Usaid K Allahwala1,2, Peter A Cistulli3,4,5, Hasthi U Dissanayake5, Michael Ward6,3, James C Weaver3,7, Ravinay Bhindi6,3. 1. Department of Cardiology, Royal North Shore Hospital, Reserve Rd, St. Leonards, Sydney, 2065, Australia. usaid.allahwala@sydney.edu.au. 2. The University of Sydney, Sydney, Australia. usaid.allahwala@sydney.edu.au. 3. The University of Sydney, Sydney, Australia. 4. Department of Respiratory & Sleep Medicine, Centre for Sleep Health and Research, Royal North Shore Hospital, Sydney, Australia. 5. Sleep Research Group, Charles Perkins Centre, School of Medicine, University of Sydney, Sydney, Australia. 6. Department of Cardiology, Royal North Shore Hospital, Reserve Rd, St. Leonards, Sydney, 2065, Australia. 7. Department of Cardiology, Royal Prince Alfred Hospital, Sydney, Australia.
Abstract
PURPOSE: Obstructive sleep apnoea (OSA) which results in hypoxia may affect the ability to recruit coronary collaterals. The aim of this study was to determine whether the severity of OSA affects collateral recruitment in patients with total coronary occlusions. METHODS: Patients with total coronary artery occlusion were reviewed. Records from the sleep investigation laboratory were reviewed to identify those patients who had undergone diagnostic polysomnography. Robust coronary collaterals were those with Rentrop grade 2 or 3 collaterals. RESULTS: Sixty-four patients with a total coronary occlusion had polysomnography performed, of whom 60 patients had OSA. Thirty-two patients (53.3%) had poor collaterals, whilst 28 (46.7%) had robust collaterals. Twenty-four (40%) patients had mild OSA, 10 (16.7%) had moderate OSA and 26 (43.3%) had severe OSA. Patients with robust collaterals were more likely to be males (96.4% vs 74.3%, p < 0.05) and have a history of hypercholesterolaemia (88.9% vs 51.6%, p < 0.01). Patients with robust collaterals had a lower apnoea-hypopnoea index (13.6 vs 45.5, p < 0.05), a higher MinSaO2 (85.4% vs 79.8%, p < 0.05), less time SaO2 < 90% (0 min vs 30.4 min, p < 0.05) and lower oxygen desaturation index (6.9 vs 26.8, p < 0.05). Those with moderate OSA had a higher mean Rentrop grade (1.6 ± 0.3) than those with mild OSA (1.5 ± 1.1) and severe OSA (0.6 ± 0.2). CONCLUSION: The presence of more severe OSA is associated with poorer coronary collateral recruitment in patients with total coronary artery occlusion. The effect of treatment of OSA on subsequent ability to recruit collaterals and other cardioprotective mechanisms requires further research.
PURPOSE: Obstructive sleep apnoea (OSA) which results in hypoxia may affect the ability to recruit coronary collaterals. The aim of this study was to determine whether the severity of OSA affects collateral recruitment in patients with total coronary occlusions. METHODS: Patients with total coronary artery occlusion were reviewed. Records from the sleep investigation laboratory were reviewed to identify those patients who had undergone diagnostic polysomnography. Robust coronary collaterals were those with Rentrop grade 2 or 3 collaterals. RESULTS: Sixty-four patients with a total coronary occlusion had polysomnography performed, of whom 60 patients had OSA. Thirty-two patients (53.3%) had poor collaterals, whilst 28 (46.7%) had robust collaterals. Twenty-four (40%) patients had mild OSA, 10 (16.7%) had moderate OSA and 26 (43.3%) had severe OSA. Patients with robust collaterals were more likely to be males (96.4% vs 74.3%, p < 0.05) and have a history of hypercholesterolaemia (88.9% vs 51.6%, p < 0.01). Patients with robust collaterals had a lower apnoea-hypopnoea index (13.6 vs 45.5, p < 0.05), a higher MinSaO2 (85.4% vs 79.8%, p < 0.05), less time SaO2 < 90% (0 min vs 30.4 min, p < 0.05) and lower oxygen desaturation index (6.9 vs 26.8, p < 0.05). Those with moderate OSA had a higher mean Rentrop grade (1.6 ± 0.3) than those with mild OSA (1.5 ± 1.1) and severe OSA (0.6 ± 0.2). CONCLUSION: The presence of more severe OSA is associated with poorer coronary collateral recruitment in patients with total coronary artery occlusion. The effect of treatment of OSA on subsequent ability to recruit collaterals and other cardioprotective mechanisms requires further research.
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