Obstructive Sleep Apnea and Carotid-Artery Intima-Media Thickness

Suzuki, Takahiro; Nakano, Hiroshi; Maekawa, Junko; Okamoto, Yukinori; Ohnishi, Yoshinobu; Yamauchi, Motoo; Kimura, Hiroshi

doi:10.1093/sleep/27.1.129

Cited by 117 publications

(99 citation statements)

References 42 publications

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“…Recent studies have evaluated the effect of OSAS on most of the aforementioned arterial characteristics. [14][15][16][17][18][19][20] These studies demonstrated an increase in carotid IMT and arterial stiffness in patients with OSAS, suggesting that OSAS may promote vascular disease. However, some of these studies excluded patients with cardiovascular or cerebrovascular disease, hypertension, diabetes mellitus, hyperlipidaemia or severe obesity 17,20 and therefore were not representative of the usual population of patients with OSAS encountered in clinical practice who exhibit a high burden of cardiovascular risk factors.…”

Section: Introductionmentioning

confidence: 73%

Structural and functional arterial properties in patients with obstructive sleep apnoea syndrome and cardiovascular comorbidities

Protogerou

Czernichow

et al. 2007

J Hum Hypertens

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The increased severity of obstructive sleep apnoea syndrome (OSAS) is associated with a parallel increase in the incidence of cardiovascular events. Whether the increased severity of OSAS is in fact associated with impaired arterial properties has never been thoroughly studied. In patients with OSAS who carry a high burden of cardiovascular risk factors, we investigated whether the severity of OSAS is associated with deterioration in the arterial properties, independent of classical cardiovascular risk factors. In 74 consecutive patients with OSAS, we non-invasively assessed, by means of tonometry and high-resolution ultrasound: carotid intima-media thickness (IMT), carotid diameter and plaques, carotid-femoral pulse wave velocity (PWV), central augmentation index (AI) and central blood pressures. The respiratory disturbance index was an independent predictor of IMT and PWV but not of carotid plaques, carotid diameter, AI or central blood pressures. Several parameters of nocturnal hypoxaemia were independently correlated with carotid IMT and PWV. In conclusion, arterial stiffening and thickening are modulated by the severity of OSAS, independently from age and cardiovascular risk factors.

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Section: Introductionmentioning

confidence: 73%

Structural and functional arterial properties in patients with obstructive sleep apnoea syndrome and cardiovascular comorbidities

Protogerou

Czernichow

et al. 2007

J Hum Hypertens

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“…Of note, the mean BMI of patients with RDI .50 in the current study was 32.8 Kg?m -2 . Moreover, recent studies from the authors' own laboratory, and by others, have shown that sleep apnoea patients free of any cardiovascular disease have evidence of oxidative stress and inflammatory/immune cell activation, which may initiate atherogenic processes that cause accumulated damage to the vasculature [1][2][3][4]. This was also corroborated by reports that sleep apnoea patients free of any cardiovascular disease suffer from endothelial dysfunction, a subclinical state of atherosclerosis [39][40][41] that was shown to be predictive of future cardiovascular events [42,43].…”

Section: Discussionmentioning

confidence: 99%

“…here is a large body of evidence linking obstructive sleep apnoea (OSA) syndrome with atherogenic processes [1][2][3][4], cardiovascular morbidity, in particular with hypertension [5][6][7][8][9][10][11], as well as with vehicle accidents and work-related accidents [12][13]. Although there have been reports of increased rates of mortality in sleep apnoea patients [14][15][16], these reports, based on small groups, did not examine the contributing role of obesity, nor the relationship with the severity of sleep apnoea syndrome.…”

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confidence: 99%

All-cause mortality in males with sleep apnoea syndrome: declining mortality rates with age

Lavie¹

2005

European Respiratory Journal

281

134

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The objective of this study was to assess whether an increasing severity of sleep apnoea is associated with increased all-cause mortality hazards and to assess whether the syndrome is associated with excess mortality, in comparison with the general population.Participants included 14,589 adult males, aged 20-93 yrs, referred to the sleep clinics with suspected sleep apnoea or diagnosed with sleep apnoea.Altogether, 372 deaths were recorded after a median follow-up of 4.6 yrs. The crude all-cause mortality rate was 5.55/1,000 patient yrs, increasing with apnoea severity. Cox proportional analysis revealed that both respiratory disturbance index (RDI) and body mass index significantly influenced all-cause mortality hazard but there was no interaction between them. Males with respiratory disturbance index .30 had a significantly higher mortality hazard rate than the reference group of males with RDI f10. Comparing mortality rates of males with moderate/severe sleep apnoea to the general population revealed that only males aged ,50 yrs showed an excess mortality rate.The hazard of mortality in sleep apnoea increases with apnoea severity as indexed by respiratory disturbance index. Moderate and severe levels of sleep apnoea are moderately associated with an increased risk of all-cause mortality, in comparison with the general population, particularly in males aged ,50 yrs. The lack of information about possible confounders and treatment effects should be taken into consideration in the interpretation of these results.

