title: [Obstructive sleep apnea-related cardiovascular disease].
abstract: The clinical spectrum of obstructive sleep apnea-(OSA-)related cardiovascular disease (CVD) comprises systemic arterial hypertension (prevalence: 40-60%), pulmonary hypertension (20-30%), coronary artery disease (20-30%), congestive heart failure (5-10%), and stroke (5-10%). During sleep, heart rhythm disorders such as atrioventricular blocks, sinus arrests and atrial fibrillation can be induced by OSA. OSA-related CVD mainly affects those patients with an apnea-hypopnea index > 30/h and, if left untreated, is linked to increased mortality. Epidemiologic data have clearly shown that cardiovascular risk is increased in OSA independent of confounding factors such as obesity and concomitant metabolic disease. In recent years, the pathophysiology of OSA-related CVD has been further elucidated showing that apart from the well-known sympathetic activation, increased oxidative stress and pro-inflammatory changes seem to play major roles. Furthermore, studies using high resolution ultrasonography have demonstrated endothelial dysfunction and enhanced atherosclerosis in these patients. Finally, animal models of OSA have delineated that daytime arterial hypertension is the consequence of the OSA-associated chronic intermittent hypoxia. Therapy of OSA by continuous positive airway pressure (CPAP) ventilation exerts cardioprotective effects. It has been shown to rectify the vascular micromilieu, restore endothelium-dependent vasodilation, lower 24-h blood pressure, eliminate nocturnal heart rhythm disorders, and improve left ventricular function. Furthermore, long-term CPAP therapy leads to a reduction in important clinical endpoints such as the rates of myocardial infarction and stroke.
authors.affiliation: Medizinische Klinik II/Schlaflabor, Universitätsklinikum Giessen und Marburg, Standort Giessen, 35392 Giessen. Richard.Schulz@innere.med.uni-giessen.de
authors.forename: Richard
authors.initials: R
authors.lastname: Schulz
authors.forename: Mathias
authors.initials: M
authors.lastname: Grebe
authors.forename: Hans-Joachim
authors.initials: HJ
authors.lastname: Eisele
authors.forename: Konstantin
authors.initials: K
authors.lastname: Mayer
authors.forename: Norbert
authors.initials: N
authors.lastname: Weissmann
authors.forename: Werner
authors.initials: W
authors.lastname: Seeger
mesh_terms: D000818:Animals; D001145:Arrhythmias, Cardiac / Q000453:epidemiology; D002318:Cardiovascular Diseases / Q000453:epidemiology* / Q000401:mortality; D045422:Continuous Positive Airway Pressure; D003327:Coronary Disease / Q000453:epidemiology; D004195:Disease Models, Animal; D004285:Dogs; D004730:Endothelium, Vascular / Q000503:physiopathology; D006333:Heart Failure / Q000453:epidemiology; D006801:Humans; D006973:Hypertension / Q000453:epidemiology; D006976:Hypertension, Pulmonary / Q000453:epidemiology; D018384:Oxidative Stress; D015995:Prevalence; D051381:Rats; D012307:Risk Factors; D020181:Sleep Apnea, Obstructive / Q000150:complications* / Q000503:physiopathology / Q000628:therapy*; D020521:Stroke / Q000453:epidemiology; D013997:Time Factors; D016277:Ventricular Function, Left