Inflammatory Aspects of Sleep Apnea and Their Cardiovascular Consequences

Abstract

Obstructive sleep apnea (OSA) is a common medical condition that occurs in a considerable percentage of the population. Substantial evidence shows that patients with OSA have an increased incidence of hypertension compared with individuals without OSA, and that OSA is a risk factor for the development of hypertension. It is established that OSA may be implicated in stroke and transient ischemic attacks. OSA is associated with coronary heart disease, heart failure, and cardiac arrhythmias. Pulmonary hypertension may be associated with OSA, especially in patients with pre-existing pulmonary disease. Although the exact cause that links OSA with cardiovascular disease is unknown, there is evidence that OSA is associated with a group of proinflammatory and prothrombotic factors that have been identified as important in the development of atherosclerosis. OSA is associated with increased daytime and nocturnal sympathetic activity. Autonomic abnormalities seen in patients with OSA include increased resting heart rate, decreased R-R interval variability, and increased blood pressure variability. Both atherosclerosis and OSA are associated with endothelial dysfunction, increased C-reactive protein, interleukin 6, fibrinogen, plasminogen activator inhibitor, and reduced fibrinolytic activity. OSA has been associated with enhanced platelet activity and aggregation. Leukocyte adhesion and accumulation on endothelial cells are common in both OSA and atherosclerosis. Clinicians should be aware that OSA may be a risk factor for the development of cardiovascular disease.

Obstructive sleep apnea in patients with central serous chorioretinopathy

“…Respiratory disturbance could compromise choriocapillary perfusion by sympathetic activation, as well as by inflammatory and procoagulant mechanisms [18,19]. Also, OSAS may cause systemic hypertension [10], while CSC too has been found to be associated with hypertension [20,21].…”

Inflammatory cytokines in pediatric obstructive sleep apnea

“…[8][9][10] The most acceptable hypothesis associates occurrence of chronic systemic inflammation with OSA. [11][12] Increase in proinflammatory cytokines (C-reactive protein [CRP], tumor necrosis factor alpha [TNF-a], interleukin 6 [IL -6], and interleukin 10 [IL -10] in adult OSA patients, and high-sensitivity C-reactiveprotein [HS-CRP] in pediatric OSA patients) supports this hypothesis, [13][14][15] with a possible association between the apnea-hypopnea index (AHI) and inflammatory cytokine levels. The inflammatory responses may be reversed after OSA treatment.…”

Biological consequences of oxygen desaturation and respiratory effort in an acute animal model of obstructive sleep apnea (OSA)

“…The current evidence available shows that OSA is associated with systemic inflammation and endothelial dysfunction (2,(5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15), and this has been considered one of the potential mechanisms linking OSA with cardiovascular disease. In most cases, however, the data are partial and sometimes even contradictory.…”