may have endothelial dysfunction that leads to impaired exercise capacity via exercise-induced pulmonary hypertension. If our hypothesis is correct, non-invasive measurements of endothelial function could be used clinically to risk stratify patients or follow response to treatment.
Type d'étude
Inscription (Réel)
Contacts et emplacements
Lieux d'étude
-
-
California
-
San Diego, California, États-Unis, 92093
- University of California, San Diego
-
-
Critères de participation
Critère d'éligibilité
Âges éligibles pour étudier
Accepte les volontaires sains
Sexes éligibles pour l'étude
Méthode d'échantillonnage
Population étudiée
La description
Inclusion Criteria:
- BMI < 30
- OSA group: diagnosis of untreated moderate-to-severe OSA (apnea-hypopnea index (AHI) ≥ 15 events/h).
- Control group: no OSA (AHI < 5 events/h).
Exclusion Criteria:
- Currently using Continuous Positive Airway Pressure (CPAP) or oral appliance treatment for OSA
- Uncontrolled cardiac co-morbidity, e.g. ischemic heart disease, heart failure, or valvular heart disease that would prevent exercise
- Uncontrolled pulmonary co-morbidity, e.g. asthma or chronic obstructive pulmonary disease (COPD)
- Comorbidities that may severely impair peripheral circulation, e.g. uncontrolled diabetes mellitus, or systemic scleroderma
- Neurological conditions limiting the ability to perform walking or cycling
- Orthopedic condition limiting the ability to perform walking or cycling
- Current smokers, alcohol (> 3 oz/day) or use of illicit drugs.
- Psychiatric disorder, other than mild and controlled depression; e.g. schizophrenia, bipolar disorder, major depression, panic or anxiety disorders.
- Pregnancy
Plan d'étude
Comment l'étude est-elle conçue ?
Détails de conception
Cohortes et interventions
Groupe / Cohorte |
---|
OSA Group
Apnea-hypopnea index (AHI) ≥ 15 events/h
|
Control Group
Apnea-hypopnea index (AHI) < 5 events/h
|
Que mesure l'étude ?
Principaux critères de jugement
Mesure des résultats |
Description de la mesure |
Délai |
---|---|---|
Endothelial function, as measured by endoPAT, between OSA patients and matched healthy controls
Délai: Baseline
|
EndoPAT is a non-invasive measurement of endothelial function, using peripheral arterial tonometry.
Exercise tolerance is measured by Cardiopulmonary exercise testing (CPET).
Effects of OSA on exercise tolerance and endothelial function will be evaluated.
|
Baseline
|
Mesures de résultats secondaires
Mesure des résultats |
Description de la mesure |
Délai |
---|---|---|
Right ventricular systolic pressure (RVSP) in response to exercise
Délai: Baseline
|
Measured by Echocardiogram, between OSA patients and matched healthy controls
|
Baseline
|
Pulmonary systolic pressure (PASP) in response to exercise
Délai: Baseline
|
Measured by Echocardiogram, between OSA patients and matched healthy controls
|
Baseline
|
Right ventricular outflow track (RVOT) peak velocity in response to exercise
Délai: Baseline
|
Measured by Echocardiogram, between OSA patients and matched healthy controls
|
Baseline
|
Velocity time interval (VTI) in response to exercise
Délai: Baseline
|
Measured by Echocardiogram, between OSA patients and matched healthy controls
|
Baseline
|
Pulmonary artery acceleration time in response to exercise
Délai: Baseline
|
Measured by Echocardiogram, between OSA patients and matched healthy controls
|
Baseline
|
Systolic peak tricuspid myocardial annular velocity
Délai: Baseline
|
Measured by Echocardiogram, between OSA patients and matched healthy controls
|
Baseline
|
Diastolic peak tricuspid myocardial annular velocity
