Obstructive Sleep Apnea and Atherosclerosis
Section snippets
General Mechanisms of Atherosclerosis
Coronary heart disease and stroke, both resulting from atherosclerosis (fatty deposits), account for 80% of deaths from cardiovascular diseases. Age-specific incidence rates for cardiovascular disease have fallen by half for the past 30 years in the economically advanced European nations, as a result of better prevention and treatments based on growing knowledge of vascular biology. Although these measures are becoming widely disseminated, an additional dramatic effect on cardiovascular disease
Atherosclerosis in Animal Models of Intermittent Hypoxia
Sleep apnea syndrome is a multicomponent disease including intermittent hypoxia (IH), respiratory efforts, and sleep fragmentation. Intermittent hypoxia has been proposed in rodents to mimic one of the major consequences of sleep apnea. As a partial model of sleep apnea, IH allows to test the specific role of IH on atherogenesis and to assess both plasma and tissue alterations that may contribute to atherosclerosis development and progression.
Atherosclerotic remodeling as evidenced by plaques
Clinical and Biological Findings in OSA
There have been significant efforts in this field of clinical research in reducing the number of confounding factors and comorbid conditions. In 2005, 3 reports were published nearly at the same time evidencing that sleep apnea may lead to early atherosclerosis as reflected at the carotid level by increase in IMT and occurrence of plaques, in the absence of any significant comorbidity.7, 8, 74 In our series of patients, severity of oxygen desaturation and BP status were the best predictors for
Conclusions
Sleep apnea and IH are associated with early vascular changes. There are both animal and clinical data supporting a specific role for IH in promoting cellular changes at the vascular wall level thus triggering atherosclerosis. These early changes as evidenced by subclinical markers in OSA patients are also seen in rodents exposed to IH for only several weeks. Lesions seem to be partly reversible as far as the inflammatory component is concerned. In OSA, CPAP impact needs certainly to be studied
References (96)
- et al.
Long-term cardiovascular outcomes in men with obstructive sleep apnoea-hypopnoea with or without treatment with continuous positive airway pressure: an observational study
Lancet
(2005) - et al.
Ambulatory blood pressure after therapeutic and subtherapeutic nasal continuous positive airway pressure for obstructive sleep apnoea: a randomised parallel trial
Lancet
(2002) - et al.
The severity of oxygen desaturation is predictive of carotid wall thickening and plaque occurrence
Chest
(2005) Leukocyte-endothelial cell recognition: three (or more) steps to specificity and diversity
Cell
(1991)- et al.
Recurrent obstructive apneas trigger early systemic inflammation in a rat model of sleep apnea
Respir Physiol Neurobiol
(2007) - et al.
The relative importance of vascular structure and function in predicting cardiovascular events
J Am Coll Cardiol
(2004) - et al.
Simvastatin attenuates plaque inflammation: evaluation by fluorodeoxyglucose positron emission tomography
J Am Coll Cardiol
(2006) - et al.
Functional assessment of vascular reactivity after chronic intermittent hypoxia in the rat
Respir Physiol Neurobiol
(2006) - et al.
Vascular reactivity to norepinephrine and acetylcholine after chronic intermittent hypoxia in mice
Respir Physiol Neurobiol
(2003) Effect of episodic hypoxia on sympathetic activity and blood pressure
Respir Physiol
(2000)