Sleep Disordered Breathing CPAP Sleep Apnea & Health Risks – USA Medical Supply
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Sleep Disordered Breathing CPAP Sleep Apnea & Health Risks

Posted by Richard Spafford on

SDB and cardiovascular disease

Sleep-disordered breathing (SDB) and cardiovascular issues

An abundance of research has focused on the connection between sleep apnea and cardiovascular or heart issues. Some of the key findings about SDB are that it:

  • Causes hypoxia, increased intrathoracic pressure swings due to the attempts to breathe during an apnea, and activation of the sympathetic nervous system—all of which have many negative consequences for the cardiovascular system.1-4
  • Is strongly associated with hypertension, independent of all relevant risk factors.5-8
  • Is present in more than 30% of patients with hypertension.9
  • Occurs in 80% patients with drug resistant hypertension.10
  • Treated with CPAP may result in a clinically significant drop in blood pressure. This drop is sufficient to reduce risk of a coronary heart disease event by 37% and stroke risk by 56%.11,12,13
  • Treatment with CPAP in patients who also have heart failure, improves left ventricular function.15
  • Is common in patients with cardiovascular disease and occurs in 50% atrial fibrillation patients.16
  • Patients have increased levels of inflammatory, oxidative and vascular endothelial effect markers, which are associated with atherogenesis. These markers are improved when the sleep apnea is treated with CPAP.17-20
  • When severe, significantly increases the risk of cardiovascular events. Treatment with CPAP reduces this risk.21,22

SDB and hypertension


People with sleep-disordered breathing (SDB) have an increased risk of developing hypertension, independent of all relevant risk factors.1-4, 7 This risk is related to SDB severity; the more severe the SDB, the greater the risk of developing hypertension.

During healthy sleep, blood pressure decreases, but SDB patients instead tend to experience:

  • Elevated blood pressure during sleep
  • Prolonged cardiovascular stress, which can lead to increased blood pressure also occurring during the day.

SDB is present in more than 30% of patients with hypertension,5 and in around 80% of patients with drug resistant hypertension.6 For this group of patients in particular, treatment with positive airway pressure therapy may be especially important.8


SDB and stroke


The majority of patients who have experienced a stroke and transient ischemic attack (TIA) also have SDB,1  which is sometimes undiagnosed. Stroke patients with SDB also have worse functional outcomes2.

Stroke has the potential to cause SDB, by either affecting:

  • Central mechanisms resulting in central sleep apnea, or
  • Muscle tone resulting in obstructive sleep apnea.

People with SDB may be predisposed to stroke through a number of symptoms they experience. In particular:

  • Repetitive drops in nocturnal blood oxygen levels caused by SDB can result in intermittent hypoxia which has been shown to be associated with systemic inflammation.4
  • Sleep fragmentation from SDB results in hypersympathetic activity.5

Patients with both SDB and stroke usually show poor compliance with post-stroke rehabilitation programs. This is mainly due to the combination of:

  • The deficits caused by the stroke; and
  • The symptoms of SDB (such as excessive daytime sleepiness, fatigue, and impaired cognitive functioning).



  • 01

    Aaronson JA et al. Obstructive sleep apnea is related to impaired cognitive and functional status after stroke. Sleep 2015;38(9):1431–7.

  • 02

    Wessendorf TE et al. Sleep-disordered breathing among patients with first-ever stroke. J Neurol2000;247(1):41–7.

  • 03

    Drager LF, Polotsky VY and Lorenzi-Filho G. Obstructive sleep apnea: an emerging risk factor for atherosclerosis. Chest 2011;140(2):534–42.

  • 04

    Jelic S and Le Jemtel TH. Inflammation, oxidative stress, and the vascular endothelium in obstructive sleep apnea. Trends Cardiovasc Med 2008(7):253–60.

  • 05

    Marin JM et al. Association between treated and untreated obstructive sleep apnea and risk of hypertension. JAMA 2012;307(20):2169–76.

  • 06

    Montesi SB et al. The effect of continuous positive airway pressure treatment on blood pressure: a systematic review and meta-analysis of randomized controlled trials. J Clin Sleep Med2012;8(5):587–96.

