Obstructive sleep apnea (OSA) is the most common type of sleep apnea wherein the affected person experiences brief breathing pauses during sleep due to an obstructed airway. The partial or complete blockage of the airway is caused by the relaxation of the throat muscles, allowing the tongue and the neck fatty tissues to fall and press on the back of the throat. With oxygen’s entry restricted, the blood oxygen levels go down which then signals the brain to partly rouse the body from sleep and force it to breathe. This is often followed by loud snorting, gasping, or choking as air forcibly enters, eliminating the airway obstruction. This could happen multiple times in an hour’s sleep depending on the severity of the disease rendering the patient unable to rest well. People with severe obstructive sleep apnea experience excessive daytime sleepiness and have trouble concentrating during the day due to headaches.
According to a global surveillance study by the World Health Organization (WHO), an estimated 100 million people worldwide suffer from obstructive sleep apnea.
Risk Factors, Diagnosis, and Treatment
Obesity is the number one risk factor for developing obstructive sleep apnea. This is because obese or overweight individuals have more fatty tissues in the neck area that can fall and press on the back of the throat during sleep. While obstructive sleep apnea is prevalent among people with excess weight, it can also affect those who weigh within normal limits. Aging can also contribute in brief breathing pauses during sleep as muscles lose their structural integrity with age. With weak throat muscles, the surrounding structures are more likely to collapse into the airway causing a blockage. Other risk factors include a strong family history of the disease, enlarged tonsils and adenoids, frequent alcohol consumption, and smoking.
Obstructive sleep apnea is usually diagnosed through a polysomnography or sleep study where the patient is hooked up to a series of medical equipment that monitors the heart, lung, and brain activity, breathing patterns, extremity movements, and blood oxygen levels during sleep. The study is done all night. In some cases, split-night sleep studies are conducted wherein the patient is monitored for the first half of the night. When diagnosed with OSA, the second half of the test continues with the patient being treated with continuous positive airway pressure (CPAP).
Continuous positive airway pressure (CPAP) is the most widely used method of treating obstructive sleep apnea. This breathing device delivers greater air pressure than that of room air through a mask worn over the nose, preventing upper respiratory pathway blockage. While it is the most recommended treatment for obstructive sleep apnea, some patients find wearing the CPAP mask uncomfortable and sometimes end up not using the device at all. Other breathing devices are also available for OSA treatment like the bilevel positive airway pressure (BiPAP) and expiratory positive airway pressure (EPAP). In some cases, oral appliances are used to keep the airway open during sleep.
Surgery is often the last resort when conservative breathing treatments and oral appliances fail. The patient could opt for either having the tonsils removed, moving the jaw forward, getting implants into the soft palate, or surgically creating a new airway through an incision in the neck where a plastic tube is placed.
OSA and Cardiovascular Disease: An Observational Association
According to data by the National Commission on Sleep Disorders Research, an estimate of 38,000 cardiovascular deaths each year can be attributed to OSA. Also, higher risks were estimated for heart failure by 140%, stroke by 60%, and coronary heart disease by 30%. However, there is not enough evidence to support the association due to it being entirely observational. In two independent studies, investigators performed a tracheostomy in sleep apnea patients to reduce comorbid conditions. In these two investigations, there is an observed disappearance of atrial flutter (the severe ones), as well as the decrease in systemic blood pressure postoperatively. Despite these amazing results, critics still point out that present data is still insufficient to rule out confounding factors.
A number of mechanisms have been proposed to explain the link between obstructive sleep apnea and cardiovascular disease. One of them is the causation between cardiovascular diseases and the intermittent hypercapnic hypoxemia and recurrent arousal from sleep that characterize obstructive sleep apnea. Another proposed mechanism is the presence of increased sympathetic nervous system activity in patients with obstructive sleep apnea with indications for impaired glucose homeostasis, vascular inflammation, and oxidative stress. All the physiological events mentioned above are some of the scientifically proven contributors to the development of certain cardiovascular diseases like coronary artery disease (CAD) and stroke.
Many clinical cohort studies had shown that obstructive sleep apnea patients receiving CPAP for treatment demonstrated decreased blood pressure as compared to those receiving no treatment. While this can be safely assumed to mean decreased risk of myocardial infarctions and strokes, randomized clinical trials (RCTs) are yet to cement the interplay between obstructive sleep apnea and cardiovascular diseases.
Research Efforts at Proving the OSA-Cardiovascular Disease Interaction
A number of studies had already been conducted during the past few years to provide sufficient evidence that OSA may be a risk factor for developing certain cardiovascular diseases. An example of these studies is steered by a group of researchers back in July 2015 wherein they related the presence and severity of obstructive sleep apnea to increased QT prolongation corrected for heart rate (QTc), an important biomarker for sudden cardiac death (SCD). The subjects of this study were OSA patients with congenital long QT syndrome (LQTS). The results of the study revealed that patients with OSA and LQTS demonstrated increased respiratory disturbance index, apnea-hypopnea index (AHI), and arousal index as compared to those without OSA and LQTS. QTc was also significantly increased in OSA and LQTS patients both during sleep and while awake.
Another study in November 2015 by a different research team exhibited association between obstructive sleep apnea and cardioembolic (CE) strokes. Among 53 subjects, CE strokes were 72% more common in OSA patients than those without OSA with majority of the CE strokes occurring in patients with moderate to severe obstructive sleep apnea. Atrial fibrillation was also documented to be prevalent in OSA patients by 59% as compared to the control group.
Still a Long Way to Go
While there are already many studies that yielded significant and positive results for proving the association between obstructive sleep apnea and cardiovascular diseases, there are still too many confounding factors to fully declare an interaction from the clinical standpoint. This is because obstructive sleep apnea and many cardiovascular diseases share the same risk factors like obesity and age. Moreover, critics also point out that people with obstructive sleep apnea are generally unhealthy.
Research still has a long way to go in proving that OSA treatments can reduce the risk for developing cardiovascular disease. As of late, what we know is that the physiological events triggered by decreased blood oxygen levels in people with obstructive sleep apnea do not necessarily reflect cardiovascular impairment. Nonetheless, it is still too early to conclude that the bodily responses that characterize obstructive sleep apnea are not enough at all to cause debilitating heart and vascular conditions. After all, everything in our body is connected and the fall of a single part could lead to the fall of another. For now, all we can do is let science run its course of discovery.