The prevalence of calcified carotid artery atheromas in patients with obstructive sleep apnea syndrome

Friedlander, Arthur H.; Yueh, Ronald; Littner, Michael R.

doi:10.1016/s0278-2391(98)90657-7

Cited by 34 publications

(16 citation statements)

References 28 publications

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“…Such studies have examined the endpoint of carotid artery intima-media thickness and reported a significant positive association between SA and increased carotid artery intima-media thickness. 5,10–13,15–17,21,23,24 Importantly, to our knowledge, no study to date has investigated the association between SA and the ankle-brachial index (ABI), an indicator of significant obstructive peripheral atherosclerotic burden in the lower extremities that independently predicts mortality. 25 …”

Section: Introductionmentioning

confidence: 99%

Sleep Apnea Is Independently Associated With Peripheral Arterial Disease in the Hispanic Community Health Study/Study of Latinos

Shah

Allison

Teng

et al. 2015

ATVB

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Objective Sleep apnea (SA) has been linked with various forms of cardiovascular disease, but little is known about its association with peripheral artery disease (PAD) measured using the ankle- brachial index (ABI). This relationship was evaluated in the Hispanic Community Health Study/Study of Latinos (HCHS/SOL). Approach and Results We studied 8,367 HCHS/SOL participants who were 45 to 74 years of age. Sleep symptoms were examined with the self-reported Sleep Health Questionnaire. SA was assessed using an in-home sleep study. Systolic blood pressure was measured in all extremities to compute the ABI. PAD was defined as ABI < 0.90 in either leg. Multivariable logistic regression was utilized to investigate the association between moderate-to-severe SA, defined as apnea-hypopnea index (AHI) ≥15, and the presence of PAD. Analyses were adjusted for covariates. The prevalence of PAD was 4.7% (n=390). The mean AHI was significantly higher among adults with PAD compared to those without (11.1 vs. 8.6 events/hour, p=0.046). After adjusting for covariates, moderate-to-severe SA was associated with a 70% increase in the odds of PAD (odds ratio 1.7, 95% CI: 1.1 – 2.5, p=0.0152). This association was not modified by sex (p=0.8739). However, there was evidence that the association between moderate-to-severe SA and PAD varied by Hispanic/Latino background (p < 0.01). Specifically, the odds were stronger in Mexican (adjusted OR 2.9, 95% CI: 1.3, 6.2) and in Puerto Rican Americans (adjusted OR 2.0, 95% CI: 0.97 – 4.2) than in other backgrounds. Conclusions Moderate-to-severe SA is associated with higher odds of PAD in Hispanic/Latino adults.

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Section: Introductionmentioning

confidence: 99%

Sleep Apnea Is Independently Associated With Peripheral Arterial Disease in the Hispanic Community Health Study/Study of Latinos

Shah

Allison

Teng

et al. 2015

ATVB

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“…Extensive reviews on cardiovascular morbidity and mortality in OSAHS and the association of OSAHS with components of the metabolic syndrome have been recently published [6][7][8]. Moreover, patients with OSAHS without overt cardiovascular diseases show subclinical signs of atherosclerosis that are related both to the structure of the vasculature, such as increased intima-media thickness, arterial plaque formation and calcified artery atheromas [9][10][11][12], and to its function, such as endothelial dysfunction and higher pulse wave velocity [13][14][15][16]. Some of these subclinical conditions were improved by treatments with nasal continuous positive airway pressure (nCPAP) or a dental device [17][18][19].…”

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confidence: 99%

Molecular mechanisms of cardiovascular disease in OSAHS: the oxidative stress link

Lavie¹,

Lavie²

2009

Eur Respir J

324

223

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Obstructive sleep apnoea/hypopnoea syndrome (OSAHS) is a highly prevalent breathing disorder in sleep that is an independent risk factor for cardiovascular morbidity and mortality. A large body of evidence, including clinical studies and cell culture and animal models utilising intermittent hypoxia, delineates the central role of oxidative stress in OSAHS as well as in conditions and comorbidities that aggregate with it. Intermittent hypoxia, the hallmark of OSAHS, is implicated in promoting the formation of reactive oxygen species (ROS) and inducing oxidative stress. The ramifications of increased ROS formation are pivotal. ROS can damage biomolecules, alter cellular functions and function as signalling molecules in physiological as well as in pathophysiological conditions. Consequently, they promote inflammation, endothelial dysfunction and cardiovascular morbidity. Oxidative stress is also a crucial component in obesity, sympathetic activation and metabolic disorders such as hypertension, dyslipidaemia and type 2 diabetes/insulin resistance, which aggregate with OSAHS. These conditions and comorbidities could result directly from the oxidative stress that is characteristic of OSAHS or could develop independently. Hence, oxidative stress represents the common underlying link in OSAHS and the conditions and comorbidities that aggregate with it.

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“…A strong association was demonstrated between OSAS and hypertension, but also with ischemic heart disease, stroke, arrhythmia, chronic heart failure, and cardiovascular morbidity and mortality initially by small-scale studies that were followed by well-designed large-scale epidemiological, and prospective studies [14,15,16,17]. Importantly, patients with OSAS without overt CVD show structural and functional subclinical signs of atherosclerosis, such as increased intima-media thickness, arterial plaque formation, calcified artery atheromas [18,19,20,21], and endothelial dysfunction [22,23,24,25], suggesting that atherosclerosis may precede the development of CVD morbidity in OSAS. Treatments with nasal continuous positive airway pressure (nCPAP) or dental device, which alleviates the apneic events and normalizes breathing during sleep, were shown to improve some of these subclinical conditions [26,27,28].…”

Section: Cardiovascular Morbidity In Sleep Apneamentioning

confidence: 99%

Cardiovascular Aspects in Obstructive Sleep Apnea Syndrome – Molecular Issues, Hypoxia and Cytokine Profiles

Lavie

Polotsky

2009

Respiration

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Obstructive sleep apnea syndrome (OSAS), which is a highly prevalent breathing disorder in sleep, is an independent risk factor for cardiovascular morbidity and mortality. Results from clinical studies as well as animal models and cell culture studies utilizing intermittent hypoxia implicate oxidative stress and inflammation in the pathogenesis of OSAS. However, the underlying mechanisms are not entirely understood. Both oxidative stress and inflammation are major components in the initiation and development of endothelial dysfunction and consequently atherosclerosis. Yet, these fundamental mechanisms are associated with obesity and with components of the metabolic syndrome that also cluster with OSAS. Accumulated evidence indicates that inflammatory cytokines such as TNF-α that are under the control of nuclear factor κB actively participate in endothelial damage. The current review highlights some of the recent findings on oxidative stress and inflammation in OSAS with specific emphasis on the role of inflammatory pathway activation and expression of cytokines and their possible role in OSAS-related cardiovascular morbidity. In light of the new findings in the field of cytokines, their potential involvement in endothelial dysfunction and cardiovascular morbidity in OSAS is discussed.

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The prevalence of calcified carotid artery atheromas in patients with obstructive sleep apnea syndrome

Cited by 34 publications

References 28 publications

Sleep Apnea Is Independently Associated With Peripheral Arterial Disease in the Hispanic Community Health Study/Study of Latinos

Sleep Apnea Is Independently Associated With Peripheral Arterial Disease in the Hispanic Community Health Study/Study of Latinos

Molecular mechanisms of cardiovascular disease in OSAHS: the oxidative stress link

Cardiovascular Aspects in Obstructive Sleep Apnea Syndrome – Molecular Issues, Hypoxia and Cytokine Profiles

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