Heavy NFL players are at increased risk of Death

"The heaviest athletes are more than twice as likely to die before their 50th birthday than their teammates, according to a Scripps Howard News Service study of 3,850 professional-football players who have died in the last century."

http://www.sleepdt.com/heavy-nfl-players-twice-as-likely-to-die-before-50/

Many of these athletes likely had untreated or inadequately treated obstructive sleep apnea (OSA). The heavier NFL players tend to have large necks. Increased neck size (greater than 16 inches in men) is a risk factor for OSA, whether the increased neck size is due to fat or muscle. Obstructive sleep apnea increases the risk of various types of heart disease, including coronary artery disease, heart attack, and congestive heart failure.

An earlier 1994 study found that "offensive and defensive linemen had a 52 percent greater risk of dying from heart disease than the general population."

Sleep and coronary artery calcification

Several medical bloggers have posted about a recent study in which increased sleep time was associated with a decreased incidence of coronary artery disease (as measured by coronary artery calcification).

The problem with these observational studies looking at sleep duration and mortality/morbidity is that they don't distinguish between 1) voluntary sleep deprivation, 2) primary insomnia, and 3) insomnia secondary to medical/sleep disorders.

How is a doctor to use the data from this study???
I doubt writing a prescription for a sleeping pill would improve someone's coronary artery calcification score. However, advising someone with voluntary sleep deprivation (due to work pressures, etc) to extend their sleep hours might (if they take your advice)- I base this conclusion on prior studies which demonstrated that voluntary sleep restriction does lead to adverse metabolic consequences. And of course, treating any obstructive sleep apnea present is important, especially in patients with pre-existing coronary artery disease, atrial fibrillation, or congestive heart failure.

More from Baltimore

Earlier this week preliminary data from the Sleep Heart Health Study was presented. It appears that in patients without significant preexisting cardiovascular disease, moderate to severe osa (apnea-hypopnea index of greater than 30 with events requiring a 4% desat) over a 10 year period led to only modest increases in the risk of incident coronary artery disease in men younger than 70 (about 1.35x risk), and no to minimal increased risk in older men and in women. The stroke risk however was significantly elevated in men, but not in women with an ahi of greater than 30. Sleepiness appeared to increase the risk of the development of coronary artery disease and stroke.

The implications of this large (over 6000 subjects) prospective cohort study is that osa may not increase the risk of developing cardiovascular disease (angina, coronary artery disease, congestive heart failure) as much as previously thought, though the risk of developing ischemic stroke is increased in younger men (about 2.7x).
Patients without significant cardiovascular disease should be treated if symptomatic (significant sleepiness). This study does not change the need to aggresively treat osa in patients with preexisting cardiovascular disease.

sleep apnea and cardiovascuar disease

The evidence linking obstructive sleep apnea to cardiovascular disease continues to grow. Obstructive sleep apnea (OSA) is a thought to be a risk factor for the development of hypertension, stroke, coronary artery disease, and congestive heart failure. The evidence is strongest for hypertension. A recent study adds to the evidence linking OSA to stroke:

But the real question, Dr. Mohsenin said, is whether there is an independent association between sleep apnea and stroke, and a recent study on which he was an author shows that there is indeed such an association.
In the observational cohort study of 697 patients with obstructive sleep apnea and 325 controls (mean apnea-hypopnea index of 35 vs. 2 in the patients and controls, respectively), obstructive sleep apnea was found to have a statistically significant association with stroke or death (hazard ratio of 1.91) after adjustment for numerous factors, including age, sex, race, smoking status, alcohol consumption, body mass index, diabetes, hyperlipidemia, atrial fibrillation, and hypertension.
A trend analysis also showed a significant dose-response relationship between sleep apnea severity at baseline and development of a composite end point of stroke or death from any cause (N. Engl. J. Med. 2005;353:2034–41).
While randomized controlled trials are needed to firmly establish a causal link between sleep apnea and stroke—to “put the last nail in the coffin and say, ‘ok, sleep apnea is indeed a cause of stroke in a high-risk patient population,’” as Dr. Mohsenin put it, the findings increasingly suggest this is the case. Also, sleep apnea occurs as commonly in transient ischemic attack as it does in stroke, further underscoring the need for sleep apnea treatment in affected patients, he noted.
Additionally, a number of studies have shown that sleep apnea is associated with worse functional outcomes in stroke patients, Dr. Mohsenin said.
Patients with stroke who have sleep apnea have been shown to have more delirium, depression, impaired functional capacity, longer rehabilitation time, and longer hospitalization, he said.
“Sleep apnea does affect the outcome of stroke,” he said, noting that in some studies these effects lasted out to 12 months.
Patients who have had a stroke should be evaluated for sleep disordered breathing, he advised.

That the treatment of OSA improves cardiovascular outcomes is an unproven assumption. We know that in sleep apnea patients, CPAP can improve cardiac functioning (ejection fraction) and reduce blood pressure. However, it has not been proven that CPAP improves mortality or decreases the rate of myocardial infarction. A randomized controlled trial looking at this question would be difficult to carry out.