[Obstructive sleep apnoea and metabolic syndrome]. / Obstruktive Schlaf-Apnoe und metabolisches Syndrom.

Metabolic syndrome, i. e., the combined occurrence of obesity, arterial hypertension, insulin resistance and dyslipidaemia (increased triglycerides, reduced HDL cholesterol), is associated with a marked increase in cardiovascular risk. The prevalence of metabolic syndrome in patients with obstructive sleep apnoea (OSA) is very high. Obesity is the main risk factor for OSA and OSA itself is now considered to be the most frequent cause of secondary arterial hypertension. Due to the confounding influence of obesity, the causal connection between OSA and metabolic disturbances is less well established, however, epidemiological data are at least in favour of an independent link between OSA and insulin resistance. It is known that CPAP therapy can ameliorate OSA-associated hypertension. In contrast, the effects of CPAP treatment on insulin resistance and dyslipidaemia have to be further elucidated by large, randomised interventional trials.

[Sleep apnea and cardiovascular disease--results from animal studies]. / Schlaf-Apnoe und Herz-Kreislauf-Erkrankungen: Ergebnisse tierexperimenteller Studien.

Over the last decade the pathophysiology of obstructive sleep apnea (OSA)-related cardiovascular disease has been further elucidated in animal models employing dogs and rats/mice. It was demonstrated that, under the conditions of chronic intermittent hypoxia (CIH), endothelial dysfunction, i. e., a reduction in endothelial-dependent vasorelaxation, occurs. Furthermore, animals were shown to develop arterial hypertension when subjected to CIH for some weeks. Other aspects of the cardiovascular morbidity linked to OSA such as pulmonary hypertension, heart failure and atherosclerosis were also found in these animal models. The common result of these studies is that, apart from sympathetic over-activity, an increased oxidative stress seems to play a key role in the development of OSA-associated cardiovascular disease. It is anticipated that animal studies will continue to enhance our understanding of the pathogenesis of these disorders.

[Pulmonary hypertension and sleep-related breathing disorders]. / Pulmonale Hypertonie und schlafbezogene Atmungsstörungen.

Pulmonary hypertension (PH), i. e. an increase of mean pulmonary artery pressure above 20 mm Hg under resting conditions, can be observed in different forms of sleep-disordered breathing (SDB). In obstructive sleep apnea (OSA) the apnea-associated triggers of hypoxia and intrathoracic pressure swings lead to repetitive rises of pulmonary artery pressure during sleep. In 20 - 30 % of these patients daytime PH occurs. PH in the setting of OSA is usually mild and rarely causes clinically evident cor pulmonale. Effective CPAP therapy has a beneficial influence on pulmonary hemodynamics in OSA. Severe congestive heart failure (i. e. with a LVEF < 40 %) might provoke pulmonary venous hypertension and thereby stimulation of pulmonary stretch and irritant receptors. The ensuing hyperventilation leads to a decrease of pCO (2) levels below the apneic threshold and thus contributes to the emergence of Cheyne Stokes respiration (CSR) in up to one half of the affected patients. Patients suffering from advanced idiopathic pulmonary arterial hypertension (IPAH) might show a similar breathing pattern while asleep. Possible pathogenetic factors of the nocturnal periodic breathing occurring in end-stage IPAH are prolonged circulation times and hypocapnia. In conclusion, SDB might cause PH (OSA-associated PH). On the other hand, PH might lead to the development of SDB (CSR in congestive heart failure, periodic breathing in IPAH).