Myocardial Perfusion by Myocardial Contrast Echocardiography and Endothelial Dysfunction in Obstructive Sleep Apnea

Butt, Mehmood; Khair, Omer; Dwivedi, Girish; Shantsila, Alena; Shantsila, Eduard; Lip, Gregory Y.H.

doi:10.1161/hypertensionaha.111.170910

Cited by 52 publications

(48 citation statements)

References 46 publications

(51 reference statements)

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“…In subjects with OSA, but otherwise healthy, endothelium-dependent vasodilatation is impaired, 65 and, in randomized trials, treating OSA by CPAP improved both endothelium-dependent and/or -independent vasodilatation without reducing plasma biomarkers of inflammation. 65 Butt and colleagues 68 recently reported that otherwise healthy patients with OSA had impaired myocardial perfusion that improved with CPAP. Enhanced apoptosis of endothelial cells and fewer circulating endothelial progenitor cells in OSA patients may contribute to these processes.…”

Section: Oxidative Stress Inflammation and Endothelial Dysfunctionmentioning

confidence: 99%

Sleep Apnea and Cardiovascular Disease

Kasai

Floras²,

Bradley³

2012

Circulation

330

207

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Sleep apnea occurs in Ϸ5% to 10% of the general population, regardless of race and ethnicity. 1 By contrast, in patients with cardiovascular diseases (CVDs), its prevalence, depending on the specific disorder surveyed, can range between 47% and 83%. [2][3][4] One form, central sleep apnea (CSA), is rare in the general population, but is detected often in conditions characterized by sodium and water retention, such as heart failure (HF). 2 Such epidemiological observations raise several important and as yet unresolved questions: What accounts for this remarkable concentration of sleep apnea among patients with CVD and its association with fluid retaining states? Does obstructive sleep apnea (OSA) predispose at-risk individuals to develop, over time, hypertension, coronary artery disease, stroke, or HF? Conversely, could mechanisms engaged by CVD, such as activation of the sympathetic nervous and renin-angiotensin-aldosterone systems, with consequences including renal sodium retention, contribute over time to the development or exacerbation of sleep apnea? From the clinical perspective, is sleep apnea, when present in patients with CVD an epiphenomenon, perhaps related to ageing, or a causal contributor to worse prognosis? And if so, are there now sufficient data to recommend randomized controlled trials to determine whether specific treatment of sleep apnea can reduce mortality or cardiovascular event rates? Our objectives, in this review, are to provide novel insight into each of these specific questions by integrating into our contemporary understanding of relationships between sleep apnea and CVD 5 newer epidemiological, observational, mechanistic, and trial data; to introduce a hypothetical model of bidirectional causality; and to consider directions for future research. Normal SleepIn healthy subjects, during non-rapid eye movement sleep (which constitutes Ϸ85% of total sleep time), efferent sympathetic nerve activity (SNA) diminishes and vagal tone increases, resulting in reductions in metabolic rate, blood pressure (BP), and heart rate (HR). 6,7 Thus, although sleep is, in general, a stable state of cardiovascular quiescence, this tableau can be interrupted both normally, by the intermittent surges in SNA, BP, and HR characteristic of rapid eye movement sleep (but comprising only 15% of total sleep time), 6 and pathologically, whether because of fitful sleep or shorter overall sleep time, as evident in patients with HF or drug-resistant hypertension, 8,9 or by coexisting sleep apnea, whether obstructive (OSA) or central (CSA).

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Section: Oxidative Stress Inflammation and Endothelial Dysfunctionmentioning

confidence: 99%

Sleep Apnea and Cardiovascular Disease

Kasai

Floras²,

Bradley³

2012

Circulation

330

207

View full text Add to dashboard Cite

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“…However, interpretation of current data are limited by the cross-sectional design of certain studies, 20 and the presence of a wide range of confounding factors such as existing comorbidities and other cardiovascular risk mediators. To reduce the possibility of confounding, Butt et al 21 recently looked at normostensive patients with moderate-severe OSA (with no apparent cardiovascular disease), and performed myocardial perfusion imaging as compared with 2 sets of matched controls without OSA (hypertensive patients and healthy subjects). Patients with OSA were found to have significant abnormalities in myocardial perfusion, as well as attenuated brachial artery reactivity when compared with healthy controls, thus lending support to the hypothesis regarding endothelial dysfunction in OSA.…”

Section: The Pathogenesis Of Osa-related Cardiovascular Eventsmentioning

confidence: 99%

Association of Obstructive Sleep Apnea With Risk of Serious Cardiovascular Events

Loke

Brown

Kwok

et al. 2012

Circ: Cardiovascular Quality and Outcomes

315

189

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Background— The relationship between obstructive sleep apnea (OSA) and cardiovascular events remains unclear. We conducted a systematic review to determine the incident risk of cardiovascular events among patients with OSA. Methods and Results— We searched MEDLINE and EMBASE in January 2011 for prospective studies that followed up patients with OSA for incident ischemic heart disease, stroke, and cardiovascular mortality. Outcomes data were pooled using random effects meta-analysis and heterogeneity assessed with the I 2 statistic. Regression analysis was performed to evaluate the effects of different gradations of OSA severity based on apnea-hypopnea index. We identified 9 relevant studies from 1731 citations. OSA was associated with incident stroke in a meta-analysis of 5 studies (8435 participants), odds ratio (OR) 2.24; 95% confidence interval (CI), 1.57–3.19; I 2 =7%. A significant association was seen in studies that were predominantly on men; OR, 2.87; 95% CI, 1.91–4.31, whereas data on women were sparse. In the overall analysis of 6 studies (8785 participants), OSA was nonsignificantly associated with ischemic heart disease (OR, 1.56; 95% CI, 0.83–2.91), with significant findings in the 5 studies that recruited mainly men (OR, 1.92; 95% CI, 1.06–3.48). Substantial heterogeneity was noted (I 2 =74%). OSA was linked to cardiovascular death in 2 studies involving 2446 participants (OR, 2.09; 95% CI, 1.20–3.65, I 2 =0%). Regression analysis showed greater likelihood of stroke or cardiovascular events with increasing apnea-hypopnea index values. Conclusions— OSA appears to be associated with stroke, but the relationship with ischemic heart disease and cardiovascular mortality needs further research.

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“…9 The critical role of chronic intermittent hypoxia (CIH) exposure in the development of cardiovascular changes induced by OSA is supported not only by clinical studies reporting the beneficial cardiovascular effects of the treatment of OSA patients with continuous positive airway pressure [10][11][12][13] but also by experimental data showing that animals exposed to CIH develop sustained hypertension, 14 an effect prevented by previous denervation of peripheral chemoreceptors. 15 In this brief review, we discuss recent data about the possible mechanisms underpinning the hypertension induced by CIH exposure, with focus on the development of the sympathetic overactivity that is associated with this pathophysiological condition.…”

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confidence: 99%