与动脉粥样硬化王玮课件

OSASOSAS 与动脉粥样硬化与动脉粥样硬化 OSAS相关动脉粥样硬化 氧化应激与慢性炎症学说 血管内皮损伤 脂蛋白的氧化修饰 胰岛素抵抗 Evidence of early atherosclerotic development 动脉粥样硬化与炎症 炎症反应在AS的发病机制中起着重要的 作用。 C-反应蛋是应答于炎症白由肝脏合成的 细胞因子，也是发生糖尿病和心血管疾 病危险预测因子。 BeforenCPAPnCPAPBefore CRPIL-6 P 30 AHI 30 HOMA IR BMI = 24.4 BMI = 26.9 BMI = 28.4 BMI = 29.5 p 15 Homeostasis model assessment (HOMA) Fasting glucose 27:123 114 participants, 30 controls, 55 OSA CVD, 59 OSA + CVD114 participants, 30 controls, 55 OSA CVD, 59 OSA + CVD TBARS Thiobarbituric reactive substances (lipid peroxidation)TBARS Thiobarbituric reactive substances (lipid peroxidation) PD Peroxides (lipid peroxidation)PD Peroxides (lipid peroxidation) PON1 Paraxonase-1 (Esterase that protects LDL and HDL against lipid peroxidation)PON1 Paraxonase-1 (Esterase that protects LDL and HDL against lipid peroxidation) (TBARS and PD reversible by CPAP)(TBARS and PD reversible by CPAP) Tan K et al. Atherosclerosis 2006 Statistical comparison adjusted for age, gender, and BMI 0 2000 4000 6000 8000 10000 12000 OSAControl HDL dysfunction p 0.01 0 15 30 45 60 75 OSAControl Oxidized LDL (/L) P 0.05 N=128N=82 N=128N=82 AHIr = 0.51p 0.001 8-isoprostane (Ln)r = 0.22p 0.01 CRPr = 0.24p 0.001 HDL dysfunction in OSA Obstructive Sleep Apnea Sleep fragmentation/ Sleep Deprivation Oxidative Stress Neurohumor al changes Intermittent hypoxia Obesity Inflammation Insulin Resistance Dyslipidemia Hypertension Metabolic syndrome Type 2 diabetes Tasali & Ip, Proceedings of Am Thoracic Soc 2008 OSA, Metabo