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“…1,2 Further support of this concept is derived from studies linking SDB to atherosclerotic pathways. [3][4][5][6] These studies provide insight into the mechanisms of vascular injury secondary to SDB. Although the impact of duration of this disorder on the development of risk factors for cardiovascular disease is difficult to estimate, morbidity secondary to SDB seems to manifest gradually, often taking decades.…”

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confidence: 99%

Activity-Adjusted 24-Hour Ambulatory Blood Pressure and Cardiac Remodeling in Children with Sleep Disordered Breathing

et al. 2008

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Abstract-Questions remain as to whether pediatric sleep disordered breathing increases the risk for elevated blood pressure and blood pressure-dependent cardiac remodeling. We tested the hypothesis that activity-adjusted morning blood pressure surge, blood pressure load, and diurnal and nocturnal blood pressure are significantly higher in children with sleep disordered breathing than in healthy controls and that these blood pressure parameters relate to left ventricular remodeling. 24-hour ambulatory blood pressure parameters were compared between groups. The associations between blood pressure and left ventricular relative wall thickness and mass were measured. 140 children met the inclusion criteria. In children with apnea hypopnea index Ͻ5 per hour, a significant difference from controls was the morning blood surge. Significant increases in blood pressure surge, blood pressure load, and in 24-hour ambulatory blood pressure were evident in those whom the apnea hypopnea index exceeded 5 per hour. Sleep disordered breathing and body mass index had similar effect on blood pressure parameters except for nocturnal diastolic blood pressure, where sleep disordered breathing had a significantly greater effect than body mass index. Diurnal and nocturnal systolic blood pressure, diastolic blood pressure, and mean arterial blood pressure predicted the changes in left ventricular relative wall thickness. Therefore, sleep disordered breathing in children who are otherwise healthy is independently associated with an increase in morning blood pressure surge, blood pressure load, and 24-hour ambulatory blood pressure. The association between left ventricular remodeling and 24-hour blood pressure highlights the role of sleep disordered breathing in increasing cardiovascular morbidity. Key Words: sleep apnea Ⅲ children Ⅲ ambulatory blood pressure Ⅲ blood pressure surge Ⅲ blood pressure load Ⅲ cardiac remodeling Ⅲ hypertrophy T he association between sleep disordered breathing (SDB) and cardiovascular morbidity in adults has become an important consideration in the management of patients with SDB. Results from numerous cross-sectional and prospective studies of blood pressure (BP) control in adults support the concept that hypertension is an intermediate end point between SDB and cardiovascular disease. 1,2 Further support of this concept is derived from studies linking SDB to atherosclerotic pathways. [3][4][5][6] These studies provide insight into the mechanisms of vascular injury secondary to SDB. Although the impact of duration of this disorder on the development of risk factors for cardiovascular disease is difficult to estimate, morbidity secondary to SDB seems to manifest gradually, often taking decades. As such, with the exception of isolated cases of heart failure, children with SDB rarely show evidence of cardiovascular disease. Thus far, studies addressing whether children with SDB acquire risk factors for the early development of cardiovascular disease are inconclusive.Findings from several pediatric studies suggest ...

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Obstructive Sleep Apnea and Carotid-Artery Intima-Media Thickness

Abstract: Our results demonstrated that the severity of OSA is independently related to atherosclerosis and that the severity of OSA-related hypoxemia is more important than the frequency of obstructive events.

Cited by 117 publications

References 42 publications

Structural and functional arterial properties in patients with obstructive sleep apnoea syndrome and cardiovascular comorbidities

Structural and functional arterial properties in patients with obstructive sleep apnoea syndrome and cardiovascular comorbidities

All-cause mortality in males with sleep apnoea syndrome: declining mortality rates with age

Activity-Adjusted 24-Hour Ambulatory Blood Pressure and Cardiac Remodeling in Children with Sleep Disordered Breathing

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