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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.

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Related in: MedlinePlus

Recordings of sympathetic nerve activity (SNA), respiration (RESP) and intra-arterial blood pressure (BP) in the same subject when awake (top left), with obstructive sleep apnea (OSA) during rapid eye movement (REM) sleep (bottom), and with elimination of obstructive apnea by continuous positive airways pressure (CPAP) therapy during REM sleep (top right). SNA is very high during wakefulness, but increases even further secondary to OSA during REM. BP increases from 130/65 mmHg when awake to 256/110 mmHg at the end of apnea. Overall, nocturnal blood pressure is increased. Elimination of apnea by CPAP therapy (top right) results in decreased sympathetic traffic and prevents BP surges during REM sleep. Reproduced with permission from [16].
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Figure 1: Recordings of sympathetic nerve activity (SNA), respiration (RESP) and intra-arterial blood pressure (BP) in the same subject when awake (top left), with obstructive sleep apnea (OSA) during rapid eye movement (REM) sleep (bottom), and with elimination of obstructive apnea by continuous positive airways pressure (CPAP) therapy during REM sleep (top right). SNA is very high during wakefulness, but increases even further secondary to OSA during REM. BP increases from 130/65 mmHg when awake to 256/110 mmHg at the end of apnea. Overall, nocturnal blood pressure is increased. Elimination of apnea by CPAP therapy (top right) results in decreased sympathetic traffic and prevents BP surges during REM sleep. Reproduced with permission from [16].

Mentions: During sleep, repetitive episodes of airway occlusion, with consequent hypoxemia, hypercapnia and dramatic changes in intrathoracic pressure, elicit a wide variety of autonomic, hemodynamic, humoral and neuroendocrine responses. These responses themselves evoke acute changes in cardiovascular function, as well as more sustained effects that carry over into the daytime even when breathing is normal. First, hypoxemia and hypercapnia result in chemoreflex activation with consequent increases in sympathetic vasoconstrictor traffic to peripheral blood vessels [16] (Fig. 1). This reflex response results in striking increases in blood pressure as well as increased levels of circulating catecholamines. The sympathetic activity and surges in blood pressure are markedly attenuated by effective treatment with CPAP therapy [17]. Stradling et al. reported that both nocturnal desaturations and respiratory effort (indirectly measured using pulse transit times) were significant independent predictors of an increase in blood pressure between night-time and morning [18].


Obstructive sleep apnea and vascular disease.

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

Recordings of sympathetic nerve activity (SNA), respiration (RESP) and intra-arterial blood pressure (BP) in the same subject when awake (top left), with obstructive sleep apnea (OSA) during rapid eye movement (REM) sleep (bottom), and with elimination of obstructive apnea by continuous positive airways pressure (CPAP) therapy during REM sleep (top right). SNA is very high during wakefulness, but increases even further secondary to OSA during REM. BP increases from 130/65 mmHg when awake to 256/110 mmHg at the end of apnea. Overall, nocturnal blood pressure is increased. Elimination of apnea by CPAP therapy (top right) results in decreased sympathetic traffic and prevents BP surges during REM sleep. Reproduced with permission from [16].
© Copyright Policy
Related In: Results  -  Collection

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

Figure 1: Recordings of sympathetic nerve activity (SNA), respiration (RESP) and intra-arterial blood pressure (BP) in the same subject when awake (top left), with obstructive sleep apnea (OSA) during rapid eye movement (REM) sleep (bottom), and with elimination of obstructive apnea by continuous positive airways pressure (CPAP) therapy during REM sleep (top right). SNA is very high during wakefulness, but increases even further secondary to OSA during REM. BP increases from 130/65 mmHg when awake to 256/110 mmHg at the end of apnea. Overall, nocturnal blood pressure is increased. Elimination of apnea by CPAP therapy (top right) results in decreased sympathetic traffic and prevents BP surges during REM sleep. Reproduced with permission from [16].
Mentions: During sleep, repetitive episodes of airway occlusion, with consequent hypoxemia, hypercapnia and dramatic changes in intrathoracic pressure, elicit a wide variety of autonomic, hemodynamic, humoral and neuroendocrine responses. These responses themselves evoke acute changes in cardiovascular function, as well as more sustained effects that carry over into the daytime even when breathing is normal. First, hypoxemia and hypercapnia result in chemoreflex activation with consequent increases in sympathetic vasoconstrictor traffic to peripheral blood vessels [16] (Fig. 1). This reflex response results in striking increases in blood pressure as well as increased levels of circulating catecholamines. The sympathetic activity and surges in blood pressure are markedly attenuated by effective treatment with CPAP therapy [17]. Stradling et al. reported that both nocturnal desaturations and respiratory effort (indirectly measured using pulse transit times) were significant independent predictors of an increase in blood pressure between night-time and morning [18].

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