The Price of Obstructive Sleep Apnea-Hypopnea: Hypertension and Other Ill Effects

Friedman, Oded; Logan, Alexander G.

doi:10.1038/ajh.2009.43

Cited by 48 publications

(37 citation statements)

References 151 publications

(121 reference statements)

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“…This is a condition that affects 9-25% of the adult population, 18,19 and untreated OSA represents an independent risk for hypertension, myocardial ischaemia and stroke. [20][21][22][23][24][25] However, the mechanisms underling the association between OSA and cardiovascular factor risk, such as hypertension, are not well understood. Most recently it has been hypothesized that an excess of aldosterone could be caused by OSA.…”

Section: Resultsmentioning

confidence: 99%

Renin-angiotensin-aldosterone system in patients with sleep apnoea: prevalence of primary aldosteronism

Murro

Petramala

Cotesta

et al. 2010

J Renin Angiotensin Aldosterone Syst

109

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Obstructive sleep apnoea (OSA) is a sleep disorder characterized by recurrent episodes of oxygen desaturation during sleep, representing an independent risk factor for cardiovascular disease, such as myocardial infarction, stroke, congestive heart failure and resistant hypertension. Several neurohormonal mechanisms have been suggested to account for blood pressure increases, such as sympathetic nervous system hyperactivity, oxidative stress, renin-angiotensin-aldosterone system (RAAS) activation, endothelin system activation, and endothelial dysfunction. The aim of this study was to evaluate the behaviour of RAAS and the presence of primary aldosteronism (PA) in these patients and possible correlations between RAAS and the severity of OSA. From October 2007 to November 2008 we studied 325 consecutive newly diagnosed hypertensive patients; 71 patients (21.8%) presented with clinical signs of sleep disorders, evaluated also through a specific questionnaire (Epworth Sleepiness Scale). In hypertensive patients with sleep disorders, 53 patients were affected by OSA; in this group 18 patients were affected by PA (five with aldosterone-producing adenoma (APA) and 13 with bilateral hyperplasia (IHA)); obesity was also demonstrated (BMI > 30 kg/m 2 ). Overall, in patients with OSA PRA levels correlated positively with apnoea/hypopnoea index (AHI; r = 0.35; p<0.01), and in all groups the waist circumference and the neck circumference were correlated positively with AHI (r = 0.3 p<0.02 and r = 0.3 p<0.03, respectively). We revealed a high prevalence of PA in patients with OSA, and we can conclude that patients with hypertension and OSA, especially those who are newly diagnosed, must be evaluated for PA.

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Section: Resultsmentioning

confidence: 99%

Renin-angiotensin-aldosterone system in patients with sleep apnoea: prevalence of primary aldosteronism

Murro

Petramala

Cotesta

et al. 2010

J Renin Angiotensin Aldosterone Syst

109

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Section: Discussionmentioning

confidence: 99%

“…Furthermore, despite all subjects receiving instructions to reduce dietary sodium intake, there was a greater dietary sodium intake in the DRH group (Table S1, available in the onliine-only Data Supplement); parenthetically, however, the LBPP-induced leg fluid volume reduction remained significantly greater in the DRH group despite adjustment for the sodium excretion rate (P<0.0001). Moreover, although the literature on the effect of specific nondiuretic antihypertensive medications on OSA severity is limited, 29 it remains possible that certain antihypertensive drug classes may be potential confounders (eg, calcium channel blockers, especially dihydropyridines that can cause peripheral edema), despite there being no significant interactions between BP status and antihypertensive drug class.Given that the effects of LBPP application on neck circumference and upper airway cross-sectional area were assessed during the wake period, the findings may not be wholly applicable to those occurring during the sleep period. However, it would have been impractical for subjects to sleep uninterrupted while undergoing simultaneous LBPP application and acoustic pharyngometry, because they would be unable to sleep or would move if they did fall asleep causing artifactual changes in the acoustic pharyngometry signal.…”

mentioning

confidence: 99%

Influence of Lower Body Positive Pressure on Upper Airway Cross-Sectional Area in Drug-Resistant Hypertension

