IMD1-53 Role In Hypertension Carotid Atheromatous Plaque Formation And Intervention Study

Objectives:Explore intermedin 1-53(IMD1-53)in hypertension carotid atheromatous plaque(atheromatous plaque,AP)role in the formation of and intervention study.Methods:In January 2012 to June 2014 in our hospital without drug therapy(including a history of high blood pressure,but not the medication,a new diagnosis of hypertension)grade Ⅰ～Ⅱ hypertension patients,a total of 138 cases,76 cases of male,female 62 cases,aged 42～78(55.21 + 10.43);Average duration(11.61 + 8.32)years.Ambulatory blood pressure and carotid ultrasound,blood IMD1-53 level check,etc.Based on carotid ultrasound check for plaques in carotid artery atheromatous plaque formation groups(hereinafter referred to as the AP group)and carotid artery atheromatous plaque group(hereinafter referred to as the NAP group),setting up a group of 30 cases of healthy people,the comparison between groups,dynamic characteristics of blood pressure,blood pressure level IMD1-53 level indicator,etc.According to the plaque risk AP into a stable plaque group and group of vulnerable plaques,compared two groups of blood pressure levels,carotid intima-media thickness,carotid intima-media thickness,cIMT),IMD1-53.According to different intervention treatment to AP group is divided into three groups,respectively,to give without perindopril captopril tablet 4 mg qd,amlodipine capsule 5 mg qd and hydrochlorothiazide tablets 12.5 mg qd 12 months intervention,intervention after end of carotid artery ultrasound,blood IMD1-53 level,such as inspection,compared before and after the intervention of blood pressure level,cIMT,IMD1-53 levels,carotid atheromatous plaque and total integral Crouse indicators.Results:AP group,the NAP group office blood pressure,cIMT,IMD1-53 levels were higher than in normal group,the difference was statistically significant(P<0.05);AP group office blood pressure,cIMT,IMD1-53 levels higher than the NAP group,the difference was statistically significant(P<0.05).In ambulatory blood pressure parameters,AP group of 24 24 HNSBP HSBP,24 HDSBP,the NAP group is high,the difference was statistically significant(P<0.05),the dipper type blood pressure ratio in the AP group is slightly lower than the NAP group,but there was no statistically significant difference between(P>0.05).In ambulatory blood pressure of various parameters,24 HNSBP high relatively stable plaque group,the difference was statistically significant(P<0.05),and IMD1-53 level is high stable plaque group,the difference was statistically significant(P<0.05).Without perindopril captopril group,amlodipine group,hydrochlorothiazide IMD1-53 level before treatment,patch parameters(including patch number,patch diameter,the maximum thickness and total integral Crouse plaque),cIMT indicators no significant difference in statistics(P>0.05).Group after intervention treatment,without perindopril split and amlodipine group IMD1-53 levels before and after the treatment,each patch parameters except(number of patches),cIMT indicators are significantly lower,the difference was statistically significant(P<0.05).Hydrochlorothiazide group IMD1-53 levels before and after the treatment,plaque parameters,cIMT index declined,but there was no significant difference statistically(P>0.05).Without perindopril split with amlodipine group IMD1-5 3 level between the two groups after treatment,plaque parameters,cIMT index is no significant difference statistically(P>0.05).Conclusions:IMD1-53 levels rise,as the blood pressure increases in hypertension in the formation of carotid artery atheromatous plaque increased more obviously,and particularly elevated in patients with vulnerable plaques.After drug intervention,as the blood pressure to drop,IMD1-53 level also fell,after carotid atheromatous plaque improve IMD1-53 level drops more apparent.In clinic,this study concludes that IMD1-53 from many aspects involved in the formation of carotid atherosclerotic plaques,resistance or slow down the role of carotid artery atheromatous plaque formation,its mechanism is complicated,but independent of the RAS system,expanded the mechanism of vascular remodeling.