ESSEN, GERMANY--Elevated levels of circulating fibrinogen—perhaps a response to insufficient blood hemoglobin oxygenation—may help explain why individuals with obstructive sleep apnea (OSA) are at high risk of stroke.[1]

Although previous research has suggested a link between OSA and vascular disease, the pathophysiological mechanisms that underlie this relationship are not well understood, and few studies have used objective measurements of sleep disturbance. Thomas E. Wessendorf, MD, et al in the Department of Respiratory Medicine at the University of Essen, in Germany, investigated the relationship between OSA, which was evaluated using complete overnight polysomnography, and circulating fibrinogen levels in patients with recent ischemic stroke.

The final study population consisted of 113 patients (82 men; average age, 58). The median time between stroke and fibrinogen assay was 30 days, and between stroke and polysomnography was 37 days.

Stroke patients with OSA had significantly higher plasma fibrinogen concentrations than did those without OSA (mean, 372 mg/dL vs 318 mg/dL, respectively). Plasma fibrinogen concentrations correlated moderately but significantly with the average number of respiratory events per hour of sleep and with the duration of longest apnea. When patients with stroke of suspected cardiac origin were excluded from the analysis, the correlation between respiratory events and fibrinogen levels increased slightly, although the correlation between longest apnea duration and fibrinogen levels was no longer statistically significant.

Plasma fibrinogen concentrations were inversely correlated with the average minimum oxygen saturation measured during respiratory events and the minimum oxygen saturation recorded during sleep; they were directly correlated with average oxygen desaturation. In a multiple regression analysis, minimum average oxygen saturation, but not respiratory disturbance index, was found to be an independent predictor of fibrinogen concentration.

These results of his study have two important implications, Dr. Wessendorf told PULMONARY REVIEWS. "First, sleep apnea detected after stroke, even if asymptomatic in terms of sleepiness, may mean something—higher morbidity and mortality, for instance. Second, epidemiological studies on vascular risk factors, including fibrinogen, should take sleep apnea into account as a possible cofactor," he added.

In an accompanying editorial that he co-authored, Virend K. Somers, MD, PhD, suggested that sleep apnea should be viewed as a potential risk factor for stroke.[2] Dr. Somers, a Professor of Medicine in the Divisions of Hypertension and Cardiovascular Diseases at the Mayo Clinic in Rochester, Minnesota, noted that fibrinogen is likely to be only one of several important pathophysiological mechanisms. He told PULMONARY REVIEWS, "Fibrinogen is one component of a bigger question: What are the abnormalities in blood and cardiovascular homeostasis that link sleep apnea to cardiovascular disease generally and stroke in particular? The challenge lies in defining these abnormalities and determining if they can be attenuated with appropriate therapy."

--Mark Bowes

References
1. Wessendorf TE, Thilmann AF, Wang Y-M, et al. Fibrinogen levels and obstructive sleep apnea in ischemic stroke. Am J Respir Crit Care Med. 2000;162:2039-2042.

2. Shamsuzzaman ASM, Somers VK. Fibrinogen, stroke, and obstructive sleep apnea. An evolving paradigm of cardiovascular risk [editorial]. Am J Respir Crit Care Med. 2000;162:2018-2020.

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