Obstructive sleep apnoea in acute coronary syndrome

Abstract

Obstructive sleep apnoea (OSA) syndrome affects about 13% of the male and 7–9% of the female population. Hypoxia, oxidative stress and systemic inflammation link OSA and cardiovascular and metabolic consequences, including coronary artery disease. Current research has identified several clinical phenotypes, and the combination of breathing disturbances during sleep, systemic effects and end-organ damage might help to develop personalised therapeutic approaches. It is unclear whether OSA is a risk factor for acute coronary syndrome (ACS) and might affect its outcome. On the one hand, OSA in patients with ACS may worsen prognosis; on the other hand, OSA-related hypoxaemia could favour the development of coronary collaterals, thereby exerting a protective effect. It is unknown whether positive airway pressure treatment may influence adverse events and consequences of ACS. In non-sleepy patients with OSA and stable coronary artery disease, randomised controlled trials failed to show that continuous positive airway pressure (CPAP) treatment protected against cardiovascular events. Conversely, uncontrolled studies suggested positive effects of CPAP treatment in such patients. Fewer data are available in subjects with ACS and OSA, and results of randomised controlled studies on the effects of CPAP are expected shortly. Meanwhile, the search for reliable markers of risk continues. Recent studies suggest that daytime sleepiness may indicate a more severe OSA phenotype with regard to cardiovascular risk. Finally, some studies suggest sex-related differences. The picture is still incomplete, and the potential role of OSA in patients with ACS awaits confirmation, as well as clear definition of subgroups with different degrees of risk.

Association of Obstructive Sleep Apnea With the Risk of Repeat Adverse Cardiovascular Events in Patients With Newly Diagnosed Acute Coronary Syndrome: A Systematic Review and Meta-Analysis

“…Obstructive sleep apnea, which results in nocturnal intermittent hypoxic-reoxygenation cycle, can trigger endothelial dysfunction, sympathetic activation, and oxidative stress, subsequently leading to the formation and development of atherosclerotic plaques. 27 ApoE( À/À ) mice exposed to intermittent hypoxic environment exhibit structural vascular remodeling of the aorta that is characterized by increased intima-media thickness. 28 Similarly, patients with OSA show a larger total atheroma volume compared to non-OSA patients through intravascular ultrasound equipment.…”

Frecuencia de factores de riesgo cardiovascular en pacientes con síndrome de apnea obstructiva del sueño

“…Los resultados al respecto en la literatura son controvertidos. Si bien, como mencionamos previamente, esta relación está descrita en múltiples estudios, en 2012 se publicó un metaanálisis en el que se concluyó que la AOS parece estar asociada con ACV, pero la relación con la cardiopatía isquémica y la mortalidad cardiovascular necesita más investigación23 y otra publicación actual plantea la duda sobre si la hipoxia crónica puede estimular el desarrollo de vasos colaterales cumpliendo un papel protector o si es un factor de riesgo para un peor pronóstico después de padecer un evento cardiovascular 24 . Además, podemos atribuir el bajo RCV calculado a 10 años al bajo promedio de edad de nuestra población.…”

The relationship between inflammation and neurocognitive dysfunction in obstructive sleep apnea syndrome

“…Compared with other parts of the body, the brain requires more energy and oxygen consumption and is more sensitive to hypoxia [129]. Data provided by previous studies have generally considered that the activation of inflammation in OSAS patients is a major pathological factor associated with CVD, diabetes mellitus, and nervous system diseases such as dementia, Parkinson's disease, Alzheimer's disease, and epilepsy [8,130,131]. More importantly, inflammation causes endothelial cell dysfunction and atherosclerosis within the brain, decreasing the brain blood flow and lowering the metabolic function and oxygen consumption in neurons [132].…”