原发性高血压患者动态脉压、收缩压、舒张压、平均动脉压与内皮功能损害及左心室肥厚的关系

Associations of ambulatory pulse pressure, systolic pressure, diastolic pressure and mean arterial pressure with endothelial dysfunction and left ventricular hypertrophy in patients with essential hypertension

目的:探讨原发性高血压患者诊室或动态脉压、收缩压、舒张压及平均动脉压变化与内皮功能损害、左心室肥厚之间的关系,以了解原发性高血压后左心室肥厚、血管内皮损伤的可能机制。方法:选择1998-06/2002-11在首都医科大学宣武医院心血管内科高血压门诊就诊的初诊或停服所有降压药物2周以上的轻中度原发性高血压患者555例。根据诊室脉压及24h动态脉压水平将555例患者分为脉压≤40mmHg(1mmHg=0.133kPa)组,40mmHg<脉压≤50mmHg组,50mmHg<脉压≤60mmHg,脉压>60mmHg。以左室心肌质量指数:男性>134g/m2,女性>110g/m2作为左室肥厚的标准分为肥厚组237例,非肥厚组318例。结果:随24h动态脉压增大,血浆内皮素水平增加(P<0.01),一氧化氮水平减少(P<0.05),内皮素与一氧化氮比值增加(P<0.05)。24h动态脉压、白天脉压、夜间脉压、诊室脉压均与内皮素、内皮素/一氧化氮比值呈显著正相关(r=0.171～0.377,P<0.01);与一氧化氮呈显著负相关(r=-0.269,-0.259,-0.167,P<0.01;r=-0.141,P<0.05)。脉压较收缩压、24h动态脉压较诊室脉压与内皮素、一氧化氮的相关性更明显。而舒张压及平均动脉压与以内皮素、一氧化氮水平均无相关性。左室肥厚组较非肥厚组收缩压及脉压明显增高(P<0.001),舒张压无明显差异。

AIM:To investigate the relationships of clinical or ambulatory pulse pressure(cPP or aPP),systolic blood pressure(SBP),diastolic blood pressure(DBP),and mean arterial pressure(MAP) with endothelial dysfunction and left ventricular hypertrophy(LVH) in patients with essential hypertension(EH),so as to study the possible mechanism of LVH and endothelial damage after EH. METHODS:Totally 555 patients with mild to moderate EH were selected from the Hypertension Clinic,Department of Cardiology,Xuanwu Hospital,Capital University of Medical Sciences from June 1998 to November 2002,they were all diagnosed for the first time or had stopped all antihypertensive drugs for more than 2 weeks.According to the levels of cPP and 24-hour aPP, the 555 cases were divided into PP≤40 mm Hg(1 mm Hg=0.133 kPa)group,40 mm Hg< PP ≤50 mm Hg group,50 mm Hg< PP≤60 mm Hg group,PP >60 mm Hg group;According to their left ventricular mass index(LVMI),they were divided into LVH group(n=237,LVMI >134 g/m2 in males and >110 g/m2 in females) and non-LVH group(n=318). RESULTS:With the increase of 24-hour aPP,plasma endothelin(ET) level was increased(P< 0.01), nitric oxide(NO) level was decreased(P< 0.05),and the ratio of ET to NO(ET/NO) was increased(P< 0.05). The 24-hour aPP,day PP,night PP and cPP had significant positive correlations with ET level and ET/NO(r=0.171 to 0.377,P< 0.01),while had remarkable negative correlation with plasma No level(r=-0.269,-0.259,-0.167,P< 0.01;r=-0.141,P< 0.05).PP and 24-hour aPP had more obvious correlation with ET and NO than SBP and cPP respectively;while DBP and MAP had no correlation with ET and NO levels.SBP and PP in the LVP group were remarkably increased as compared with those in the non-LVP group(P< 0.001),while there was unobvious difference in DBP,and the main reason for the increased PP was the increase of SBP.Taking ET and NO as the dependent variables, and cPP or ambulatory SBP,DBP,PP and MAP as the independent variables,only cPP or aPP were involved in the regression equation[Results of clinical blood pressure(BP) indexes:ET =0.497×cPP+44.613(R2=0.029,P< 0.01);NO=-0.398×cPP +100.454.Results of 24-hour BP indexes:ET=1.269×24-hour PP +12.536(R2=0.090,P< 0.01);NO=-0.15×24-hour aPP +130.266(R2=0.072,P< 0.01)].Taking LVMI as the dependent variable, and cPP or 24-hour SBP, DBP,PP and MAP as independent variables, only cPP or 24-hour SBP were involved in the regression equation[Results ofclinical BP indexes:LVMI=0.405×clinical SBP+37.769(R2=0.072,P< 0.01);Results of 24-hour BP indexes:LVMI=0.611 ×24-hour SBP +19.821(R2=0.174,P< 0.01)]. CONCLUSION:Increases of both PP and SBP can lead to LVP,endothelial dysfunction and diastolic hypofunction in EH patients;Increased PP is the main decisive factor that results in the endothelial dysfunction of EH patients,with the increase of PP,vascular endothelial dysfunction is aggregated;Increased SBP is the main decisive factor that leads to LVP of EH patients;Increased DBP and MAP have no obvious influence on LVP and vascular endothelial dysfunction.