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Sleep Apnea may Increase Risk of Atherosclerosis
Helen Goodridge 07/Sep/04
Clinical Newswire Sept. 6, 2004 (GLASGOW, UK) - Increased deposition of cholesterol in the arteries may explain the link between sleep apnea and cardiovascular disease according to two studies presented at the 14th Annual Congress of the European Respiratory Society (ERS) in Glasgow, Scotland.

Patients with sleep apnea, which is characterised by frequent nocturnal disruption of breathing, experience excessive daytime sleepiness and fatigue, and additionally, may be at higher risk of developing cardiovascular disease.

Dr. Viliam Donic and colleagues at the Kosice University Hospital in Slovakia examined the relationship between apnea and atherosclerosis by ultrasound scanning of the carotid arteries. The thickness of the internal layers of the artery walls (intima-media thickness, IMT) is a reliable indicator of the size of fatty deposits typically found in atherosclerosis. Dr. Donic told delegates in Glasgow that the intima-media was markedly thicker in patients with sleep apnea than healthy controls (0.83 ± 0.13 mm compared with 0.67 ± 0.12 mm; p=0.004). Furthermore, patients with either arterial hypertension or coronary artery disease had significantly more atherosclerosis when also suffering from sleep apnea, compared to non-apneic subjects (0.9 ± 0.19 mm and 0.8 ± 0.19 mm respectively; p<0.03). “An intima-media thickness of more than 0.85 mm is considered to represent coronary sclerosis,” Dr Donic explained.

Another study, performed in Italy at the Catholic University of the Sacred Heart in Rome, showed a similar correlation between IMT and sleep apnea. Dr. Flaminio Mormile and colleagues analysed 29 patients who had recently been diagnosed with sleep apnea and who had not yet been treated. They performed carotid ultrasonography in addition to cardiorespiratory monitoring, lung function tests and blood gas analysis. When patients were classified according to their IMT, a significantly higher number of abnormal respiratory events per hour of sleep were recorded among patients with an IMT greater than 1.22 mm (an apnea-hypopnea index of 47.2 ± 24 events/hour) compared to those with an IMT of less than 1.05 mm (29.3 ± 11 events/hour; p<0.05). Conversely, when patients were classified according to the severity of their sleep apnea, those with more than 45.2 events/hour had significantly thicker carotid artery walls than those with fewer than 24 events/hour (1.29 ± 0.2 mm compared with 1.0 ± 0.3 mm; p<0.023). There were no apparent differences in common risk factors for atherosclerosis between the groups to account for this variation.

Analysis of blood gases yielded some surprising results. “Patients who, in our study, presented this strong link between apnea and atherosclerosis, were found to have a normal blood oxygen concentrations,” Dr. Mormile said. In fact, there was an inverse correlation between IMT and nocturnal hypoxia. Patients with frequent apnea had higher mean oxygen pressures (mean SaO2 93.8 ± 17 mm Hg, compared with 79 ± 16 mm Hg in patients with less frequent apnea; p=0.006) and lower daytime CO2 levels.

Although investigation of larger patient groups is required, these two studies indicate that effective treatment of sleep apnea may help limit atherosclerosis and thereby prevent the development of cardiovascular disease.

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