Friedman

Bradley²,

Logan³

2013

Hypertension

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Abstract-We previously showed that in hypertensive patients the amount of fluid displaced from the legs overnight is directly related to the severity of obstructive sleep apnea and that the rostral fluid shift was greater in drug-resistant hypertensive patients. The findings suggested that this fluid redistribution increases upper airway collapsibility, yet more direct evidence is lacking. The present study examines the effects of graded lower body positive pressure on leg fluid volume, upper airway cross-sectional area, and neck circumference in patients with drug-resistant hypertension (n=25) and controlled hypertension (n=15). In both groups, the reduction in mean upper airway cross-sectional area and oropharyngeal junction area, assessed by acoustic pharyngometry, and the increase in neck circumference, determined by mercury strain gauge plethysmography, were related to the amount of fluid displaced from the legs (R 2 =0.41, P<0.0001; R 2 =0.42, P<0.0001; and R 2 =0.47, P<0.0001, respectively). Displacement of leg fluid volume was significantly greater in patients with drug-resistant hypertension than in controlled hypertension (P<0.0001), and as a consequence, the former experienced greater reductions in mean upper airway cross-sectional area and oropharyngeal junction area (P=0.001 and P<0.0001, respectively). The findings support the concept that in hypertensive subjects, rostral fluid displacement may participate in the pathogenesis of obstructive sleep apnea by narrowing the upper airway and making it more susceptible to collapse during sleep. The exaggerated fluid volume displacement from the legs and upper airway response to lower body positive pressure in patients with drug-resistant hypertension provide additional evidence of an important link between drug-resistant hypertension and obstructive sleep apnea. 112.203547/-/DC1Correspondence to Alexander G. Friedman et al Lower Body Positive Pressure in Hypertension 241increases pharyngeal resistance and upper airway collapsibility in healthy subjects. [14][15][16] In this study, we examined the effects of LBPP on the upper airway cross-sectional area of patients with DRH and controlled hypertension (CH). We hypothesized that the degree of upper airway narrowing would be related to the amount of fluid shifted from the legs and the extent of narrowing would be greater in patients with DRH than those with CH. Methods Study DesignThe study was carried in a human physiology laboratory during the daytime. The human subjects review committee of Mount Sinai Hospital, University Health Network, and Toronto Rehabilitation Institute, all in Toronto, approved the study. All subjects provided written informed consent before participation. Study SubjectsPatients with CH and DRH were recruited from the Hypertension Clinic at the Mount Sinai Hospital in Toronto. DRH was defined as uncontrolled hypertension on optimal doses of a diuretic and 2 additional antihypertensive medications or normal blood pressure (BP) on ≥4 drugs and CH as normal BP on ≤3 agents.1 In deter...

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“…3 Obesity is associated both with decreased responsiveness to antihypertensive medications 4 and with OSA. 5 Whether obesity is the factor that explains the association between DRH and OSA, however, is unclear, because increased body weight and neck girth only account for approximately one third of the variability in the frequency of apneas and hypopneas per hour of sleep (ie, the apneahypopnea index [AHI]). 6 Moreover, the factors accounting for weight-related antihypertensive drug resistance have not been identified.…”

mentioning

confidence: 99%

Relationship Between Overnight Rostral Fluid Shift and Obstructive Sleep Apnea in Drug-Resistant Hypertension

et al. 2010

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Abstract-Obstructive sleep apnea occurs frequently in patients with drug-resistant hypertension. The factors accounting for this observation, however, are unclear. Both conditions demonstrate clinical features suggestive of extracellular fluid volume overload. The aims of this study were to examine whether the spontaneous overnight fluid shift from the legs to the upper body is associated with obstructive sleep apnea in hypertensive subjects and whether its magnitude is greater in drug-resistant hypertension. Leg fluid volume and the circumference of the calf and neck were measured before and after sleep in drug-resistant hypertensive (nϭ25) and controlled hypertensive (nϭ15) subjects undergoing overnight polysomnography. The severity of obstructive sleep apnea was greater in the drug-resistant hypertensive group than in the controlled hypertensive group (apnea-hypopnea index: 43.0Ϯ5.4 versus 18.1Ϯ4.2 events per hour of sleep; Pϭ0.02, case-mix adjusted). In both groups, the apnea-hypopnea index strongly related to the amount of leg fluid volume displaced (R 2 ϭ0.56; PϽ0.0001), although the magnitude of change was greater in the drug-resistant hypertensive group (346.7Ϯ24.1 versus 175.8Ϯ31.3 mL; Pϭ0.01, propensity-score adjusted). The overnight reduction in calf circumference and increase in neck circumference were also greater in drug-resistant hypertension (both PՅ0.02). In hypertensive subjects, rostral fluid displacement strongly relates to the severity of obstructive sleep apnea with its magnitude being greater in drug-resistant hypertension. Our findings support the concept that fluid redistribution centrally during sleep accounts for the high prevalence of obstructive sleep apnea in drug-resistant hypertension. rug-resistant hypertension (DRH) is emerging as a major and growing problem in managing hypertension. It accelerates the atherosclerotic burden of aging and is associated with a significant increased risk of hypertensive target organ damage. 1 In a previous study, we reported that patients with DRH had a very high prevalence of obstructive sleep apnea (OSA) 2 and subsequently demonstrated that treatment of OSA with continuous positive airway pressure was accompanied by a significant fall in both nighttime and daytime blood pressure (BP). 3 Obesity is associated both with decreased responsiveness to antihypertensive medications 4 and with OSA. 5 Whether obesity is the factor that explains the association between DRH and OSA, however, is unclear, because increased body weight and neck girth only account for approximately one third of the variability in the frequency of apneas and hypopneas per hour of sleep (ie, the apneahypopnea index [AHI]). 6 Moreover, the factors accounting for weight-related antihypertensive drug resistance have not been identified.Many studies have demonstrated abnormalities in extracellular fluid volume regulation in DRH and OSA. Plasma renin is generally suppressed in both conditions, 7,8 and primary aldosteronism is a common finding in DRH. 9 BP of DRH patients often falls dr...

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The Price of Obstructive Sleep Apnea-Hypopnea: Hypertension and Other Ill Effects

Cited by 48 publications

References 151 publications

Renin-angiotensin-aldosterone system in patients with sleep apnoea: prevalence of primary aldosteronism

Renin-angiotensin-aldosterone system in patients with sleep apnoea: prevalence of primary aldosteronism

Influence of Lower Body Positive Pressure on Upper Airway Cross-Sectional Area in Drug-Resistant Hypertension

Relationship Between Overnight Rostral Fluid Shift and Obstructive Sleep Apnea in Drug-Resistant Hypertension

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