Obstructive Sleep Apnea and Cardiovascular Risk

Abstract

Obstructive sleep apnea syndrome (OSAS) is a chronic condition characterized by recurrent episodes of partial or complete upper airway collapse during sleep. OSAS presents with intermittent hypoxia, increased respiratory effort, sleep fragmentation, and disruptive snoring together with daytime somnolence. Observational data showed that OSAS is associated with an increased risk of cardiovascular (CV) events. The increased incidence of cardiac arrhythmias (atrial fibrillation, ventricular arrhythmias, and sudden cardiac death) and heart failure could help explain the high CV mortality associated with OSAS. Since all these complications are manifestations of atherosclerotic vascular disease, it was postulated that OSAS may promote atherosclerosis. Therefore, it is relevant to investigate potential associations of OSAS with established vascular risk factors. Hypertension is an established CV risk factor associated with the presence of OSAS. This association may be independent of the presence of obesity. Treatments for OSAS may achieve small decreases in blood pressure (BP). Intermittent hypoxia promotes persistent elevations of BP by enhancing sympathetic tone, while inducing oxidative stress, inflammation, and endothelial dysfunction. The OSASrelated hypertension has a diastolic predominance and a nondipping pattern, while resistant hypertension is frequent due to increased levels of plasma aldosterone. Of interest, it was suggested that OSAS and hypertension may have additive independent effects on atherosclerosis. In this context, hypertension may not be the only CV risk factor associated with OSAS. The predominance of small dense low-density lipoprotein (sdLDL) particles is considered a predictor of CV events. In this issue of Angiology, Sopkova et al report that the presence of metabolic syndrome (MetS), but not OSAS, independently predicted the small size of lowdensity lipoprotein particles in patients with OSAS. MetS is a cluster of risk factors that include abdominal obesity, insulin resistance, elevated BP, and atherogenic dyslipidemia (levels of high triglycerides [TG] and low highdensity lipoprotein cholesterol [HDL-C]). MetS is considered a proinflammatory and procoagulant state associated with increased sympathetic activity, endothelial dysfunction, and higher cholesterol concentration of the atherogenic sdLDL. Thus, MetS promotes atherogenesis and increases the risk of CV events. In the study by Sopkova et al, among MetS components, levels of low HDL-C and high TG were the major independent determinants of sdLDL in patients with OSAS. This is in accordance with our previous findings that increased levels of TG and waist circumference comprise the main predictors of increased concentration of sdLDL in MetS. This finding implies that increased atherogenesis in OSAS may, at least in part, be mediated by the presence of MetS. All components of MetS, including hypertension, insulin resistance, and low HDL-C, together with high levels of TG are frequent in patients with OSAS. Furthermore, HDL may be dysfunctional in these patients. Habitual snoring, as a surrogate marker of OSAS, was associated with the number of MetS components in a dose-dependent manner. Therefore, it is not surprising that the prevalence of MetS is increased in patients with OSAS. In this context, OSAS was considered as a ‘‘manifestation of MetS.’’ Also, the coexistence of these conditions has been termed as ‘‘syndrome Z.’’ It is difficult to settle a causal relationship between MetS and OSAS since they share common predisposing factors. These factors include increased age, obesity, and unhealthy lifestyle (sedentary lifestyle, smoking, and excessive alcohol intake). Interestingly, it was suggested that the association of MetS, or its components, with OSAS may be independent of