Limits...
Obstructive sleep apnea and vascular disease.

Lanfranchi P, Somers VK - Respir. Res. (2001)

Bottom Line: This relationship may be independent of co-morbidity, such as obesity.Untreated OSA may possibly contribute to the initiation and/or progression of pathophysiologic mechanisms involved in hypertension, heart failure, cardiac ischemia and stroke.This brief commentary will examine the evidence and mechanisms linking OSA to vascular disease.

View Article: PubMed Central - HTML - PubMed

Affiliation: Mayo Clinic, Rochester, Minnesota 55905, USA.

ABSTRACT
There is emerging evidence linking obstructive sleep apnea (OSA) to vascular disease, including hypertension. This relationship may be independent of co-morbidity, such as obesity. Even apparently healthy OSA patients have evidence of subtle functional vascular abnormalities that are known to occur in patients with hypertension and atherosclerosis. Untreated OSA may possibly contribute to the initiation and/or progression of pathophysiologic mechanisms involved in hypertension, heart failure, cardiac ischemia and stroke. This brief commentary will examine the evidence and mechanisms linking OSA to vascular disease.

Show MeSH

Related in: MedlinePlus

Comparison of mean arterial pressure (MAP) and endothelin 1 (ET-1) in 22 patients with severe obstructive sleep apnea (OSA) before sleep at approximately 22:00 hours, before nasal continuous positive airways pressure (CPAP) therapy at approximately 02:00 hours, and on waking at approximately 07:00 hours after 5 hours of CPAP therapy. Measurements in control subjects without sleep apnea are shown on the right. Data are means ± SEM. Reproduced with permission from [21].
© Copyright Policy
Related In: Results  -  Collection


getmorefigures.php?uid=PMC64798&req=5

Figure 2: Comparison of mean arterial pressure (MAP) and endothelin 1 (ET-1) in 22 patients with severe obstructive sleep apnea (OSA) before sleep at approximately 22:00 hours, before nasal continuous positive airways pressure (CPAP) therapy at approximately 02:00 hours, and on waking at approximately 07:00 hours after 5 hours of CPAP therapy. Measurements in control subjects without sleep apnea are shown on the right. Data are means ± SEM. Reproduced with permission from [21].

Mentions: While sympathetic activation is one mechanism that may contribute to increased daytime blood pressures after repetitive nocturnal apneas, a second possibility is the pressor effect of endothelin [19]. Hypoxemia results in increased levels of endothelin production [20]. Endothelin is a potent vasoconstrictor. In untreated patients, 4–5 hours of repetitive nocturnal apneas results in significant increases in both endothelin and blood pressure. Treatment of the OSA over the subsequent 4 hours dramatically reduces both blood pressure and endothelin levels when the subject is awake [21] (Fig. 2). Since endothelin has sustained hypertensive effects that persist for a number of hours, hypoxemia-mediated endothelin release during sleep may result in sustained daytime blood pressure elevation in patients with obstructive apnea.


Obstructive sleep apnea and vascular disease.

Lanfranchi P, Somers VK - Respir. Res. (2001)

Comparison of mean arterial pressure (MAP) and endothelin 1 (ET-1) in 22 patients with severe obstructive sleep apnea (OSA) before sleep at approximately 22:00 hours, before nasal continuous positive airways pressure (CPAP) therapy at approximately 02:00 hours, and on waking at approximately 07:00 hours after 5 hours of CPAP therapy. Measurements in control subjects without sleep apnea are shown on the right. Data are means ± SEM. Reproduced with permission from [21].
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC64798&req=5

Figure 2: Comparison of mean arterial pressure (MAP) and endothelin 1 (ET-1) in 22 patients with severe obstructive sleep apnea (OSA) before sleep at approximately 22:00 hours, before nasal continuous positive airways pressure (CPAP) therapy at approximately 02:00 hours, and on waking at approximately 07:00 hours after 5 hours of CPAP therapy. Measurements in control subjects without sleep apnea are shown on the right. Data are means ± SEM. Reproduced with permission from [21].
Mentions: While sympathetic activation is one mechanism that may contribute to increased daytime blood pressures after repetitive nocturnal apneas, a second possibility is the pressor effect of endothelin [19]. Hypoxemia results in increased levels of endothelin production [20]. Endothelin is a potent vasoconstrictor. In untreated patients, 4–5 hours of repetitive nocturnal apneas results in significant increases in both endothelin and blood pressure. Treatment of the OSA over the subsequent 4 hours dramatically reduces both blood pressure and endothelin levels when the subject is awake [21] (Fig. 2). Since endothelin has sustained hypertensive effects that persist for a number of hours, hypoxemia-mediated endothelin release during sleep may result in sustained daytime blood pressure elevation in patients with obstructive apnea.

Bottom Line: This relationship may be independent of co-morbidity, such as obesity.Untreated OSA may possibly contribute to the initiation and/or progression of pathophysiologic mechanisms involved in hypertension, heart failure, cardiac ischemia and stroke.This brief commentary will examine the evidence and mechanisms linking OSA to vascular disease.

View Article: PubMed Central - HTML - PubMed

Affiliation: Mayo Clinic, Rochester, Minnesota 55905, USA.

ABSTRACT
There is emerging evidence linking obstructive sleep apnea (OSA) to vascular disease, including hypertension. This relationship may be independent of co-morbidity, such as obesity. Even apparently healthy OSA patients have evidence of subtle functional vascular abnormalities that are known to occur in patients with hypertension and atherosclerosis. Untreated OSA may possibly contribute to the initiation and/or progression of pathophysiologic mechanisms involved in hypertension, heart failure, cardiac ischemia and stroke. This brief commentary will examine the evidence and mechanisms linking OSA to vascular disease.

Show MeSH
Related in: MedlinePlus