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[Sleep apnea and cardiovascular risk].
Z Kardiol. 1995 Nov; 84(11):871-84.ZK

Abstract

Obstructive sleep apnea syndrome (OSAS) is the most important form of sleep-related breathing disorders due to its high prevalence and its potential for developing cardiovascular diseases. The increased morbidity of these patients is explained by the coincidence with cardiovascular diseases, and the increased mortality of untreated patients is due to cardiovascular complications, which depend on the degree of the breathing disorder. Heavy snoring, as a partial obstruction of the upper airways, and OSAS are independent risk factors for the development of cardiovascular diseases and stroke. Causal associations exist between acute hemodynamic changes, pressure and volume load, changes in the humoral and the central nervous system, and blood gas alterations during the obstructive apnea and the long-term condition due to OSAS. Obstructive apnea can be divided into an early phase, a late phase, and a phase of the postapneic hyperventilation with respect to hemodynamic changes, blood gas alterations, and the autonomic nervous system. The most striking changes in these parameters are seen at the end of apnea and in the first resumption of breathing, with an increase in systemic and pulmonary blood pressure, decrease in stroke volume, and a distinct change in heart rate. Manifestation of systemic hypertension even in the awake state is promoted by changes in the volume system, with activation of neurohumoral changes and by a resetting of baro- and chemoreceptors. Similar mechanisms are discussed in the development of pulmonary hypertension. In this circumstance the role of hypoxemia as a causal factor for pulmonary hypertension or as a consequence due to structural changes of the pulmonary vessels is controversial. OSAS is frequent in patients with coronary heart disease and these patients must be classified as a particular risk group because of apnea-associated silent myocardial ischemia and electric instability of the myocardium. The occurrence of arrhythmia in patients with OSAS is closely related to the apnea and hyperventilation events and depends on the sympathovagal balance. Early diagnosis and suitable therapy of patients at risk not only abolishes the sleep-related breathing disorder but also improves long-term outcome.

Authors+Show Affiliations

Medizinische Universitätsklinik und Poliklinik Bonn.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

English Abstract
Journal Article
Review

Language

ger

PubMed ID

8571638

Citation

Schäfer, H, et al. "[Sleep Apnea and Cardiovascular Risk]." Zeitschrift Fur Kardiologie, vol. 84, no. 11, 1995, pp. 871-84.
Schäfer H, Koehler U, Hasper E, et al. [Sleep apnea and cardiovascular risk]. Z Kardiol. 1995;84(11):871-84.
Schäfer, H., Koehler, U., Hasper, E., Ewig, S., & Lüderitz, B. (1995). [Sleep apnea and cardiovascular risk]. Zeitschrift Fur Kardiologie, 84(11), 871-84.
Schäfer H, et al. [Sleep Apnea and Cardiovascular Risk]. Z Kardiol. 1995;84(11):871-84. PubMed PMID: 8571638.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - [Sleep apnea and cardiovascular risk]. AU - Schäfer,H, AU - Koehler,U, AU - Hasper,E, AU - Ewig,S, AU - Lüderitz,B, PY - 1995/11/1/pubmed PY - 1995/11/1/medline PY - 1995/11/1/entrez SP - 871 EP - 84 JF - Zeitschrift fur Kardiologie JO - Z Kardiol VL - 84 IS - 11 N2 - Obstructive sleep apnea syndrome (OSAS) is the most important form of sleep-related breathing disorders due to its high prevalence and its potential for developing cardiovascular diseases. The increased morbidity of these patients is explained by the coincidence with cardiovascular diseases, and the increased mortality of untreated patients is due to cardiovascular complications, which depend on the degree of the breathing disorder. Heavy snoring, as a partial obstruction of the upper airways, and OSAS are independent risk factors for the development of cardiovascular diseases and stroke. Causal associations exist between acute hemodynamic changes, pressure and volume load, changes in the humoral and the central nervous system, and blood gas alterations during the obstructive apnea and the long-term condition due to OSAS. Obstructive apnea can be divided into an early phase, a late phase, and a phase of the postapneic hyperventilation with respect to hemodynamic changes, blood gas alterations, and the autonomic nervous system. The most striking changes in these parameters are seen at the end of apnea and in the first resumption of breathing, with an increase in systemic and pulmonary blood pressure, decrease in stroke volume, and a distinct change in heart rate. Manifestation of systemic hypertension even in the awake state is promoted by changes in the volume system, with activation of neurohumoral changes and by a resetting of baro- and chemoreceptors. Similar mechanisms are discussed in the development of pulmonary hypertension. In this circumstance the role of hypoxemia as a causal factor for pulmonary hypertension or as a consequence due to structural changes of the pulmonary vessels is controversial. OSAS is frequent in patients with coronary heart disease and these patients must be classified as a particular risk group because of apnea-associated silent myocardial ischemia and electric instability of the myocardium. The occurrence of arrhythmia in patients with OSAS is closely related to the apnea and hyperventilation events and depends on the sympathovagal balance. Early diagnosis and suitable therapy of patients at risk not only abolishes the sleep-related breathing disorder but also improves long-term outcome. SN - 0300-5860 UR - https://www.unboundmedicine.com/medline/citation/8571638/[Sleep_apnea_and_cardiovascular_risk]_ DB - PRIME DP - Unbound Medicine ER -