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The vascular micromilieu in obstructive sleep apnoea

Obstructive sleep apnoea (OSA) is increasingly recognised as an important cardiovascular risk factor. In particular, OSA has been shown to increase the risk of diurnal arterial hypertension in a dose-dependent manner, and is now considered as one of the most common causes of secondary arterial hypertension 1, 2. Furthermore, OSA increases the likelihood of developing vaso-occlusive disease, notably myocardial infarction and stroke, although this association seems to be weaker than that observed for arterial hypertension 3. Of note, the epidemiological studies demonstrating a genuine relationship between OSA and cardiovascular disorders have been controlled with respect to confounding factors such as age, body weight and metabolic disease.

How does one explain the causal link between OSA and cardiovascular disease? The repetitive collapse of the upper airway during sleep generates a unique pattern of hypoxia, with frequent cycles of hypoxia and re-oxygenation during the night, and a constant normoxia while awake. Accumulating evidence suggests that this chronic intermittent hypoxia causes a specific disturbance in the vascular micromilieu, with vasoconstrictive, pro-inflammatory and pro-coagulant forces predominating. Finally, the disturbance in the vascular micromilieu leads to endothelial dysfunction in these patients 4. This reduction in endothelial-dependent vasorelaxation has been established as a pathogenic factor in both systemic arterial hypertension and atherosclerosis. Treatment of OSA by continuous positive airway pressure (CPAP) ventilation not only eliminates apnoeas and nocturnal oxygen desaturations, but also exerts cardio-protective effects. …