Relationship between plasma fibrinogen level and obstructive sleep apnea

Abstract Background Obstructive sleep apnea (OSA), which causes recurring hypoxemia owing to upper airway closure, is one of the most frequent sleep disorders. OSA patients are more prone to suffer cardiovascular disease (CVD) and stroke. One primary mechanism connecting OSA with cardiovascular problems is the prothrombotic state. Our goal in this research is to confirm the relationship between plasma fibrinogen levels and OSA. Results A case–control study involved 20 adults, non-obese participants who had been recently diagnosed with OSA, had never been treated for OSA before, and did not have any other preexisting conditions, and 20 controls underwent measurement of plasma fibrinogen levels following whole night polysomnography. The patient's plasma fibrinogen levels were substantially more significant than the controls' (399.8 ± 54.7 versus 309.8 ± 26.7 mg/dL, respectively), with a p -value of less than 0.001. Plasma fibrinogen levels in moderate and severe OSA (383.6 ± 20.6 mg/dL and 454.4 ± 25.6 mg/dL, respectively) were significantly higher than in controls (309.8 ± 26.7 mg/dL) ( p < 0.001 and p < 0.001) and mild OSA patients (335 ± 27.8 mg/dL) ( p = 0.013 and p < 0.001). Plasma fibrinogen levels were not significantly different between the controls and patients with mild OSA ( p = 0.219). Apnea–hypopnea index, arousal index, and oxygen desaturation index showed positive correlations with plasma fibrinogen ( r = 0.953, 0.888, and 0.894, p = < 0.001, < 0.001, and < 0.001, respectively). The total sleep time, sleep efficiency, N3%, REM%, and lowest oxygen saturation showed negative correlations ( r = − 0.860, − 0.877, − 0.611, − 0.844, and − 0.745, p = < 0.001, < 0.001, < 0.001, and < 0.001, respectively). Conclusion Elevated levels of plasma fibrinogen in individuals with moderate-to-severe OSA may be attributed to sleep apnea and these increased levels could serve as a significant risk factor that establishes a connection between OSA and pathology of the cardiovascular and cerebrovascular systems. These results could significantly affect OSA diagnosis, therapy monitoring, and outcome.