Abstract

Patients with obstructive sleep apnoea are at increased risk of atherosclerotic morbidity and mortality. Abnormalities in lipid metabolism that occur in response to chronic intermittent hypoxia in patients with sleep-disordered breathing may increase the cardiovascular risk in an already susceptible population. Atherogenic lipoprotein phenotype and small, dense LDL have an independent predictive role for future cardio- and cerebro-vascular events in patients with the metabolic syndrome. Therefore, testing the hypothesis that therapy of obstructive sleep apnoea may reduce atherogenic lipoprotein phenotype might have significant clinical implications. We suggest that abolition of obstructive sleep apnoea by continuous positive airway pressure results in reductions in circulatory levels of small, dense LDL by improvements in oxygen saturation, reductions in oxidative stress, improvements in insulin sensitivity, and reductions in triglyceride biosynthesis. Testing the proposed hypothesis may contribute to improvements in clinical management of patients with obstructive sleep apnoea by early recognition of atherogenic dyslipidaemia followed by both, vigorous treatment of the underlying sleep-disordered breathing by noninvasive ventilation and targeted therapeutic modulation of hypertriglyceridaemia, low HDL-cholesterol and increased levels of small, dense LDL. Implementing this strategy to patients with obstructive sleep apnoea may potentially contribute to substantial reduction of their high cardiovascular risk.

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