Progress in cardiovascular diseases
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Obstructive sleep apnea, aldosterone excess, and resistant hypertension are common comorbidities in obese patients. The mechanisms that link these conditions are not fully elucidated, but sympathetic nervous system activation, sodium retention, renin-angiotensin-aldosterone system stimulation, endothelial dysfunction, and increased production of reactive oxidative species may be contributing factors. Patients diagnosed with this triad should be treated with low-salt diet, weight-loss counseling, and continuous positive airway pressure, as well as aggressive antihypertensive therapy, usually with multiple agents, including a mineralocorticoid receptor antagonist. Patients with aldosterone-producing adenoma may require adrenalectomy.
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Obstructive sleep apnea (OSA) is associated with repetitive nocturnal arterial oxygen desaturation and hypercapnia, large intrathoracic negative pressure swings, and acute increases in pulmonary artery pressure. Rodents when exposed to brief, intermittent hypoxia for several hours per day to mimic OSA developed pulmonary vascular remodeling and sustained pulmonary hypertension and right ventricular hypertrophy within a few weeks. Until recently, however, it was unclear whether episodic nocturnal hypoxemia associated with OSA was sufficient to cause similar changes in humans. ⋯ The pulmonary hypertension associated with OSA appears to be mild and may be due to a combination of precapillary and postcapillary factors including pulmonary arteriolar remodeling and hyperreactivity to hypoxia and left ventricular diastolic dysfunction and left atrial enlargement. Although measurable changes in the structure and function of the right ventricle have been reported in association with OSA, the clinical significance of these changes is uncertain. Right ventricular failure in OSA appears to be uncommon and is more likely if there is coexisting left-sided heart disease or chronic hypoxic respiratory disease.
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Prog Cardiovasc Dis · Mar 2009
ReviewObstructive sleep apnea and cardiovascular disease: a perspective and future directions.
Data from animal and human studies provide a biological plausibility to the notion that obstructive sleep apnea activates pathways that lead to insulin resistance, atherosclerosis and hypertension. Sleep apnea thus activates the same pathways as does obesity. That obstructive sleep apnea is a risk factor for cardiovascular disease is supported by epidemiological association studies. ⋯ Data from randomized treatment trials for cardiovascular endpoints will likely not be available for many years. In the interim, physicians need to consider how to treat such patients. It is proposed that given that CPAP treatment for obstructive sleep apnea is highly effective and essentially totally safe, and that the evidence is suggestive that sleep apnea is a risk factor for cardiovascular disease, then we propose all patients with severe sleep apnea should be treated to reduce cardiovascular risk.
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Obstructive sleep apnea (OSA) is associated with significant cardiovascular morbidity and excess in mortality. Atherosclerosis has been shown to occur in OSA patients free of any other significant risk factors. In particular, intima media thickness, an early marker of atherosclerosis, may be increased at the carotid level in OSA. ⋯ Early changes at the vascular wall level have been shown in OSA patients and its reversibility under continuous positive airway pressure has also been suggested. Several biological markers potentially linked with early atherosclerosis development are under study in OSA patients. Further studies are needed to identify at-risk subjects prone to develop vascular changes because OSA treatment may either be initiated earlier or combined with specific drug treatments.
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Prog Cardiovasc Dis · Jan 2009
ReviewCardiovascular, inflammatory, and metabolic consequences of sleep deprivation.
That insufficient sleep is associated with poor attention and performance deficits is becoming widely recognized. Fewer people are aware that chronic sleep complaints in epidemiologic studies have also been associated with an increase in overall mortality and morbidity. This article summarizes findings of known effects of insufficient sleep on cardiovascular risk factors including blood pressure, glucose metabolism, hormonal regulation, and inflammation with particular emphasis on experimental sleep loss, using models of total and partial sleep deprivation, in healthy individuals who normally sleep in the range of 7 to 8 hours and have no sleep disorders. These studies show that insufficient sleep alters established cardiovascular risk factors in a direction that is known to increase the risk of cardiac morbidity.