Research On The Correlation Of Serum Copeptin With Obstructive Sleep Apnea Hypopnea Syndrome Associated Hypertension

ObjectivesObstructive sleep apnea-hypopnea syndrome（OSAHS）is considered the most common breathing disorder that occurs during sleep and has been already shown to be an independent risk factor of systemic diseases such as hypertension,ischemic heart disease and cerebral vascular disease.Many factors could regulate OSAHS associated hypertension in pathogenesis mechanism.The purpose of this study was to investigate the roles of plasma copeptin in the pathophysiology of OSAHS and OSAHS associated hypertension.MethodsFollowing the overnight polysomnographic examinations,all patients with OSAHS were divided into two groups:29 patients with obstructive sleep apnea-hypopnea syndrome without complications（OSAHS group）and27 patients with OSAHS associated hypertension（OSAHS+HT group）.There were 30 healthy adults in control subjects（N group）who were excluded OSAHS and HT.First,the plasma concentrations of copeptin by the ELISA method,right upper extremity arteria brachialis blood pressure before sleep（MAPn）and after wakening（MAPd）,apnea-hypopnea index（AHI）,oxygen desatur-ation index（ODI）,the percentage of total sleep time spent with SpO₂<90%（Ts90%）,the longest apnea time（LAT）,mean arterial oxygen saturation（MSaO₂）and lowest arterial oxygen saturation（LSaO₂）were measured respectively.Compare the difference of the variables among 3 groups and the correlations between copeptin and the variables in OSAHS group and OSAHS+HT group.Second,the patients with OSAHS+HT accepted nasal continuous positive airway pressure（nCPAP）therapy.The plasma concen-trations of copeptin,right upper extremity arteria brachialis blood pressure before sleep and after wakening,AHI,ODI,Ts90%,LAT,MSaO₂ and LSaO₂ were measured and compared again after 3-month treatment with nCPAP.Results1.The differences in the polysomnographic parameters in sleep-disordered breathing such as AHI、ODI、Ts90%、LAT、MSaO₂ and LSaO₂ among the three groups were statistically significant each other（P<0.001）.There were significant differences of AHI,Ts90%and MSaO₂among any two groups（P<0.05）.2.The plasma copeptin concentrations gradually increased among control group,OSAHS group and OSAHS+HT group[separately were（170.57±59.68）pg/ml,（203.32±53.71）pg/ml,（233.11±39.05）pg/ml].There were significant differences among three groups（F=11.431,P<0.001）and the significant differences was observed among any two groups（P<0.05）.There were significant differences of MAPn and MAPd among three groups（P<0.001）.3.The plasma copeptin concentrations were correlated positively with AHI,ODI,Ts90%,LAT and negatively with the MSaO₂ both in OSAHS and OSAHS+HT patients（P<0.05）,but no closely correlation with LSaO₂.4.The plasma copeptin levels were correlated positively withMAPn（r=0.631,P<0.05）and MAPd（r=0.756,P<0.05）in OSAHS patients and were correlated positively with MAPn（r=0.756,P<0.05）and MAPd（r=0.808,P<0.05）OSAHS+HT patients as well.5.The regression equation obtained by multiple regression analysis was as follow:copeptin=5.506+0.939×AHI+1.426×MAPn+0.849×ODI（F=31.604,P<0.001）and suggested that AHI,MAPn and ODI were independently associated with plasma copeptin level.6.After the three-month nCPAP therapy,improvements were noted in the polysomnographic parameters in sleep-disordered breathing such as AHI（4.33±1.80）,ODI（4.28±2.64）,Ts90%[median,2.9（Q1-Q3:2.1-4.8%）],LAT（23.46±12.89s）,MSaO₂[median,96（Q1-Q3:95-97%）]and LSaO₂[median,84.5（Q1-Q3:80.6-86.8%）]（P<0.001）.MAPn（103.54±6.14mmHg）and MAPd（107.39±9.46mmHg）were significantly decreased（P<0.001）.The plasma copeptin concentrations（223.25±52.73pg/ml）were also significantly decreased（P=0.027）.ConclusionsCopeptin levels were high in OSAHS patients and more pronounced in OSAHS+HT patients.It indicated that hyperactivation of the arginine vasopressin system which was closely related to copeptin seems to be a contributor and/or a consequence in the occurrence and development of OSAHS associated hypertension.