Background: Obstructive sleep apnea hypopnea syndrome (OSAHS) is the mostcommon type of sleep-disordered breathing.It is result of repeated upper airwaycollapse during sleep caused apnea.Performance of the mouth-nasal airflow to stop butthe thoracic-abdominal respiratory movements still. American Academy of SleepMedicine will apnea is defined as more than the respiratory airflow during sleepintensity reduced by90%compared with baseline, accompanied by more than4%oxygen desaturation. Apnea the airway is completely collapse lead to the ventilationairflow interruption. The hypopnea part due to airway collapse lead to reducedventilation air flow. Studies have shown that OSAHS independently related tohypertension.The pathophysiological mechanisms of OSAHS lead to hypertension maybe intermittent hypoxia leads to sympathetic activation, RAAS system activation,oxidative stress, inflammation and endothelial dysfunction.Sympathetic activityenhancement is the main mechanism of occurrence and development of the OSASmerged EH. These mechanisms lead to the promotion of hypertension with patientswith OSAHS rhythm of blood pressure and left ventricular structure change are of greatsignificance. Neuropeptide Y (NPY) is a peptide containing36amino acid residuesneuromodulation, which widely distributed in the neurons of the central and peripheralnerve tissue. NPY and catecholamine (CA) class of neurotransmitters to norepinephrine(NE) secretory vesicles coexist in the sympathetic which released after receivingstimulation. It is also marks the sympathetic activity and in the body is relatively stablecompared with the CA, more convenient detection. Have important significance for thestudy of the OSAHS autonomic nervous system activity changeObjective To study the impact of obstructive sleep apnea-hypopnea syndrome (OSAHS) on blood pressure rhythm, left vent ricular configuration in patients with hypertensionas well as the relationship between OSAHS and autonomous nerve system.Methods Selected108patients with snore or blood pression abnormal from December2010to June2011in Department of Cardiology and Respiratory of our hospital.OSAHSpatients with hypertension (EH+OSAHS group, n=39); OSAHS patient s withouthypertension (OSAHS group, n=36); Hypertensives without OSA HS (EH group, n=33); volunteers without OSAHS and hypertension (control group, n=35).Hypertension diagnosis depend on Published diagnostic criteria of hypertensionHypertension Prevention Guide Revision Committee of Hypertension Prevention Guide(2005Revision). Hypertension was defined that:systolic BP(SBP)140mmHg and/ordiastolic BP(DBP)90mmHg to delimit the upper bounds of normal without used drug tocontrol that and previous history of hypertension, is currently used antihypertensivedrugs, blood pressure, although lower than140/90mmHg (1mmHg=0.133kPa).OSAHS used the2002Chinese Society of Respiratory credits enacted by the diagnosticcriteria: Sleep breathing process in a night7h apnea and hypopnea repeated episodes ofmore than30times or Sleep apnea-hypopnea index (AHI)≥5/h.All participants underwent polysomnography (PSG),24-hour ambulatory bloodpressure monitor (ABPM), echocardiography and measured the concentration of plasmaNPY. The diurnal mean arterial pressure values, incidence of the non-dipper bloodpressure rhythm, left vent ricular configuration and autonomous nerve system werecompared among four groups.The experimental datas were statistically analyzed bySPSS19.0software. The value of P<0.05was considered statistically significant.Results (1)The concentration of NPY in four groups were(59.4±15.1)pmol/L in controlgroup,(89.7±16.8)pmol/L in EH group,(101.1±11.6)pmol/L in OSAHS groupand(126.9±26.5)pmol/L in EH+OSAHS group.Among the groups were statisticallysignificant(P<0.05).(2)Compared with EH+OSAHS group and EH group, nodifference in the SBP day. SBP night,DBPday and DBPnight are different, are higherthan the EH group(P<0.05). SBP night, DBPnight in EH+OSAHS group are elevatoryas well as in OSAHS group, but this change was more significant in EH+OSAHS groupthan in OSAHS group(P<0.05).(3)The percentage of patient s with non-dipper blood pressure rhythm was raised gradually f rom cont rol, EH, OSAHS, to EH+OSAHSgroup. The percentage of non-dipper was significantly higher in OSAHS andEH+OSAHS than in EH(P<0.05).(4) LVDd, LVST, PWT, LVMI, RWT and thepercentage of abnormal of left ventricular configuration were significantly higher inEH+OSAHS group than in EH group. Simultaneously, the percentage of normal of leftventricular configuration was lower in EH+OSAHS group than in EH group (P<0.05).The concentration of NPY and occurrence of non-dipper blood pressure rhythm waspositively correlated. Besides concentration of NPY, BMI and hypertension, OSAHSwas the independent risk factor of left ventricular remodeling.Conclusion (1) OSAHS enhanced in hypertensive patients day and night, especiallynight sympathetic activity, destruction of the sympathetic and vagal balance andautonomic nervous system dysfunction.(2) OSAHS elevated nighttime blood pressure,so that "non-dipper blood pressure rhythm in an increased incidence.(3) OSAHShypertension in patients with baseline blood pressure levels were significantly increasedand diastolic blood pressure more.(4) OSAHS is an independent risk factor for leftventricular remodeling, and high blood pressure induced left ventricular remodeling,two concurrent, the role of overlay. |