Obstructive Sleep Apnea: From Intermittent Hypoxia to Cardiovascular Complications via Blood Platelets

Abstract

Obstructive sleep apnea is a chronic condition characterized by recurrent episodes of apneas or hypopneas during sleep leading to intermittent hypoxemia and arousals. The prevalence of the sleep disordered breathing is estimated that almost 50% of men and 24% of women suffer from moderate to severe form of the disorder. Snoring, collapse of upper airways and intermittent hypoxia are main causes of smoldering systemic inflammation in patients suffering from obstructive sleep apnea. The systematic inflammation is considered one of the key mechanisms leading to significant cardiovascular complications. Blood platelets, formerly not even recognized as cells, are currently gaining attention as crucial players in the immune continuum. Platelet surface is endowed with receptors characteristic for cells classically belonging to the immune system, which enables them to recognize pathogens, immune complexes, and interact in a homo- and heterotypic aggregates. Platelets participate in the process of transcellular production of bioactive lipids by delivering both specific enzymes and substrate molecules. Despite their lack of nucleus, platelets synthetize proteins in a stimuli-dependent manner. Atherosclerosis and consequent cardiovascular complications result from disruption in homeostasis of both of the platelet roles: blood coagulation and inflammatory processes modulation. Platelet parameters, routinely evaluated as a part of complete blood count test, were proposed as markers of cardiovascular comorbidity in patients with obstructive sleep apnea. Platelets were found to be excessively activated in this group of patients, especially in obese subjects. Persistent activation results in enhanced spontaneous aggregability and change in cytokine production. Platelet-lymphocyte ratio was suggested as an independent marker for cardiovascular disease in obstructive sleep apnea syndrome and continuous positive air pressure therapy was found to have an impact on platelet parameters and phenotype. In this literature review we summarize the current knowledge on the subject of platelets involvement in obstructive sleep apnea syndrome and consider the possible pathways in which they contribute to cardiovascular comorbidity.

Association between excessive daytime sleepiness, REM phenotype and severity of obstructive sleep apnea

“…Obstructive sleep apnea syndrome (OSA) is characterized by recurrent episodes of apneas or hypopneas during sleep leading to intermittent hypoxemia and arousals. The severity of OSA is by convention assessed by apneahypopnea index (AHI) 1 . A few distinct phenotypes of OSA have been recognized with the main division lying between patients with sleep disordered breathing (SDB) independent of body position and sleep stage (usually obese with severe disease) and those with SDB dependent on supine position and/or REM sleep (usually non-obese, with mild to moderate disease) 2,3 .…”

Comparison of erythrocyte distribution width, mean platelet volume and platelet distribution width in patients with obstructive sleep apnea syndrome

“…Inflammation plays a key role in endothelial dysfunction and atherosclerotic vascular disease. Platelets are related to inflammation, thrombosis and atherogenesis [9,10] in the following way: Active platelets stimulate leukocyte activation by forming aggregates through physical interaction with leukocytes. These platelet-leukocyte complexes are considered as markers in platelet activating conditions such as stable coronary artery disease, unstable atherosclerosis, and vascular disease [11].…”

Neutrophil-to-lymphocyte ratio (NLR) and Platelets-to-lymphocyte (PLR) Ratio in Patients with Exacerbation of Bronchiectasis

“…Platelets have an important role in the immune system due to the surface receptors that enable them to recognize pathogens and immune complexes. Activated and adherent platelets release cytokines, including chemokines that stimulates inflammatory recruitment of immune cells [20,21]. The aim of this study is to evaluate the utility of NLR and PLR as inflammatory markers in patients with exacerbation of bronchiectasis compared with classical markers such as C-reactive protein, erytrocite sedimentation rate and white blood cells.…”