Apnea: ‘Sleeping Gun’ in Sudden Death?

Post on June 12, 2013 by André Broussard, D.C.

June 12, 2013

Obstructive sleep apnea may place adults at a greater risk for sudden cardiac death, researchers found.

After adjustment for other risk factors, each 10% decrease in the lowest nocturnal oxygen saturation among adults undergoing a first-time polysomnogram for suspected sleep-disordered breathing was associated with a 14% greater risk of sudden cardiac death or resuscitated cardiac arrest (HR 1.14, 95% CI 1.01 to 1.27), according to Virend Somers, MD, PhD, of the Mayo Clinic in Rochester, Minn., and colleagues.

Sleep factors associated with a significantly greater likelihood of remaining free from sudden cardiac death or resuscitated cardiac arrest included an apnea-hypopnea index of less than 20 events per hour (HR 1.60, 95% CI 1.14-2.24), a mean nocturnal oxygen saturation of 93% or higher (HR 2.93, 95% CI 1.98-4.33), and a lowest nocturnal oxygen saturation of 78% or higher (HR 1.81, 95% CI 1.28-2.56), the researchers reported online in the Journal of the American College of Cardiology.

“These findings should encourage ongoing research of the mechanisms of sudden cardiac death in individuals with obstructive sleep apnea, as well as the development of clinical trials of obstructive sleep apnea therapy in select populations at risk for sudden cardiac death,” they wrote.

Erik Altman, MD, of the North Shore-LIJ Health System, said “this study is important because the patients who have sudden cardiac death often have a lack of structural heart disease … that we can [use to] pick them out of a general population and deem them more at risk.”

“Here we have obstructive sleep apnea, which is a risk factor which shows us these patients are far more likely to have experienced sudden cardiac death, whether survived sudden cardiac death or fatal sudden cardiac death,” he said in an interview.

Obstructive sleep apnea has been associated with increased risks of cardiovascular disease and mortality in prior studies, with some findings suggesting a relationship with sudden cardiac death.

“A specific link to sudden cardiac death was suggested by the finding that sudden cardiac death is more likely to occur during usual sleep hours in individuals with obstructive sleep apnea, which is the time when sudden cardiac death is least likely in individuals without [the sleep disorder] and in the general population,” the authors wrote.

They analyzed longitudinal data from 10,701 adults (mean age 53; 68% male) who underwent their first, overnight diagnostic polysomnogram at the Mayo Clinic Sleep Disorders Center from 1987 to 2003 and did not have a history of cardiac arrest. Most were referred for suspected sleep-disordered breathing.

The average apnea-hypopnea index was 31 events per hour, and about three-quarters of the individuals were ultimately diagnosed with obstructive sleep apnea.

During an average follow-up of 5.3 years, 121 patients had a sudden cardiac death and 21 patients had a resuscitated cardiac arrest (either through advanced life support or with a shock from an implantable cardioverter-defibrillator). The annual rate of sudden cardiac death or resuscitated arrest was 0.27%, which is higher than the 0.1% to 0.2% estimated rate seen in the general population.

After multivariate adjustment, the only sleep-related predictor of sudden cardiac death or resuscitated arrest was the lowest nocturnal oxygen saturation. Increasing apnea-hypopnea index and decreasing mean nocturnal oxygen saturation were not significantly related.

Looking at a worsening of those three variables according to various thresholds, however, revealed significant associations with sudden cardiac death or resuscitated cardiac arrest.

As for potential mechanisms, the researchers said that the repetitive oxygen desaturation that occurs in patients with sleep apnea “may cause ventricular ectopy.”

“Hypoxemia, with associated hypercapnia, also activates the chemoreflex, which increases vascular sympathetic nerve activity and serum catecholamines,” they continued. “Tachycardia and surges in blood pressure at the end of apneas result in increased myocardial oxygen demand at a time when oxygen saturation is at its lowest, a situation that may lead to myocardial ischemia and potentially dysrhythmic consequences.”

Mechanisms might also include increases in coagulability during the night among patients with obstructive sleep apnea and cardiac autonomic dysfunction.

The authors acknowledged a number of limitations including a sample that included only Minnesota residents who were referred for a sleep study, potentially hindering generalizability. Other limitations included the retrospective design, and the lack of details on the use of continuous positive airway pressure therapy.

From the American Heart Association:

This research was supported by grants from the NIH.

Somers has served as a consultant for ResMed, Medtronics, and NeuPro; has received support from a gift from the Philips-Respironics Foundation to the Mayo Foundation; and is working on intellectual property related to sleep and heart disease with Mayo Health Solutions. One of the other authos has served as a consultant for Medtronic, Boston Scientific, and St. Jude Medical.

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