AIM: The aim of this long-term prospective study was to evaluate the effect of treating obstructive sleep apnoea (OSA) on the rate of cardiovascular events in coronary artery disease (CAD). METHODS AND RESULTS: We prospectively studied 54 patients (mean age 57.3 +/- 10.1 years) with both CAD (> or = 70% coronary artery stenosis) and OSA (apnoea-hypopnoea index > or = 15). In 25 patients, OSA was treated with continuous positive airway pressure (n=21) or upper airway surgery (n=4); the remaining 29 patients declined treatment for their OSA. The median follow-up was 86.5 +/- 39 months. The two groups were similar at baseline in age, body mass index, smoking history, hypertension, hypercholesterolaemia, diabetes mellitus, number of diseased vessels, left ventricular ejection fraction, and CAD therapy. Treatment of risk factors other than OSA was similar in the two groups. The endpoint (a composite of cardiovascular death, acute coronary syndrome, hospitalisation for heart failure, or need for coronary revascularisation) was reached in 6 (6/25, 24%) and 17 (17/29, 58%) patients with and without OSA treatment, respectively (P<0.01). OSA treatment significantly reduced the risk of occurrence of the composite endpoint (hazard ratio 0.24; 95% confidence interval, 0.09-0.62; p<0.01) and of each of its components. CONCLUSIONS: Our data indicate that the treatment of OSA in CAD patients is associated with a decrease in the occurrence of new cardiovascular events, and an increase in the time to such events.
AIM: The aim of this long-term prospective study was to evaluate the effect of treating obstructive sleep apnoea (OSA) on the rate of cardiovascular events in coronary artery disease (CAD). METHODS AND RESULTS: We prospectively studied 54 patients (mean age 57.3 +/- 10.1 years) with both CAD (> or = 70% coronary artery stenosis) and OSA (apnoea-hypopnoea index > or = 15). In 25 patients, OSA was treated with continuous positive airway pressure (n=21) or upper airway surgery (n=4); the remaining 29 patients declined treatment for their OSA. The median follow-up was 86.5 +/- 39 months. The two groups were similar at baseline in age, body mass index, smoking history, hypertension, hypercholesterolaemia, diabetes mellitus, number of diseased vessels, left ventricular ejection fraction, and CAD therapy. Treatment of risk factors other than OSA was similar in the two groups. The endpoint (a composite of cardiovascular death, acute coronary syndrome, hospitalisation for heart failure, or need for coronary revascularisation) was reached in 6 (6/25, 24%) and 17 (17/29, 58%) patients with and without OSA treatment, respectively (P<0.01). OSA treatment significantly reduced the risk of occurrence of the composite endpoint (hazard ratio 0.24; 95% confidence interval, 0.09-0.62; p<0.01) and of each of its components. CONCLUSIONS: Our data indicate that the treatment of OSA in CAD patients is associated with a decrease in the occurrence of new cardiovascular events, and an increase in the time to such events.
Authors: Dominik Linz; Holger Woehrle; Thomas Bitter; Henrik Fox; Martin R Cowie; Michael Böhm; Olaf Oldenburg Journal: Clin Res Cardiol Date: 2015-04-23 Impact factor: 5.460
Authors: Girardin Jean-Louis; Ferdinand Zizi; Luther T Clark; Clinton D Brown; Samy I McFarlane Journal: J Clin Sleep Med Date: 2008-06-15 Impact factor: 4.062