RAS阻断剂治疗原发性高血压过程中醛固酮逃逸与左室肥厚关系研究

Relationship between aldosterone escape phenomena and left ventricular hypertrophy in essential hypertension treated by RAS blocker

目的:探讨伴有左心室肥厚(left ventricular hypertrophy,LVH)的原发性高血压(essential hypertension,EH)患者使用血管紧张素转换酶抑制剂(angiotensin-converting enzyme inhibitor,ACEI)和血管紧张素Ⅱ受体拮抗剂(angiotensinⅡreceptorinhibitor,ARB)治疗后有无醛固酮(aldosterone,Ald)逃逸现象及其与LVH的关系并探讨其机制。方法:将95例伴有LVH EH患者随机分为依那普利组(48例)和厄贝沙坦组(47例),用放射免疫法测定治疗前、治疗后1、3、6个月时血浆AngⅡ、Ald的活性,并用超声心动图测定室间隔厚度、左心室后壁厚度、左心室舒张末横径变化情况及检测血尿常规、血糖、血脂、肝肾功能检查,记录药物不良反应。结果:(1)治疗后2组血压均明显下降,比较两组的血压下降,差异无统计学意义(P>0.05)。(2)依那普利组治疗1、3、6个月后血AngⅡ较治疗前明显下降差异有统计学意义,治疗3、6个月后与1个月比较AngⅡ轻度升高,但差异无统计学意义(P>0.05);而Ald治疗1个月后下降较治疗前差异有统计学意义(P<0.05),治疗3、6个月后则升高,接近治疗前水平,与治疗前比较差异无统计学意义(P>0.05)。厄贝沙坦组血AngⅡ治疗后1个月与治疗前比较上升,但差异无统计学意义,治疗3、6个月时较治疗前上升,差异有统计学意义;血Ald治疗后1、3、6个月浓度明显下降,与治疗前比较差异有统计学意义(P<0.05)。(3)依那普利组、厄贝沙坦组均能逆转LVH。左心室重量、左心室重量指数下降(组内治疗前后比较P<0.05,组间P>0.05)。2组部分患者血浆Ald水平在初期下降,在治疗3个月以后,血浆中Ald水平再度升高且高于治疗前水平即Ald逃逸,治疗6月后依那普利组有19例,厄贝沙坦组2例。有逃逸现象的患者LVH逆转差,差异有统计学意义。结论:应用ACEI或ARB治疗EH患者过程中存在Ald逃逸现象,且该部分患者LVH逆转差,临床工作中应尽早发现并积极对症治疗。

Objective：To investigate the relationship between aldosterone escape phenomena and left ventricular hypertrophy（LVH）in essential hypertension（EH） treated by angiotensin-converting enzyme inhibitor（ACEI） and angiotensin II receptor inhibitor blocker （ARB）. Methods：Totally 95 cases of EH complicated with LVH were randomly divided into enalapril group（n=48） and irbesartan group （n=47）. Angiotensin il （Ang I[ ）, aldosterone （Aid）, interventricular septal thickness （IVST）, left ventricular posterior wall thickness （PWT）and left ventricular end diastolic diameter（LVDD） levels were examined before therapy and at 1,3,6 months after thera- py. Results：（ 1）Levels of blood pressure were decreased in both groups and there was no significant difference between two groups （P 〉0.05）. （2）In enalapril group, Ang II levels were all decreased significantly （P 〈0.05） at 1,3,6 months after therapy. Ang II levels were slightly increased at 3,6 months after therapy compared with those at 1 month after therapy, but without statistical differences （P〉0.05）. Ald levels were decreased significantly at 1 month after therapy compared with those before therapy（P〈0.05） but they were increased at 3,6 months after therapy, reaching the levels before therapy （P〉0.05）. In irbesartan group, Ang II levels were increased at 1 month after therapy compared with those before therapy, without statistical differences but they were increased at 3,6 months after therapy compared with those before therapy,with statistical differences（P〈0.05）. Levels of Aid were all decreased significantly at 1,3,6 months after therapy compared with those before therapy（P〈0.05）. （3）IVST,PWT,LVDD levels were decreased in both groupsafter therapy compared with those before therapy（P〈0.05） but there was no significance between two groups. Aid levels of some patients（19 patients in enalapril group and 2 patients in irbesartan group） were initially decreased but were increased after 3 months＇ therapy compared with those before therapy,which was called Ald escape. LVH ameliorations of these paitents were quiet. Conclusions ：Aid escape may occur in EH treated by ACEI and ARB. LVH ameliorations in these paitents with Ald escape phenomena are quiet.