  • 07

    Shamsuzzaman AS, Gersh BJ and Somers VK. Obstructive sleep apnea: implications for cardiac and vascular disease. JAMA 2003;290:1906-14.

  • 08

    Lattimore JD, Celermajer DS and Wilcox I. Obstructive sleep apnea and cardiovascular disease. J Am Coll Cardiol 2003;41:1429-37.

  • 09

    Bradley TD and Floras JS. Sleep apnea and heart failure: Part I: obstructive sleep apnea. Circulation2003;107:1671-8.

  • 10

    Peker Y et al. Increased incidence of cardiovascular disease in middle-aged men with obstructive sleep apnea: a 7-year follow-up. Am J Respir Crit Care Med 2002;166:159-165.

  • 11

    Peppard PE et al. Prospective study of the association between sleep-disordered breathing and hypertension. N Engl J Med 2000;342:1378-1384.

  • 12

    Lavie P, Herer P and Hoffstein V. Obstructive sleep apnea syndrome as a risk factor for hypertension: population study. BMJ 2000;320:479-82.

  • 13

    Nieto FJ et al. Association of sleep-disordered breathing, sleep apnea, and hypertension in a large community-based study. JAMA 2000;283:1829-1836.

  • 14

    Bixler EO et al. Association of hypertension and sleep-disordered breathing. Arch Intern Med2000;160:2289-95.

  • 15

    Sjostrom C et al. Prevalence of sleep apnea and snoring in hypertensive men: a population based study. Thorax 2002;57:602-7.

  • 16

    Logan AG et al. High prevalence of unrecognized sleep apnoea in drug-resistant hypertension. J Hypertens 2001;19:2271-7.

  • 17

    Logan AG et al. Refractory hypertension and sleep apnoea: effect of CPAP on blood pressure and baroreflex. Eur Respir J 2003;21:241-7.

  • 18

    Becker HF et al. Effect of nasal continuous positive airway pressure treatment on blood pressure in patients with obstructive sleep apnea. Circulation 2003;107:68-73.

  • 19

    Pepperell JC et al. Ambulatory blood pressure after therapeutic and subtherapeutic nasal continuous positive airway pressure for obstructive sleep apnoea: a randomized parallel trial. Lancet2002;359:204-10.

  • 20

    Shahar E et al. Sleep-disordered breathing and cardiovascular disease: cross-sectional results of the Sleep Heart Health Study. Am J Respir Crit Care Med 2001;163:19-25.

  • 21

    Kaneko Y et al. Cardiovascular effects of continuous positive airway pressure in patients with heart failure and obstructive sleep apnea. N Engl J Med 2003;348:1233-1241.

  • 22

    Gami AS et al. Association of atrial fibrillation and obstructive sleep apnea. Circulation2004;110(4):364-7.

  • 23

    Ip MS et al. Endothelial function in obstructive sleep apnea and response to treatment. Am J Respir Crit Care Med 2004;169:348-53.

  • 24

    Ip MS et al. Circulating nitric oxide is suppressed in obstructive sleep apnea and is reversed by nasal continuous positive airway pressure. Am J Respir Crit Care Med 2000;162:2166–2171.

  • 25

    Shamsuzzaman AS et al. Elevated C-reactive protein in patients with obstructive sleep apnea. Circulation 2002;105:2462-4.

  • 26

    Dyugovskaya L, Lavie P and Lavie L. Increased adhesion molecules expression and production of reactive oxygen species in leukocytes of sleep apnea patients. Am J Respir Crit Care Med2002;165:934-9.

  • 27

    Marin JM et al. Long-term cardiovascular outcomes in men with obstructive sleep apnoea-hypopnoea with or without treatment with continuous positive airway pressure: an observational study. Lancet 2005;365(9464):1046-53.

  • 28

    Doherty LS et al. Long-term effects of nasal continuous positive airway pressure therapy on cardiovascular outcomes in sleep apnea syndrome. Chest 2005;127(6):2076-84.

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