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An update on cardiovascular effects of obstructive sleep apnoea syndrome
  1. Meral Uyar1,
  2. Vedat Davutoglu2
  1. 1Department of Respiratory Medicine, Gaziantep University, Gaziantep, Turkey
  2. 2Department of Cardiology, Gaziantep University, Gaziantep, Turkey
  1. Correspondence to Dr Meral Uyar, Department of Pulmonary Medicine, University of Gaziantep, School of Medicine, Gaziantep 27310, Turkey; meraluyar1{at}


Obstructive sleep apnoea syndrome is an important health problem which may cause or worsen systemic diseases. Chronic intermittent hypoxia during repetitive airflow cessations may cause endothelial dysfunction. Sleep apnoea is also shown to be associated with hypercoagulability which may be due to decreased nitric oxide levels and impaired vasodilatation. Endothelial dysfunction, increased systemic inflammation, sympathetic nervous system activation, increased oxidative stress and dysglycaemia may all contribute to cardiovascular processes such as hypertension, arrhythmia, stroke, heart failure and coronary artery disease in patients with obstructive sleep apnoea. Treatment approaches in patients with obstructive sleep apnoea mainly focus on maintaining upper airway patency either with positive airway pressure devices or upper airway appliances. Strategies involving positive airway pressure therapy are associated with decreased morbidity and mortality. Obstructive sleep apnoea should be suspected as an underlying mechanism in patients with cardiovascular disease and warrants appropriate treatment.

  • endothelium
  • oxidative stress
  • sleep

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