Délai: Baseline
|
Measured by Echocardiogram, between OSA patients and matched healthy controls
|
Baseline
|
Peak tricuspid myocardial annular velocity during isovolumic contraction
Délai: Baseline
|
Measured by Echocardiogram, between OSA patients and matched healthy controls
|
Baseline
|
Peak tricuspid myocardial annular velocity during isovolumic relaxation
Délai: Baseline
|
Measured by Echocardiogram, between OSA patients and matched healthy controls
|
Baseline
|
Right ventricular (RV) wall stress
Délai: Baseline
|
Measured by Echocardiogram, between OSA patients and matched healthy controls
|
Baseline
|
3-D right ventricular ejection fraction (3D-RVEF)
Délai: Baseline
|
Measured by Echocardiogram, between OSA patients and matched healthy controls
|
Baseline
|
Systolic peak right ventricular (RV) strain
Délai: Baseline
|
Measured by Echocardiogram, between OSA patients and matched healthy controls
|
Baseline
|
Early diastolic peak right ventricular (RV) strain
Délai: Baseline
|
Measured by Echocardiogram, between OSA patients and matched healthy controls
|
Baseline
|
Late diastolic peak right ventricular (RV) strain
Délai: Baseline
|
Measured by Echocardiogram, between OSA patients and matched healthy controls
|
Baseline
|
Collaborateurs et enquêteurs
Parrainer
Dates d'enregistrement des études
Dates principales de l'étude
Début de l'étude
Achèvement primaire (Réel)
Achèvement de l'étude (Réel)
Dates d'inscription aux études
Première soumission
Première soumission répondant aux critères de contrôle qualité
Première publication (Estimation)
Mises à jour des dossiers d'étude
Dernière mise à jour publiée (Réel)
Dernière mise à jour soumise répondant aux critères de contrôle qualité
Dernière vérification
Plus d'information
Termes liés à cette étude
Termes MeSH pertinents supplémentaires
Autres numéros d'identification d'étude
- UCSD150468
Ces informations ont été extraites directement du site Web clinicaltrials.gov sans aucune modification. Si vous avez des demandes de modification, de suppression ou de mise à jour des détails de votre étude, veuillez contacter register@clinicaltrials.gov. Dès qu'un changement est mis en œuvre sur clinicaltrials.gov, il sera également mis à jour automatiquement sur notre site Web .
Essais cliniques sur Apnée obstructive du sommeil
-
Shree Birendra HospitalBP Koirala Institute of Health SciencesComplétéIctère obstructif | Corrélation radiologique de l'ictère obstructifNépal
-
University Hospital, Strasbourg, FranceInconnuePathologie respiratoire | Syndrome obstructifFrance
-
University of Sao Paulo General HospitalInconnueSyndrome obstructif des voies urinaires inférieuresBrésil
-
Kartal Kosuyolu Yuksek Ihtisas Education and Research...InconnueThrombus obstructifTurquie
-
Sohag UniversityRecrutementIctère calculaire obstructifEgypte
-
University Hospital, Strasbourg, FranceComplétéMégauretère obstructif congénitalFrance
-
Turkish Ministry of Health Izmir Teaching HospitalComplétéPatients atteints d'ictère obstructifTurquie
-
Pearl Therapeutics, Inc.ComplétéTrouble pulmonaire obstructif chroniqueÉtats-Unis, Canada, Allemagne, Hongrie, Corée, République de, Pologne, Fédération Russe, Tchéquie
-
Pearl Therapeutics, Inc.ComplétéTrouble pulmonaire obstructif chroniqueÉtats-Unis, L'Autriche, Belgique, Canada, Danemark, Allemagne, Italie, Espagne, Suède, Royaume-Uni, Pérou, Brésil, Afrique du Sud, Argentine, Fédération Russe, Mexique, Porto Rico, Chili, Norvège
-
RWTH Aachen UniversityComplétéSyndrome coronarien aigu | Syndrome pulmonaire obstructif chroniqueAllemagne