INTRODUCTION: Obstructive sleep apnea (OSA) has been associated with an elevated rate of cardiovascular mortality. However, this issue has not been investigated in patients with elevated proneness to cardiovascular diseases. Our hypothesis was that OSA would have an especially adverse effect on the risk of cardiovascular mortality in Finnish individuals exhibiting elevated proneness for coronary heart diseases. METHODS: Ambulatory polygraphic recordings from 405 men having suspected OSA were retrospectively analyzed. The patients were categorized regarding sleep disordered breathing into a normal group (apnea hypopnea index (AHI) < 5, n = 104), mild OSA group (5 ≤ AHI < 15, n = 100), and moderate to severe OSA group (AHI ≥ 15, n = 201). In addition, basic anthropometric and health data were collected. In patients who died during the follow-up period (at least 12 years and 10 months), the primary and secondary causes of death were recorded. RESULTS: After adjustment for age, BMI, and smoking, the patients with moderate to severe OSA suffered significantly (p < 0.05) higher mortality (hazard ratio 3.13) than their counterparts with normal recordings. The overall mortality in the moderate to severe OSA group was 26.4 %, while in the normal group it was 9.7 %. Hazard ratio for cardiovascular mortality was 4.04 in the moderate to severe OSA and 1.87 in the mild OSA group. CONCLUSIONS: OSA seems to have an especially adverse effect on the cardiovascular mortality of patients with an elevated genetic susceptibility to coronary heart diseases. When considering that all our patients had possibility of continuous positive airway pressure treatment and our reference group consisted of patients suffering from daytime somnolence, the hazard ratio of 4.04 for cardiovascular mortality in patients with moderate to severe disease is disturbingly high.
INTRODUCTION:Obstructive sleep apnea (OSA) has been associated with an elevated rate of cardiovascular mortality. However, this issue has not been investigated in patients with elevated proneness to cardiovascular diseases. Our hypothesis was that OSA would have an especially adverse effect on the risk of cardiovascular mortality in Finnish individuals exhibiting elevated proneness for coronary heart diseases. METHODS: Ambulatory polygraphic recordings from 405 men having suspected OSA were retrospectively analyzed. The patients were categorized regarding sleep disordered breathing into a normal group (apnea hypopnea index (AHI) < 5, n = 104), mild OSA group (5 ≤ AHI < 15, n = 100), and moderate to severe OSA group (AHI ≥ 15, n = 201). In addition, basic anthropometric and health data were collected. In patients who died during the follow-up period (at least 12 years and 10 months), the primary and secondary causes of death were recorded. RESULTS: After adjustment for age, BMI, and smoking, the patients with moderate to severe OSA suffered significantly (p < 0.05) higher mortality (hazard ratio 3.13) than their counterparts with normal recordings. The overall mortality in the moderate to severe OSA group was 26.4 %, while in the normal group it was 9.7 %. Hazard ratio for cardiovascular mortality was 4.04 in the moderate to severe OSA and 1.87 in the mild OSA group. CONCLUSIONS: OSA seems to have an especially adverse effect on the cardiovascular mortality of patients with an elevated genetic susceptibility to coronary heart diseases. When considering that all our patients had possibility of continuous positive airway pressure treatment and our reference group consisted of patients suffering from daytime somnolence, the hazard ratio of 4.04 for cardiovascular mortality in patients with moderate to severe disease is disturbingly high.
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