Daytime Sleepiness as a Stroke and Cardiac Risk Factor
Brief Report
Daytime Sleepiness as a Stroke and Cardiac Risk Factor
By Alan Z. Segal, MD, Associate Professor of Clinical Neurology, Weill Cornell Medical College, New York, NY. Dr. Segal reports no financial relationships relevant to this field of study.
This article originally appeared in the January issue of Neurology Alert. At that time it was peer reviewed by M. Flint Beal, MD, Anne Parrish Titzel Professor, Department of Neurology and Neuroscience, Weill Cornell Medical Center, New York, NY. Dr. Beal reports no financial relationships relevant to this field of study.
Synopsis: Excessive daytime sleepiness appears to be an important risk factor for stroke. It is unknown whether this is related to obstructive sleep apnea or other mechanisms.
Source: Blechier M, et al. Excessive daytime sleepiness and vascular events. The Three City Study. Ann Neurol Online Oct. 31, 2011. DOI: 10.1002/ana.22656.
Excessive daytime sleepiness (EDS) is a common complaint in clinical practice. Not only does it have a direct impact on quality of life and productivity, it may have direct effects on morbidity and mortality. EDS has been shown to increase the risk of stroke and to a lesser degree coronary heart disease (CHD) in middle-aged populations and in the elderly, and it has been shown to impact cardiovascular risk, particularly in women. EDS may be a product of insufficient sleep duration or an underlying sleep disorder, most notably concomitant obstructive sleep apnea (OSA). Sleep deprivation has been shown to increase sympathetic drive, with elevated levels of catecholamines, and also results in endothelial cell dysfunction and systemic inflammation.
In the current report, from the French Three City Study (Bordeaux, Dijon, and Monpelier), 9294 elderly patients (age > 65) from the community were selected and given a face-to-face questionnaire. EDS was rated by subjects as occurring never, rarely, regularly, or frequently. Subjects also rated their sleep quality and the presence or absence of insomnia. Sleep duration was not reported. Outcomes at 2 years included CHD (angina, myocardial infarction, or cardiac related death) and stroke (classified as ischemic, hemorrhagic, or unspecified).
Results of the study showed a nearly two-fold (hazard ratio [HR] 1.92) increased risk of a combined endpoint of CHD and stroke. For stroke alone, there was a HR of 2.24, which was statistically significant, and for CHD, the HR was 1.70, which did not reach significance. Of note, the relationship between EDS and stroke applied roughly equally to ischemic compared with hemorrhagic strokes.
There were no data in this study regarding OSA, but there was no interaction between the presence of frequent or regular snoring or BMI and the vascular endpoints. As the authors acknowledge, obesity and snoring are less reliable predictors of OSA in the elderly than in younger people. Also, the relationship between EDS and vascular events was not modified by the presence or absence of insomnia, cognitive dysfunction, use of hypnotics, or depression with early morning awakening. In the absence of data on sleep itself, these variables might serve as surrogate markers to quantify sleep quality and duration.
Importantly, hypertension was a major modifying factor. When the population was split into subjects with or without hypertension at baseline, a relationship between EDS and vascular events was only demonstrated in the hypertensive group. As the authors note, hypertension is, in part, the result of sympathetic hyperactivity in EDS subjects and is such a powerful vascular risk factor on its own that it would likely mask any independent relationship between EDS and vascular events.
Among the 5262 participants who underwent B-mode ultrasound of the carotid arteries, those with EDS had higher carotid plaque burden. Adjustment for this subclinical atherosclerosis, however, did not modify the relationship between EDS and vascular events. Of note, obstructive sleep apnea is known to be associated with increased carotid plaque burdens as well.
Commentary
Because EDS was based solely on patient reports, there may be some patients who are misclassified, especially since more objective measures, such as the Epworth Sleepiness Scale, were not performed. As the authors note, subjects may not have been able to differentiate between sleepiness and fatigue.
A clear limitation of this study is the absence of data on sleep duration and OSA. Because OSA is a potent risk factor for hypertension as well as vascular events and EDS, it may be an important unifying diagnosis in a significant subset of these subjects.
It is not clear from this study or from previous reports why EDS appears to be a more potent risk factor for stroke than CHD. This may relate to the extremely powerful relationship between hypertension and stroke and could have important therapeutic implications. While EDS is multifactorial, requiring a complex set of behavioral and pharmacological interventions, the diurnal hypertension that results from EDS is an extremely modifiable stroke risk factor.
Excessive daytime sleepiness appears to be an important risk factor for stroke. It is unknown whether this is related to obstructive sleep apnea or other mechanisms.Subscribe Now for Access
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