| Affiliation: | BG-Kliniken Bergmannsheil, Universitätsklinikum der Ruhr-Universität Bochum, Med. Klinik III, Bochum, Germany; Sleep Laboratory, Pulmonary Medicine, Sahlgrenska University Hospital, Gothenburg, Sweden; Abt. Kardiologie und Pneumologie, Georg-August-Universität Göttingen, Göttingen, Germany; Med. Klinik II, Universität Giessen, Giessen, Germany; Ruhrlandklinik, Abt. Pneumologie, Schlaf- und Beatmungsmedizin, Essen, Germany; Fachklinik Rhein-Ruhr, Abt. Neurologie, Essen, Germany; Abt. für Pneumologie, Schlafmedizinisches Labor, Universität Marburg, Marburg, Germany; Ev. Johannes Krankenhaus, Neurologische Klinik, Bielefeld, Germany; Med. Klinik, Kardiologie, Pneumologie, Angiologie, Schlafmedizinisches Zentrum, Charité, Berlin, Germany; Zentrum für Pneumologie und Thoraxchirurgie, Großhansdorf, Germany; Klinik für Pneumologie, Klinik Ambrock, Universität Witten/Herdecke, Hagen, Germany; Kliniken St. Antonius, Akad. Lehrkkh. Universität Düsseldorf, Zentrum f. Innere Med., Schwerpunkt Pneumologie, Wuppertal, Germany; Bethesda Krankenhaus Wuppertal GmbH, Med. Klinik, Wuppertal, Germany; Klinikum Saarbrücken, Abt. für Pneumologie, Saarbrücken, Germany; Medizinische Fakultät / Klinikum der Universität Rostock, Abt. Pneumologie, Rostock, Germany |
| Abstract: | Summary The purpose of this review is to summarize current knowledge about the link between sleep-disordered breathing (SDB) and cardiovascular and cerebrovascular diseases. Obstructive sleep apnoea (OSA) is a well-established risk factor for systemic arterial hypertension, and its treatment with continuous positive airway pressure leads to a decrease in daytime and night-time blood pressure profiles. Pulmonary arterial hypertension occurs in 20–30% of OSA patients and is usually mild. It is not yet clear if OSA per se leads to pulmonary hypertension or if the coexistence of chronic obstructive pulmonary disease with daytime and/or sleep-related hypoxaemia is required to provoke a persistent rise in pulmonary artery pressure. Furthermore, OSA is associated with nocturnal cardiac arrhythmias, especially cyclical fluctuations of the heart rate in response to recurrent apnoeas. Atrioventricular conduction blocks and ventricular premature beats are less often observed and seem to be confined to patients with severe OSA and those with accompanying ischaemic heart disease. The association between OSA and vaso-occlusive disease (i.e. atherosclerosis) is less clear. However, accumulating experimental and epidemiological data support such a link. Thus, OSA may lead to coronary artery disease (CAD) and stroke by promoting atherosclerosis. Correspondingly, patients with CAD or acute stroke show a high prevalence of SDB. Cheyne–Stokes respiration (CSR) is a specific pattern of central sleep apnoea occurring in patients with advanced congestive heart failure (CHF). If present, CSR clearly has a negative impact on the clinical course of CHF. Although the optimal treatment strategy for CSR is less well defined than that for OSA, the successful reversal of CSR might increase overall survival in affected patients. |
