Endothelial Dysfunction and Cardiovascular Risk in Obstructive Sleep Apnea: A Review Article

Abstract

Obstructive sleep apnea (OSA) is a respiratory condition during sleep caused by repeated pauses in breathing due to upper airway obstruction. It is estimated that OSA affects 30% of the population, but only 10% are well diagnosed due to the absence of a well-defined symptomatology and poor screening tools for early diagnosis. OSA is associated to an endothelial dysfunction inducing several biological responses such as hypoxia, hypercapnia and oxidative stress, among others. OSA also triggers respiratory, nervous, metabolic, humoral and immunity system activations that increase the possibility of suffering a cardiovascular (CV) disease. In this review, we expose different studies that show the relationship between OSA and endothelial dysfunction and its association with CV pathologies like hypertension, and we define the most well-known treatments and their limitations. Additionally, we describe the potential future directions in OSA research, and we report clinical features such as endothelial progenitor cell alterations that could act as biomarkers for the development of new diagnostic tools and target therapies.

Keywords: cardiovascular disease; endothelial dysfunction; endothelial progenitor cells; obstructive sleep apnea; oxidative stress.

Figure 1

Comparative diagram between healthy people and OSA patients of the most characteristic physical and cellular process of obstructive sleep apnoea (OSA). (A). The airway inlet is block in OSA patient causing an obstruction which generates a decrease in blood oxygen which activates de nervous system (SN) leading to a micro-awake. (B). Difference in intrathoracic pressure between healthy person and OSA patient due to the obstruction of respiratory airways. (C). The cycle of reoxygenation is altered due to the obstruction, and ends up with a decrease in nitric oxide (NO), increase in oxidative stress and systemic inflammation. (D). The processes in C lead to a dysfunctional endothelium (ED) which can cause an inflammatory response that can produce different cardiac pathologies such as atherosclerosis, hypertension or thrombosis.