0445 Different Mechanisms of Cardiovascular Risk in Men with OSA: The Role of the Arousal Threshold. (27th April 2018) - Appleton, S L
Abstract: Introduction: Obstructive sleep apnea (OSA) has a multifactorial aetiology. Waking up too easily to minor airway narrowing (a low respiratory arousal threshold: ArTH) contributes to OSA pathogenesis in approximately 1/3 of OSA patients. Conversely, others require substantial respiratory stimuli (ventilatory drive) to elicit cortical arousal (high arousal threshold). The extent to which the ArTH phenotype contributes to common clinical consequences of OSA such as blood pressure and glucose control is unknown. Thus, we aimed to determine relationships between the ArTH with blood pressure and glucose control. Methods: The Men Androgen Inflammation Lifestyle Environment and Stress (MAILES) Study is a population-based biomedical cohort of men aged ≥35y in Adelaide, South Australia. In 2008–10, men underwent biomedical assessment (including blood pressure, anthropometry, fasting glucose) and in 2010–12, 837 men underwent home-based full polysomnography (Embletta X100). ArTH was estimated using a 2014 published equation based on clinical and PSG data as follows: -65.391 + 0.0636*age + 3.692*1 (male sex) - 0.0314*BMI - 0.108 *apnea hypopnea index + 0.533 *oxygen saturation nadir + 0.0906 * hypopnea fraction. Pulse pressure was defined as systolic blood pressure (SBP, mmHg) - diastolic blood pressure (DBP, mmHg). Results: OSA (AHI≥10/hr) was present in 52.9% (n=443). The mean (SD) ArTH was -17.8 cmH2 O (6.5), median (IQR) was -16.2 (-19.1, -14.3) cmH2 O, n=423. ArTh was significantly correlated with DBP (r = -0.143, p<0.05) and pulse pressure (r =0.126, p<0.05). No significant correlations were evident with SBP (r =0.024, p=0.63) or fasting glucose (r =0.025, p=0.60). In multiple regression models adjusted for age, BMI, smoking and alcohol use, the significant associations with DBP [unstandardized B (SE): -0.15 (0.07), p=0.037] and pulse pressure persisted [0.24 (0.09), p=0.008]. Conclusion: The ArTH phenotype may contribute to cardiovascular risk in OSA via different mechanisms. Large negative intrathoracic pressure swings may increase blood pressure in patients with a high ArTH whereas repetitive surges in sympathetic activity may contribute to increased pulse pressure in those with a low ArTH. Support (If Any): The ResMed Foundation and NH&MRC of Australia.