Clinical Trial Details
— Status: Enrolling by invitation
Administrative data
| NCT number |
NCT04793334 |
| Other study ID # |
UCSD HRPP 191948 |
| Secondary ID |
|
| Status |
Enrolling by invitation |
| Phase |
|
| First received |
|
| Last updated |
|
| Start date |
March 20, 2021 |
| Est. completion date |
May 31, 2026 |
Study information
| Verified date |
May 2024 |
| Source |
University of California, San Diego |
| Contact |
n/a |
| Is FDA regulated |
No |
| Health authority |
|
| Study type |
Observational
|
Clinical Trial Summary
Obesity is a common risk factor for the development of obstructive sleep apnea. However, not
all subjects with obesity develop obstructive sleep apnea. This study will attempt to
determine the mechanistic drivers between obesity and obstructive sleep apnea.
Description:
Obstructive sleep apnea (OSA) is a highly prevalent disease with major neurocognitive and
cardiovascular sequelae. Obesity is a major risk factor for OSA, but the underlying
mechanisms remain unclear. Given the rising prevalence of obesity and the lack of adequate
therapies for some afflicted patients, further mechanistic work is clearly required.
Bariatric surgery is being done increasingly with compelling outcome data emerging; however,
clinical response to weight loss is highly variable. In some patients, OSA is not present at
baseline, despite morbid obesity, in other patients, OSA resolves following bariatric
surgery, while other patients have persistence of OSA despite weight loss, and still other
patients can experience re-emergence of OSA in long term follow-up studies after bariatric
surgery. OSA can occur due to several major pathophysiological factors including pharyngeal
anatomy, pharyngeal dilator muscle dysfunction, unstable ventilatory control, end- expiratory
lung volume and arousal threshold. As a result considerable complexity exists in the
obesity/OSA relationship, suggesting the need for further research. First, the investigators
will perform a baseline evaluation of pathophysiological traits among obese people prior to
weight loss surgery. Because some people will have OSA and some will not, the investigators
will define the potential mechanisms underlying OSA and potential protective mechanisms among
obese people without OSA (pharyngeal critical closing pressure Pcrit primary outcome).
Second, the investigators will re-evaluate these same individuals from the standpoint of
sleep study and pathophysiological traits six months following bariatric surgery after a
variable degree of weight loss. The investigators anticipate that some OSA patients will have
resolution of OSA whereas others will have persistence of disease. For non-OSA patients
undergoing weight loss, the investigators will have a positive control group which will allow
the investigators to account for non-specific effects of weight loss. This aim will allow the
investigators to test the hypothesis that pharyngeal mechanics is the predominant mechanism
whereby weight loss leads to improvement in OSA. Third, the investigators will perform
magnetic resonance imaging during wakefulness at functional residual capacity, total lung
capacity and residual volume on participants at baseline and 6months following bariatric
surgery. This aim will allow the investigators to perform structure/function assessments in
our participants, to define the impact of weight loss on pharyngeal anatomy, and to quantify
the lung volume dependence of the upper airway before and after weight loss. The acquired
data will also be used for computational modeling including dynamic assessment of pharyngeal
function during tidal breathing. As a result of the proposed research, the investigators are
confident that the investigators will gain major insights into the as yet unanswered question
"why does obesity (sometimes) cause sleep apnea". This research will have major therapeutic
implications as it will allow the investigators to individualize therapy for afflicted
patients.
