A new review argues that conditions such as hypertension, obesity, and chronic obstructive pulmonary disease may contribute to the causation of obstructive sleep apnea, not just the other way around.
Obstructive sleep apnea (OSA) has long been considered a risk factor for a host of metabolic, cardiovascular, and pulmonary diseases, but a new report suggests the risk relationship between OSA and many common comorbidities may actually be bidirectional.
For instance, Gleeson and McNicholas note that hypertension is common in patients with OSA, and a significant amount of medical literature suggests the presence of OSA increases a patient’s risk of hypertension. However, they said some evidence suggests the reverse could be true, too.
“Data from animal and small human studies suggest fluctuations in BP [blood pressure] can influence upper airway tone by demonstrating inhibitory changes on electromyogram (EMG),” they wrote. “This suggests that reduction in BP may improve airflow and reduce OSA severity.”
OSA is also considered a risk factor for heart failure, with evidence suggesting that patients with untreated moderate or severe OSA face double the risk of fatal heart-failure events.
However, one study found more than half (53%) of patients with stable heart failure also have OSA, and the severity of the heart failure correlated with the severity of the patient’s OSA. Hashing out causality can be difficult, but they noted that rates of sleep-disordered breathing (SDB) are higher in patients with heart failure than in those without.
“A different clinical phenotype of OSA is common in patients with HF[heart failure], with many having lower [body mass index], which supports the view that HF may predispose to, or exacerbate SDB, in the absence of other shared risk factors such as obesity,” they wrote.
Turning toward chronic obstructive pulmonary disease (COPD), the authors said most of the existing studies looking at COPD and OSA have focused on the premise that the former contributes to the latter. However, there is limited research suggesting COPD is more common in patients with OSA, possibly due to airway inflammation caused by the sleep disorder.
Perhaps the most commonly discussed comorbidities of OSA is obesity. Previous reports have documented that obesity can increase a person’s risk of OSA, in part by contributing to oropharyngeal narrowing. However, Gleeson and McNicholas noted that the lifestyle effects of OSA, such as a reduced activity level and a tendency to snack to boost energy levels, might contribute to obesity. They added that some patients gain weight after starting therapy with continuous positive airway pressure (CPAP) devices.
“Overall, the relationship between obesity and OSA is synergistic in terms of cardiometabolic risk with a variety of potential intermediate mechanisms including inflammation, endothelial dysfunction, and insulin resistance being amplified by the concurrence of both disorders,” they noted.
The investigators said fluid retention, which can be associated with heart failure, renal dysfunction, and COPD, appears to be one of the major ways comorbidities can predispose patients to OSA.
The authors concluded that more research into potential bidirectional relationships with OSA is warranted. In the meantime, they said physicians treating patients with common OSA comorbidities should be proactive in screening patients for OSA.
“•Clinicians involved in the care of patients with metabolic, cardiovascular, renal and neuropsychiatric disorders should be alert to the possibility that many of these disorders may predispose to OSA,” they wrote.