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Is obstructive sleep apnoea an innocent bystander in the pathophysiology of arterial stiffening?
  1. Craig L Phillips1,2,3,
  2. Luciano F Drager4,5
  1. 1CIRUS, Centre for Sleep and Chronobiology, Woolcock Institute of Medical Research, University of Sydney, Sydney, New South Wales, Australia
  2. 2Department of Respiratory and Sleep Medicine, Royal North Shore Hospital, St Leonards, New South Wales, Australia
  3. 3Sydney Medical School, University of Sydney, Sydney, New South Wales, Australia
  4. 4Hypertension Unit, Heart Institute (InCor), University of Sao Paulo Medical School, Sao Paulo, Brazil
  5. 5Hypertension Unit, Renal Division, University of Sao Paulo Medical School, Sao Paulo, Brazil
  1. Correspondence to Associate Professor Craig L Phillips, Woolcock Institute of Medical Research, PO Box M77, Missenden Road, NSW 2050, Australia; craig.phillips{at}sydney.edu.au

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Arterial compliance is an important mechanical property of the arterial tree that is crucial for the maintenance of vascular homeostasis and cardiovascular health. There are a number of factors that variably decrease arterial compliance and therefore increase arterial stiffness in different arterial segments. For example, arteries become less distensible and therefore stiffer as blood pressure (BP) increases, and this effect occurs throughout the arterial tree. On the other hand, an increase in the collagen–elastin ratio in the arterial wall, such as occurs with ageing, increases arterial stiffness predominantly in large elastic arteries like the aorta. In contrast, an increase in the quantity and tone of arterial smooth muscle mainly increases arterial stiffness in the smaller conduit arteries such as the femoral arteries.1 2

Overall, a loss of arterial compliance gives rise to increased arterial stiffness and poorer maintenance of vascular homeostasis, and this is likely to be a key driver of cardiovascular disease (CVD). The process of arterial stiffening occurs in ageing populations and in conditions that are strongly associated with CVD including chronic kidney disease,3 type II diabetes and various components of the metabolic syndrome.4 This has led to the development of many methods for quantifying arterial stiffness,5 as a means of improving CVD risk stratification in populations with comorbid disease. However, in order to standardise the assessment of risk, the American Heart Association Council for high blood pressure research recommends the non-invasive measurement of the carotid-femoral pulse wave velocity as the preferred method.6 Studies have established that an increase in pulse wave velocity (PWV) of 1 m/s increases CVD events …

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